2012 Report of Cancer Statistics (PDF) - Karmanos Cancer Institute

Cancer Statisticsin Metropolitan Detroit 2012Metropolitan Detroit Cancer Surveillance SystemSurveillance, Epidemiology and End Results ProgramDecember 2012

Table of ContentsTable of Contents 1Metropolitan Detroit Cancer Surveillance System (MDCSS) 2Geographic Coverage Area 3Population Estimates 4Michigan Department of Community Health Collaboration,and MDCSS Authority to Collect Cancer Data 5Cancer Trends, Incidence, Mortality and Survival in Metropolitan Detroit 6Temporal Cancer Trends 7Cancer Incidence and Mortality: All Races 8Cancer Incidence and Mortality: Whites 10Cancer Incidence and Mortality: African-Americans 12Survival Analysis by Stage: Prostate Cancer 14Survival Analysis by Stage: Female Breast Cancer 15Survival Analysis by Stage: Lung Cancer 16Survival Analysis by Stage: Colorectal Cancer 17Cancer Research at MDCSS 18The Young Women’s Health History Study -Breast Cancer Risk Factors in Young Women 19Risk Factors for Ovarian Cancer in African-American Women 20Patterns of Care Study 21Genetic Pathways of Inflammation and Risk of Lung Cancerand Chronic Obstructive Pulmonary Disease 22The Epidemiology Research Core 24List of Studies Conducted at the MDCSS 25MDCSS/SEER Publications 2010-2012 28Affiliations and Acknowledgements 32MDCSS Participating Institutions 33Appendix A: Michigan Public Health Code and HealthInsurance Portability and Accountability Act (HIPAA) Excerpts 34Credits 36

Metropolitan Detroit Cancer Surveillance System (MDCSS)and Surveillance, Epidemiology and End Results (SEER) CancerProgram Description and GoalsProgram DescriptionProgram Goals2The Metropolitan Detroit Cancer Surveillance System (MDCSS)has been recording data on cancer in Wayne, Oakland and MacombCounties since 1973. Cancer is a reportable disease under Stateof Michigan law. The MDCSS is the arm of the Michigan Departmentof Community Health (MDCH) responsible for the collectionand reporting of cancer data for residents of the tri-county area.The MDCSS is also one of 20 cancer registries in the United Statesproviding cancer data to the National Cancer Institute as part of theSurveillance, Epidemiology and End Results (SEER) Program.The SEER Program was established pursuant to the National CancerAct of 1971. The MDCSS is a founding participant in that programand is now completing its 40th year of data collection as a SEERRegistry.The MDCSS has a staff of more than 50 people who collect datafrom hospitals, laboratories, radiation centers and other facilitiesthat serve cancer patients. A follow-up program tracks more than95% of the cancer survivors diagnosed since 1973, providing yearlyupdates on their vital status. Funding for the registry is provided bythe National Cancer Institute to Wayne State University. Additionalfunding for research studies is provided by the National CancerInstitute and other agencies through grants and contracts anddistributed to university, state and national researchers investigatingcancer-related topics. Strict rules are in place to preserve theconfidentiality of individual patient information and the hospitalsand physicians who provide these data.The national SEER Program collects cancer data on approximately28% of the United States population. Participating registries arechosen in part for the special populations represented within theirborders. The Detroit tri-county area is an ideal location because ofits urban, industrial setting and diverse population. The goals of theDetroit SEER Program are to:1. Assemble and report estimates of cancer incidence, survival andmortality in the tri-county area.2. Monitor annual cancer trends to identify unusual changes inspecific forms of cancer in population subgroups.3. Provide information on changes over time in the extent of diseaseat diagnosis, therapy and patient survival.4. Promote and conduct studies designed to identify factors leadingto cancer causes, prevention and control.5. Respond to requests from individuals and organizations for dataon cancer in the tri-county area.Over the past 40 years, we have seen remarkable improvements incancer diagnosis and therapy. Early detection leads to improved survival.In fact, mortality from cancer has decreased in recent years,which is most likely due to early detection and better therapies.

Geographic Coverage Area:Metropolitan DetroitThe MDCSS and the MetropolitanDetroit SEER Programprovide reporting for Wayne,Oakland and Macomb countiesin southeastern Michigan.These three counties are hometo 3,863,924 people, approximately39% of the total statepopulation. There are 1,820,584individuals residing in WayneCounty, 39% of those in the Cityof Detroit, which has a populationof 713,777. Oakland Countyresidents number 1,202,362and Macomb County has thesmallest population of thethree, with 840,978 residents.About 69% of the population inthe tri-county area are Whiteand 26% African-American. Anadditional 5% of the populationare of other races, primarilyAsian and Native American orare multi-racial. (U.S. Census2010.) As of the 2010 census,persons of Hispanic ethnicitymade up about 4% of the totalpopulation. The tri-county areaalso has great ethnic diversity,which includes groups of Polish-,German-, Italian-, andArab-Americans.In 2010, there were 24,651 newinvasive and in situ cancersdiagnosed in residents of themetropolitan Detroit (tricounty)area. This is about halfthe number reported for theentire state. Because of thelarge population encompassedin the metropolitan Detroitarea and the diversity foundhere, the MDCSS is especiallyvital to both State of Michiganand national cancer statisticsreporting.Newly Diagnosed Invasive and In Situ Cancersin the Metropolitan Detroit Area (2010)11,3147,7975,540New CancersWayne CountyNew CancersOakland CountyNew CancersMacomb County3

Population by Age, Sex, Race and Ethnicityin Metropolitan Detroit, 2011OAKLANDMACOMBWAYNE4WHITEAFRICAN-AMERICANAMERICAN INDIAN/ALASKA NATIVEASIAN/PACIFICISLANDERHISPANIC *ALL RACESAGE MALE FEMALE MALE FEMALE MALE FEMALE MALE FEMALE MALE FEMALE MALE FEMALE00-04 years 74,443 71,227 37,033 35,689 783 760 6,291 5,934 9,101 8,736 118,550 113,61005-09 years 82,624 78,660 36,392 34,865 777 819 6,915 6,755 8,921 8,739 126,708 121,09910-14 years 89,203 84,559 40,276 39,271 847 844 6,264 5,988 7,966 7,714 136,590 130,66215-19 years 87,808 81,699 44,995 43,715 889 923 5,211 4,599 7,346 6,890 138,903 130,93620-24 years 77,771 75,432 38,494 41,051 782 757 4,373 4,410 6,263 5,875 121,420 121,65025-29 years 79,629 78,017 27,689 32,977 673 671 5,369 5,894 6,455 6,027 113,360 117,55930-34 years 80,248 78,917 26,928 34,046 652 764 6,109 7,331 6,770 6,365 113,937 121,05835-39 years 80,373 79,405 29,062 37,611 696 739 7,062 7,992 6,221 5,975 117,193 125,74740-44 years 95,525 94,753 30,739 38,345 750 836 6,972 6,879 5,426 5,118 133,986 140,81345-49 years 104,613 104,665 29,734 36,356 742 808 5,821 5,636 4,496 4,434 140,910 147,46550-54 years 110,011 112,777 30,812 38,277 706 824 4,562 4,499 3,708 3,652 146,091 156,37755-59 years 98,606 100,855 27,536 35,233 623 687 3,611 3,895 2,776 3,028 130,376 140,67060-64 years 82,404 87,034 22,902 30,490 428 556 2,986 3,726 2,104 2,146 108,720 121,80665-69 years 56,385 62,511 14,652 19,365 238 325 2,341 2,499 1,321 1,403 73,616 84,70070-74 years 38,439 47,291 9,451 13,642 195 226 1,665 1,629 817 989 49,750 62,78875-79 years 29,004 40,223 6,809 11,413 104 145 892 1007 634 888 36,809 52,78880-84 years 25,007 38,145 4,973 9,024 53 123 451 666 521 718 30,484 47,95885+ years 20,716 44,071 4,072 9,425 53 144 310 506 389 607 25,151 54,146Total 1,312,809 1,360,241 462,549 540,795 9,991 10,951 77,205 79,845 81,235 79,304 1,862,554 1,991,832Source: Surveillance, Epidemiology, and EndResults (SEER) Program (www.seer.cancer.gov)SEER*Stat Database: Populations -*Note: Persons of Hispanic origin may be of any race, therefore Hispanic counts not added to totals.Total U.S. (1990-2011) - Linked To County Attributes - Total U.S., 1969-2011 Counties, National Cancer Institute, DCCPS,Surveillance Research Program, SurveillanceSystems Branch, released October 2012.

Michigan Department of Community Health Collaborationand the MDCSS Authority to Collect Cancer DataThe 28-year collaborationbetween the State of MichiganDepartment of CommunityHealth (MDCH) and the MetropolitanDetroit Cancer SurveillanceSystem (MDCSS) wasrecently renewed by the State ofMichigan. The following lettergrants authority to the MDCSSto collect cancer data as a designatedpublic health authority ofthe State. Because the MDCSSis designated by the MDCH asa “state-authorized entity forthe collection and reporting ofindividually identifiable cancerinformation,” HIPAA allowshospitals to disclose such informationto the MDCSS.5

Cancer Trends, Incidence, Mortalityand Survival in Metropolitan DetroitTemporal Cancer Trends 7Cancer Incidence and Mortality: All Races 8Cancer Incidence and Mortality: Whites 106Cancer Incidence and Mortality: African-Americans 12Survival Analysis by Stage: Prostate Cancer 14Survival Analysis by Stage: Female Breast Cancer 15Survival Analysis by Stage: Lung Cancer 16Survival Analysis by Stage: Colorectal Cancer 17

Temporal Cancer Trends in Metropolitan DetroitIncidence rates for prostatecancer peaked in 1992, buthave remained high due toincreased detection through thePSA (prostate specific antigen)test. Female breast cancerincidence rates have remainedsteady since the late 1980’s.Mammography screening hasplayed an important role in theearly diagnosis of this cancer.While rates of lung cancer havebeen declining among malessince the mid 1990’s, ratesamong females are only nowleveling off.Lung cancer has been theleading cause of cancermortality among males since1973, but it has declinedsomewhat since 1992.Mortality among femalesfrom lung cancer continues toincrease, reflecting an increasein smoking. Mortality ratesfor prostate and female breastcancer have been decreasingover time.RATES PER 100,000 POPULATIONAge-Adjusted Incidence for Invasive Lung & Bronchus,Prostate & Female Breast Cancers, Metropolitan Detroit, 1973 – 200930030025025020020015015010010050501975 1980 19851990 1995 2000 2005Source: Surveillance, Epidemiology, and End Results (SEER) Program (www.seer.cancer.gov) SEER*Stat Database: Incidence - SEER 9 RegsResearch Data, Nov 2011 Sub, Vintage 2009 Pops (1973-2009) - Linked To County Attributes - TotalU.S., 1969-2010 Counties, National Cancer Institute, DCCPS, Surveillance Research Program, Surveillance Systems Branch, released April2012, based on the November 2011 submission.Male Lung Female Lung Prostate Female BreastAge-Adjusted Mortality Rates for Invasive Lung & Bronchus,Prostate & Female Breast Cancers, Metropolitan Detroit, 1973 – 20097RATES PER 100,000 POPULATION100806040201975 1980 19851990 1995 2000 2005Source: Surveillance, Epidemiology, and End Results (SEER) Program (www.seer.cancer.gov) SEER*Stat Database: Mortality - All COD,Aggregated With State, Total U.S. (1969-2009) , National Cancer Institute, DCCPS, SurveillanceResearch Program, Surveillance Systems Branch, released April 2012. Underlying mortality data provided by NCHS (www.cdc.gov/nchs).

All RacesCancer Incidence, Mortality and Age Adjusted Rates per 100,000Population by Site, Race and Sex, Metropolitan Detroit, 20098All Races Incidence Rate Mortality RateTotal Male Female Total Male Female Total Male Female Total Male FemaleAll Sites (Invasive) 21,972 11,228 10,744 508.3 593.3 451.4 7,949 4,013 3,936 184 224.3 158.8Oral Cavity and Pharynx 518 345 173 11.9 17.2 7.3 90 60 30 2.1 3.1 1.2Lip 14 7 7 0.3 0.4 0.3 * * 0 * * 0Tongue 152 102 50 3.4 5 2.1 17 11 * 0.4 0.6 *Salivary Gland 59 33 26 1.4 1.8 1.1 * * * * * *Floor of Mouth 38 25 13 0.9 1.2 0.6 * * 0 * * 0Gum and Other Mouth 82 44 38 1.9 2.3 1.6 14 * * 0.3 * *Nasopharynx 19 13 6 0.4 0.6 0.2 11 * * 0.3 * *Tonsil 71 60 11 1.6 2.8 0.5 * * * * * *Oropharynx 27 19 8 0.6 0.9 0.3 10 * * 0.2 * *Hypopharynx 37 30 7 0.9 1.6 0.3 * * * * * *Other Oral Cavityand Pharynx 19 12 7 0 0.5 0 16 * * 0.4 * *Digestive System 3,997 2,098 1,899 91.7 111.1 77.2 2,040 1,111 929 46.8 60.8 36.7Esophagus 247 168 79 5.6 8.8 3.1 184 131 53 4.2 7 2.1Stomach 351 221 130 8.1 12.2 5.4 166 95 71 3.9 5.5 2.8Small Intestine 109 50 59 3 2.8 2.4 12 * * 0.3 * *Colon and Rectum 1,993 950 1,043 46 50.6 42.7 759 374 385 17.5 21.2 14.9Colon excluding Rectum 1,432 652 780 33.2 35.3 31.8 641 305 336 14.9 17.5 13.1Cecum 333 131 202 7.8 7.2 8.3 † † † † † †Appendix 30 15 15 0.7 0.8 0.7 † † † † † †Ascending Colon 287 121 166 6.7 6.6 6.7 † † † † † †Hepatic Flexure 81 36 45 1.9 2 1.8 † † † † † †Transverse Colon 113 52 61 2.6 2.7 2.4 † † † † † †Splenic Flexure 40 22 18 0.9 1.1 0.7 † † † † † †Descending Colon 80 46 34 1.9 2.6 1.5 † † † † † †Sigmoid Colon 370 185 185 8.5 9.7 7.6 † † † † † †Large Intestine, NOS 98 44 54 2.3 2.5 2.2 † † † † † †Rectum andRectosigmoid Junction561 298 263 12.8 15.4 10.9 118 69 49 2.7 3.7 1.8Rectosigmoid Junction 134 72 62 3.1 3.7 2.6 † † † † † †Rectum 427 226 201 9.7 11.6 8.3 † † † † † †Anus, Anal Canaland Anorectum 80 34 46 1.8 1.8 1.8 * * * * * *Liver and IntrahepaticBile Duct 346 260 86 7.5 12.7 3.4 254 180 74 5.7 9 3Liver 324 246 78 7.1 11.9 3.1 208 149 59 4.6 7.4 2.4Intrahepatic Bile Duct 22 14 8 0.5 0.8 0.3 46 31 15 1 1.6 0.6Gallbladder 62 21 41 1.4 1.2 1.6 25 * 22 0.6 * 0.8Other Biliary 84 45 39 1.9 2.4 1.6 19 10 * 0.4 0.6 *Pancreas 666 330 336 15.3 17.6 13.6 589 300 289 13.5 16.3 11.6Retroperitoneum 10 7 * 0.2 0.4 * * * * * * *Peritoneum, Omentumand Mesentery 26 * 25 0.6 * 1 * * * * * *Other Digestive Organs 23 11 12 1 0.6 1 12 * * 0.3 * *Respiratory System 3,575 1,865 1,710 84 101.9 71.5 2,337 1,270 1,067 54.8 70.3 44Nose, Nasal Cavityand Middle Ear 28 19 9 0.7 1 0.4 * * * * * *Larynx 184 146 38 4 7.6 2 47 37 10 1.1 2 0.4Lung and Bronchus 3,326 1,674 1,652 78.3 91.7 69.1 2,276 1,223 1,053 53.3 67.7 43.4Pleura 31 23 8 0.7 1.3 0.3 * * 0 * * 0Trachea, Mediastinum andOther Respiratory Organs 6 * * 0.1 * * * * * * * *Bones and Joints 32 18 14 0.8 0.9 0.7 19 12 * 0.4 0.6 *Soft Tissue including Heart 128 61 67 3.1 3.2 3 55 33 22 1.3 1.8 1Skin excluding Basaland Squamous 751 415 336 17.5 22.1 14.8 117 77 40 2.6 4.2 1.6Melanoma of the Skin 639 351 288 14.9 18.7 12.7 91 61 30 2.1 3.3 1.2Other Non-Epithelial Skin 112 64 48 3 3.5 2 26 16 10 0.6 0.9 0.4Breast 3,123 21 3,102 72 1.2 131.3 614 * 606 14.1 * 24.6

All Races Incidence Rate Mortality RateTotal Male Female Total Male Female Total Male Female Total Male FemaleFemale Genital System 1,309 0 1,309 29.6 0 54.7 383 0 383 8.8 0 15.7Cervix Uteri 174 0 174 4.2 0 7.9 49 0 49 1.2 0 2.2Corpus and Uterus, NOS 707 0 707 15.7 0 28.9 128 0 128 2.9 0 5.2Corpus Uteri 685 0 685 15.2 0 28 59 0 59 1.4 0 2.5Uterus, NOS 22 0 22 0.5 0 0.9 69 0 69 1.6 0 2.7Ovary 321 0 321 7.3 0 13.3 182 0 182 4.2 0 7.4Vagina 26 0 26 0.6 0 1.1 * 0 * * 0 *Vulva 64 0 64 1.5 0 2.6 14 0 14 0.3 0 0.5Other Female Genital Organs 17 0 17 0 0 0.8 * 0 * * 0 *Male Genital System 3,689 3,689 0 84 188.9 0 358 358 0 8.2 21.7 0Prostate 3,563 3,563 0 81 182.1 0 353 353 0 8.1 21.5 0Testis 102 102 0 2.7 5.5 0 * * 0 * * 0Penis 19 19 0 0.4 1 0 * * 0 * * 0Other Male Genital Organs * * 0 * * 0 0 0 0 0 0 0Urinary System 1,835 1,266 569 42.3 68.8 23.2 410 268 142 9.6 15.3 5.7Urinary Bladder 1,006 750 256 23.2 42.1 10.2 215 144 71 5 8.4 2.8Kidney and Renal Pelvis 778 486 292 17.9 25 12.2 186 119 67 4.4 6.7 2.8Ureter 30 16 14 0.7 1 0.5 * * * * * *Other Urinary Organs 21 14 7 0.5 0.8 0.3 * * * * * *Eye and Orbit 23 12 11 0.6 0.7 0.4 * * * * * *Brain and OtherNervous System 266 137 129 6.4 7.2 5.8 183 101 82 4.2 5.2 3.4Brain 241 124 117 5.8 6.6 5.3 † † † † † †Cranial Nerves OtherNervous System 25 13 12 0.6 0.7 0.5 † † † † † †Endocrine System 619 150 469 14.8 7.7 21.4 38 16 22 0.9 0.8 0.9Thyroid 593 137 456 14.2 7 20.8 23 * 16 0.5 * 0.6Other Endocrineincluding Thymus 26 13 13 0.6 0.7 0.6 15 * * 0.4 * *Lymphoma 992 526 466 23.6 28.2 20.1 308 169 139 7.2 9.7 5.6Hodgkin’s Lymphoma 130 65 65 3.3 3.5 3.1 17 * 11 0.4 * 0.5Hodgkin’s - Nodal 124 62 62 3.1 3.4 2.9 † † † † † †Hodgkin’s - Extranodal 6 * * 0.2 * * † † † † † †Non-Hodgkin’sLymphoma (NHL) 862 461 401 20.3 24.7 17 291 163 128 6.8 9.4 5.1NHL - Nodal 597 331 266 14 17.8 11.2 † † † † † †NHL - Extranodal 265 130 135 6.3 6.9 5.9 † † † † † †Myeloma 315 182 133 7.3 9.8 5.4 164 83 81 3.8 4.5 3.2Leukemia 504 295 209 12 16.2 9 330 177 153 7.8 10.3 6Lymphocytic Leukemia 221 145 76 5.3 7.9 3.3 83 48 35 1.9 2.8 1.4Acute LymphocyticLeukemia 44 27 17 1.2 1.4 0.9 11 * * 0.3 * *Chronic LymphocyticLeukemia 160 104 56 3.8 5.8 2.3 68 38 30 1.6 2.3 1.2Other LymphocyticLeukemia 17 14 * 0.4 0.7 * * * * * * *Myeloid and MonocyticLeukemia 257 136 121 6.1 7.5 5.2 161 84 77 3.8 4.8 3.2Acute Myeloid Leukemia 155 77 78 3.7 4.3 3.4 132 74 58 3.2 4.3 2.4Acute Monocytic Leukemia * 0 * * 0 * * 0 * * 0 *Chronic Myeloid Leukemia 93 54 39 2.2 2.9 1.6 19 * 14 0.4 * 0.5Other Myeloid/MonocyticLeukemia 8 * * 0.2 * * * * * * * *Other Leukemia 26 14 12 0.6 0.8 0.5 86 45 41 2 2.7 1.5Other Acute Leukemia 10 * 7 0.2 * 0.3 30 16 14 0.7 1 0.5Aleukemic, Subleukemicand NOS 16 11 * 0.4 0.6 * 56 29 27 1.3 1.7 1Miscellaneous 296 148 148 6.7 8.1 5.7 498 269 229 11.4 15.3 8.99Rates are per 100,000 and age-adjusted to the 2000 US Std Population (19 age groups - Census P25-1130) standard.† Not reported * Statistic not displayed due to fewer than 6 cases.Source: Surveillance, Epidemiology, and End Results (SEER) Program (www.seer.cancer.gov) SEER*Stat Database. Underlying mortality data provided by NCHS (www.cdc.gov/nchs).

WhitesCancer Incidence, Mortality and Age Adjusted Rates per 100,000Population by Site, Race and Sex, Metropolitan Detroit, 200910WHITE Incidence Rate Mortality RateTotal Male Female Total Male Female Total Male Female Total Male FemaleAll Sites (Invasive) 16,404 8,367 8,037 501.4 573.8 455.5 5,915 3,008 2,907 177 215.2 153.6Oral Cavity and Pharynx 383 254 129 11.7 16.6 7.3 62 40 22 1.9 2.8 1.2Lip 13 7 6 0.4 0.5 0.3 * * 0 * * 0Tongue 118 82 36 3.6 5.3 2 15 10 * 0.5 0.7 *Salivary Gland 46 25 21 1.5 1.9 1.2 * * 0 * * 0Floor of Mouth 27 19 8 0.8 1.1 0.5 * * 0 * * 0Gum and Other Mouth 63 35 28 1.9 2.5 1.6 12 * * 0.4 * *Nasopharynx 12 8 * 0.4 0.5 * * * * * * *Tonsil 53 44 9 1.6 2.7 0.5 * * 0 * * 0Oropharynx 16 10 6 0.5 0.7 0.3 * * * * * *Hypopharynx 23 18 * 0.7 1.3 * * * * * * *Other Oral Cavityand Pharynx 12 6 6 0.3 0.3 0.3 11 * * 0.3 * *Digestive System 2,792 1,497 1,295 83.5 102.5 69 1,448 812 636 42.9 56.9 32.6Esophagus 192 142 50 5.7 9.5 2.5 152 112 40 4.5 7.6 2Stomach 226 153 73 6.8 10.7 3.9 98 67 31 3 4.8 1.6Small Intestine 66 35 31 2 2.4 1.6 * * * * * *Colon and Rectum 1,419 695 724 42.8 48 38.9 540 268 272 15.9 19.2 13.5Colon excluding Rectum 1,013 475 538 30.4 33.2 28.5 454 214 240 13.4 15.7 12Cecum 234 98 136 7.1 6.9 7.1 † † † † † †Appendix 21 11 10 0.7 0.8 0.6 † † † † † †Ascending Colon 209 88 121 6.3 6.1 6.3 † † † † † †Hepatic Flexure 59 27 32 1.8 2 1.6 † † † † † †Transverse Colon 83 35 48 2.4 2.3 2.5 † † † † † †Splenic Flexure 23 15 8 0.6 1 0.4 † † † † † †Descending Colon 49 29 20 1.5 2.1 1.1 † † † † † †Sigmoid Colon 267 141 126 8.1 9.7 6.8 † † † † † †Large Intestine, NOS 68 31 37 2 2.2 2 † † † † † †Rectum andRectosigmoid Junction 406 220 186 12.3 14.8 10.4 86 54 32 2.5 3.6 1.5Rectosigmoid Junction 86 43 43 2.6 2.9 2.4 † † † † † †Rectum 320 177 143 9.7 11.9 8.1 † † † † † †Anus, Anal Canaland Anorectum 62 23 39 1.8 1.5 2.1 * * * * * *Liver and IntrahepaticBile Duct 207 158 49 6 10.2 2.5 159 113 46 4.7 7.5 2.5Liver 185 144 41 5.4 9.2 2.2 123 89 34 3.7 5.9 1.9Intrahepatic Bile Duct 22 14 8 0.6 1 0.4 36 24 12 1.1 1.6 0.7Gallbladder 41 14 27 1.2 1 1.4 19 * 16 0.5 * 0.7Other Biliary 63 33 30 1.8 2.3 1.6 15 * * 0.4 * *Pancreas 466 226 240 13.9 15.5 12.6 434 229 205 12.9 16 10.8Retroperitoneum 10 7 * 0.3 0.5 * * * * * * *Peritoneum, Omentumand Mesentery 22 * 21 0.7 * 1.1 * * * * * *Other Digestive Organs 18 10 8 0.6 0.8 0.4 * * * * * *Respiratory System 2,683 1,373 1,310 82.4 97 72.4 1,759 928 831 53.4 66.1 44.8Nose, Nasal Cavityand Middle Ear 21 15 6 0.6 1.1 0.3 * * * * * *Larynx 130 100 30 4 6.9 1.7 26 23 * 0.8 1.6 *Lung and Bronchus 2,498 1,234 1,264 76.7 87.3 69.9 1,722 897 825 52.3 63.9 44.6Pleura 31 23 8 0.9 1.6 0.4 * * 0 * * 0Trachea, Mediastinum andOther Respiratory Organs * * * * * * * * 0 * * 0Bones and Joints 27 15 12 0.9 1.1 0.8 15 * * 0.5 * *Soft Tissue including Heart 102 45 57 3.4 3.2 3.5 44 29 15 1.4 2 1Skin excluding Basaland Squamous 714 398 316 22.3 27.3 19.4 113 75 38 3.3 5.2 2.1Melanoma of the Skin 624 349 275 19.5 23.8 17.1 88 59 29 2.6 4.1 1.6Other Non-Epithelial Skin 90 49 41 2.7 3.4 2.3 25 16 * 0.7 1.1 *Breast 2,319 16 2,303 70.8 1.2 132.3 430 * 425 12.8 * 22.6

WHITE Incidence Rate Mortality RateTotal Male Female Total Male Female Total Male Female Total Male FemaleFemale Genital System 997 0 997 30 0 56.7 286 0 286 8.5 0 15.4Cervix Uteri 113 0 113 3.8 0 7.4 27 0 27 0.9 0 1.7Corpus and Uterus, NOS 552 0 552 16.2 0 30.6 89 0 89 2.6 0 4.8Corpus Uteri 545 0 545 15.9 0 30.2 43 0 43 1.3 0 2.4Uterus, NOS 7 0 7 0.2 0 0.4 46 0 46 1.4 0 2.4Ovary 250 0 250 7.5 0 14.1 149 0 149 4.4 0 7.9Vagina 16 0 16 0.5 0 1 * 0 * * 0 *Vulva 53 0 53 1.6 0 2.9 12 0 12 0.4 0 0.6Other Female Genital Organs 13 0 13 0.4 0 0.8 * 0 * * 0 *Male Genital System 2,589 2,589 0 78.6 172.5 0 248 248 0 7.2 18.8 0Prostate 2,478 2,478 0 74.5 164.1 0 243 243 0 7 18.5 0Testis 90 90 0 3.5 6.8 0 * * 0 * * 0Penis 16 16 0 0.5 1.1 0 * * 0 * * 0Other Male Genital Organs * * 0 * * 0 0 0 0 0 0 0Urinary System 1,473 1,037 436 44.3 72 23.7 343 224 119 10.3 16.2 6.4Urinary Bladder 867 657 210 25.8 46.6 11 179 123 56 5.3 9 2.9Kidney and Renal Pelvis 560 351 209 17.1 23.3 11.9 156 97 59 4.7 7 3.3Ureter 28 16 12 0.8 1.2 0.6 * * * * * *Other Urinary Organs 18 13 * 0.6 0.9 * * * * * * *Eye and Orbit 18 8 10 0.5 0.6 0.5 * * * * * *Brain and OtherNervous System 205 110 95 6.7 7.8 5.8 152 85 67 4.6 5.8 3.7Brain 186 100 86 6.1 7.1 5.2 † † † † † †Cranial Nerves OtherNervous System 19 10 9 0.6 0.7 0.5 † † † † † †Endocrine System 481 124 357 15.9 8.4 23.3 28 10 18 0.8 0.7 1Thyroid 467 118 349 15.5 8 22.8 19 * 13 0.5 * 0.7Other Endocrineincluding Thymus 14 6 8 0.4 0.4 0.4 * * * * * *Lymphoma 808 430 378 25.7 30.4 22.1 261 144 117 7.8 10.5 6Hodgkin’s Lymphoma 104 53 51 3.8 4.1 3.5 14 * * 0.4 * *Hodgkin’s - Nodal 98 50 48 3.5 3.8 3.3 † † † † † †Hodgkin’s - Extranodal 6 * * 0.3 * * † † † † † †Non-Hodgkin’sLymphoma (NHL) 704 377 327 21.9 26.3 18.6 247 139 108 7.3 10.1 5.5NHL - Nodal 486 265 221 15.1 18.5 12.4 † † † † † †NHL - Extranodal 218 112 106 6.8 7.8 6.1 † † † † † †Myeloma 191 113 78 5.8 8.1 4.1 97 48 49 2.8 3.4 2.3Leukemia 401 241 160 12.6 17.1 9.3 255 142 113 7.8 10.7 5.7Lymphocytic Leukemia 180 119 61 5.8 8.5 3.7 63 38 25 1.9 3 1.2Acute LymphocyticLeukemia 35 20 15 1.4 1.5 1.2 * * * * * *Chronic LymphocyticLeukemia 131 86 45 4 6.1 2.4 53 32 21 1.6 2.5 1.1Other LymphocyticLeukemia 14 13 * 0.4 0.9 * * * * * * *Myeloid and MonocyticLeukemia 201 111 90 6.2 7.8 5.1 118 68 50 3.6 5 2.7Acute Myeloid Leukemia 123 65 58 3.8 4.6 3.3 98 61 37 3.1 4.5 2Acute Monocytic Leukemia * 0 * * 0 * 0 0 0 0 0 0Chronic Myeloid Leukemia 71 41 30 2.2 2.8 1.6 12 * * 0.3 * *Other Myeloid/MonocyticLeukemia 6 * * 0.2 * * * * * * * *Other Leukemia 20 11 9 0.6 0.8 0.5 74 36 38 2.2 2.8 1.8Other Acute Leukemia 9 * 6 0.3 * 0.3 27 14 13 0.8 1.1 0.6Aleukemic, Subleukemicand NOS 11 8 * 0.3 0.6 * 47 22 25 1.4 1.7 1.1Miscellaneous 221 117 104 6.4 8.2 5.2 369 208 161 10.9 15 8.211Rates are per 100,000 and age-adjusted to the 2000 US Std Population (19 age groups - Census P25-1130) standard.† Not reported * Statistic not displayed due to fewer than 6 cases.Source: Surveillance, Epidemiology, and End Results (SEER) Program (www.seer.cancer.gov) SEER*Stat Database. Underlying mortality data provided by NCHS (www.cdc.gov/nchs).

African-AmericansCancer Incidence, Mortality and Age Adjusted Rates per 100,000Population by Site, Race and Sex, Metropolitan Detroit, 200912AFRICAN-AMERICAN Incidence Rate Mortality RateTotal Male Female Total Male Female Total Male Female Total Male FemaleAll Sites (Invasive) 5,026 2,595 2,431 544.1 687.3 448.4 1,951 971 980 221.7 280.2 185.3Oral Cavity and Pharynx 125 85 40 12.8 19.9 7.5 28 20 * 3 4.7 *Lip * 0 * * 0 * 0 0 0 0 0 0Tongue 32 19 13 3.2 4.4 2.3 * * * * * *Salivary Gland 11 6 * 1.2 1.3 * * * * * * *Floor of Mouth 9 * * 1.1 * * 0 0 0 0 0 0Gum and Other Mouth 18 9 9 1.8 1.8 1.7 * 0 * * 0 *Nasopharynx * * * * * * * * 0 * * 0Tonsil 18 16 * 1.8 3.8 * * * * * * *Oropharynx 11 9 * 1.1 2.1 * * * * * * *Hypopharynx 14 12 * 1.5 2.9 * * * 0 * * 0Other Oral Cavityand Pharynx 6 * * 0.6 * * * * * * * *Digestive System 1,106 552 554 122 149.1 103.9 565 286 279 63.9 81.2 52.2Esophagus 54 26 28 6 7.6 5.1 31 18 13 3.5 5.2 2.3Stomach 113 64 49 13.2 20 9.4 62 26 36 7.3 8.5 6.8Small Intestine 42 15 27 4.9 5 5.1 * * * * * *Colon and Rectum 519 227 292 57.4 61.1 54.9 214 104 110 25.3 31.8 21.1Colon excluding Rectum 380 156 224 42.9 43.7 42.5 182 89 93 21.5 27.1 17.9Cecum 91 27 64 10.6 8.1 12.5 † † † † † †Appendix 7 * * 0.8 * * † † † † † †Ascending Colon 75 31 44 8.6 8.6 8.5 † † † † † †Hepatic Flexure 21 9 12 2.3 2.4 2.2 † † † † † †Transverse Colon 27 15 12 3 4.3 2.2 † † † † † †Splenic Flexure 16 6 10 1.9 1.7 1.9 † † † † † †Descending Colon 28 16 12 3.1 4.7 2.2 † † † † † †Sigmoid Colon 88 37 51 9.4 9.6 9.4 † † † † † †Large Intestine, NOS 27 13 14 3.1 3.8 2.6 † † † † † †Rectum andRectosigmoid Junction 139 71 68 14.6 17.4 12.4 32 15 17 3.9 4.7 3.1Rectosigmoid Junction 44 27 17 4.9 7.1 3.3 † † † † † †Rectum 95 44 51 9.7 10.3 9.1 † † † † † †Anus, Anal Canaland Anorectum 17 10 7 1.7 2.3 1.2 * * * * * *Liver and IntrahepaticBile Duct 123 90 33 12.1 20.7 5.7 87 62 25 9 14.8 4.6Liver 123 90 33 12.1 20.7 5.7 80 57 23 8.2 13.6 4.2Intrahepatic Bile Duct 0 0 0 0 0 0 * * * * * *Gallbladder 20 6 14 2.2 1.5 2.6 * 0 * * 0 *Other Biliary 18 11 7 2.1 3.1 1.5 * * * * * *Pancreas 193 102 91 21.5 27.7 17.2 149 69 80 16.5 18.8 14.8Retroperitoneum 0 0 0 0 0 0 * * 0 * * 0Peritoneum, Omentumand Mesentery * 0 * * 0 * 0 0 0 0 0 0Other Digestive Organs * * * * * * * * * * * *Respiratory System 843 465 378 93.6 126.9 71.1 563 334 229 64 94 44.4Nose, Nasal Cavityand Middle Ear * * * * * * * * 0 * * 0Larynx 51 43 8 5.1 10.9 1.3 21 14 * 2.3 3.8 *Lung and Bronchus 784 416 368 87.6 114.5 69.5 539 318 221 61.3 89.7 42.7Pleura 0 0 0 0 0 0 * * 0 * * 0Trachea, Mediastinum andOther Respiratory Organs * * * * * * * 0 * * 0 *Bones and Joints * * * * * * * * * * * *Soft Tissue including Heart 24 15 9 2.4 3.5 1.6 11 * * 1.2 * *Skin excluding Basaland Squamous 31 15 16 3.3 3.9 2.9 * * * * * *Melanoma of the Skin 10 * 9 1 * 1.6 * * * * * *Other Non-Epithelial Skin 21 14 7 2.2 3.7 1.3 * 0 * * 0 *Breast 715 * 710 76.5 * 129.4 175 * 172 19.3 * 31.8

AFRICAN-AMERICAN Incidence Rate Mortality RateTotal Male Female Total Male Female Total Male Female Total Male FemaleFemale Genital System 280 0 280 29.5 0 50.5 93 0 93 10.6 0 17.8Cervix Uteri 55 0 55 5.7 0 9.9 20 0 20 2.2 0 3.7Corpus and Uterus, NOS 142 0 142 15 0 25.5 39 0 39 4.6 0 7.5Corpus Uteri 127 0 127 13.4 0 22.9 16 0 16 1.9 0 3.1Uterus, NOS 15 0 15 1.5 0 2.6 23 0 23 2.7 0 4.4Ovary 60 0 60 6.4 0 10.9 31 0 31 3.7 0 6.1Vagina 10 0 10 1.1 0 1.8 * 0 * * 0 *Vulva 10 0 10 1.1 0 1.8 * 0 * * 0 *Other Female Genital Organs * 0 * * 0 * 0 0 0 0 0 0Male Genital System 989 989 0 104.9 256 0 108 108 0 13.3 37.2 0Prostate 976 976 0 103.5 253 0 108 108 0 13.3 37.2 0Testis 10 10 0 1 2.3 0 0 0 0 0 0 0Penis * * 0 * * 0 0 0 0 0 0 0Other Male Genital Organs 0 0 0 0 0 0 0 0 0 0 0 0Urinary System 321 201 120 35.5 56.9 21.8 64 42 22 7.5 12.5 4.1Urinary Bladder 122 80 42 14 24.2 7.7 35 20 15 4.2 5.9 2.8Kidney and Renal Pelvis 195 120 75 21.1 32.3 13.7 28 21 * 3.2 6.2 *Ureter * 0 * * 0 * 0 0 0 0 0 0Other Urinary Organs * * * * * * * * 0 * * 0Eye and Orbit * * * * * * 0 0 0 0 0 0Brain and OtherNervous System 48 21 27 4.9 4.9 5 29 15 14 3 3.3 2.7Brain 43 18 25 4.4 4.1 4.7 † † † † † †Cranial Nerves OtherNervous System * * * * * * † † † † † †Endocrine System 103 15 88 10.5 4 15.6 * * * * * *Thyroid 93 10 83 9.4 2.6 14.6 * * * * * *Other Endocrineincluding Thymus 10 * * 1.1 * * * * * * * *Lymphoma 153 83 70 16.2 20.9 12.9 45 25 20 4.9 6.7 3.8Hodgkin’s Lymphoma 18 8 10 1.8 1.9 1.8 * * * * * *Hodgkin’s - Nodal 18 8 10 1.8 1.9 1.8 † † † † † †Hodgkin’s - Extranodal 0 0 0 0 0 0 † † † † † †Non-Hodgkin’sLymphoma (NHL) 135 75 60 14.3 19 11.1 42 24 18 4.6 6.5 3.4NHL - Nodal 97 58 39 10.2 14.7 7.1 † † † † † †NHL - Extranodal 38 17 21 4.1 4.3 4 † † † † † †Myeloma 121 68 53 13.3 17.8 10.1 65 35 30 7.4 9.5 5.9Leukemia 87 45 42 9.9 12.7 8 69 32 37 7.8 9 7Lymphocytic Leukemia 34 20 14 3.8 5.3 2.7 20 10 10 2 2.3 1.8Acute LymphocyticLeukemia 9 7 * 0.9 1.4 * * * 0 * * 0Chronic LymphocyticLeukemia 23 12 11 2.7 3.6 2.1 15 * * 1.5 * *Other LymphocyticLeukemia * * * * * * * 0 * * 0 *Myeloid and MonocyticLeukemia 47 22 25 5.4 6.6 4.8 37 13 24 4.5 4 4.7Acute Myeloid Leukemia 28 11 17 3.3 3.4 3.3 28 10 18 3.4 3.2 3.5Acute Monocytic Leukemia 0 0 0 0 0 0 * 0 * * 0 *Chronic Myeloid Leukemia 17 11 6 1.9 3.2 1.1 * * * * * *Other Myeloid/MonocyticLeukemia * 0 * * 0 * * * 0 * * 0Other Leukemia 6 * * 0.7 * * 12 * * 1.3 * *Other Acute Leukemia * 0 * * 0 * * * * * * *Aleukemic, Subleukemicand NOS * * * * * * * * * * * *Miscellaneous 71 30 41 8 8.2 7.7 121 58 63 14.2 18 11.813Rates are per 100,000 and age-adjusted to the 2000 US Std Population (19 age groups - Census P25-1130) standard.† Not reported * Statistic not displayed due to fewer than 6 cases.Source: Surveillance, Epidemiology, and End Results (SEER) Program (www.seer.cancer.gov) SEER*Stat Database. Underlying mortality data provided by NCHS (www.cdc.gov/nchs).

Survival Analysis of Prostate Cancer by StageOver the past 31 years, thetreatment of men with prostatecancer diagnosed at an earlystage has improved. In thetri-county area, the currentfive-year relative survival formen diagnosed with local stageprostate cancer is near 100%.Dramatic improvement insurvival of men with prostatecancer that is diagnosed afterit has spread to other parts ofthe body has not been seen.The five-year relative survivalfor men diagnosed with distantstage disease has fluctuatedfor the last 31 years between20-38%, with African-Americanmen showing a better trend inthe last decade than White men.Armed with successful treatmentfor early stage disease,there has been a concertedeffort to identify these cancerswhile they are in local stage.Currently, about 95% of themen who are newly diagnosedwith prostate cancer in thetri-county area are diagnosed atlocal or regional stages. A fewof the risk factors for developingthe disease are age, race(African-American), and familyhistory (men with close bloodrelatives such as fathers orbrothers who have been diagnosedwith the disease).Localized/RegionalDistant14Invasive Prostate Cancer – White Males100 Stage Distribution 1973 – 2009 Metropolitan Detroit100Invasive Prostate Cancer – African-American MalesStage Distribution 1973 – 2009 Metropolitan Detroit8010080100PERCENTAGE PERCENTAGE60806080606040 40404020 20PERCENTAGE PERCENTAGE20201975 1980 1975 198019751980 1985 1990 1995 2000 2005YEAR DIAGNOSED - 3 YEAR MOVING AVERAGE19751980 1985 1990 1995 2000 2005YEAR DIAGNOSED - 3 YEAR MOVING AVERAGE1005-Year Relative Survival Rates for Prostate Cancer –White Males by Stage, 1973 – 2009 Metropolitan Detroit5 -Year Relative Survival Rates for Prostate Cancer –African-American Males by Stage, 1973 – 2009 Metropolitan Detroit1001008080PERCENTAGE6040PERCENTAGE604020201975 1980200019751980 1985 1990 1995 2000 2005YEAR DIAGNOSED - 3 YEAR MOVING AVERAGE19751980 1985 1990 1995 2000 2005YEAR DIAGNOSED - 3 YEAR MOVING AVERAGE

Survival Analysis of Female Breast Cancer by StageBoth diagnosis and treatmentfor female breast cancer haveimproved since 1973. Due tomammography screening, morecases are diagnosed at an earlierstage. Currently, five-year relativesurvival for cases diagnosedat local stage is 95% for womenin the general population. Forwomen with regional stagedisease, survival also has improved.For women diagnosedwith late stage disease, survivalhas remained relatively steady,at 10-20% for women in thegeneral population. African-American women tend to have ahigher proportion of late stagediagnoses and five-year survival,regardless of stage, tends to bepoorer than for White women.Gender and age are the greatestrisk factors for developingbreast cancer. Breast cancer canstrike men and women both,but women are many timesmore likely to develop the diseasethan men. A family historyof breast cancer has also beenlinked to increasing a woman’slikelihood of developing thedisease. Gender, age, and familyhistory are things that cannotbe prevented, however womencan increase their chances ofsurviving this disease by consultingwith their physician, andfollowing recommended screeningfor their specific age and riskgroup. Women who are at anincreased risk due to a familyhistory should consult withtheir doctor about whether theyshould begin mammographyscreening at an earlier age.LocalizedRegionalDistant100Invasive Breast Cancer – White FemalesStage Distribution 1973 – 2009 Metropolitan DetroitInvasive Breast Cancer – African-American FemalesStage Distribution 1973 – 2009 Metropolitan Detroit151001008080PERCENTAGE6040PERCENTAGE6040202019751980 1985 1990 1995 2000 2005YEAR DIAGNOSED - 3 YEAR MOVING AVERAGE19751980 1985 1990 1995 2000 2005YEAR DIAGNOSED - 3 YEAR MOVING AVERAGE5-Year Relative Survival Rates for Breast Cancer –100White Females by Stage, 1973 – 2009 Metropolitan Detroit5-Year Relative Survival Rates for Breast Cancer –African-American Females by Stage, 1973 – 2009 Metropolitan Detroit1001008080PERCENTAGE6040PERCENTAGE6040202019751980 1985 1990 1995 2000 2005YEAR DIAGNOSED - 3 YEAR MOVING AVERAGE19751980 1985 1990 1995 2000 2005YEAR DIAGNOSED - 3 YEAR MOVING AVERAGE

Survival Analysis of Lung Cancer by StageDiagnosis of lung cancer inlocal stage is difficult becausesymptoms usually do not appearuntil the disease is advanced.Only about 23% of lung cancersin Whites and 18-19% inAfrican-Americans are diagnosedat the local stage. Mostearly stage lung cancer casesare diagnosed incidentally. Thefive-year survival rate for localstage cancer is less than 50% forthe general population. The fiveyearsurvival for distant stagecancer is approximately 2%. Aneffective method for screeningfor lung cancer has not yet beendeveloped although promisingmethods are being tested. Whena new method is developed,the hope is that it will be aseffective and universally usedas mammography screeninghas been for breast cancer andthe PSA blood test has been forprostate cancer.The major risk factor for lungcancer is tobacco smoking.The risk increases over timeas a person continues to smoke.However, if a person is ableto quit smoking before cancerhas developed, the lung tissuecan begin to repair itself. Anex-smoker can lower his risk oflung cancer, but his risk will stillbe higher than that of someonewho has never smoked. Nonsmokerswho are exposed tosecond hand smoke in the homeor workplace are also at increasedrisk for developing lungcancer. Exposure to carcinogensin the workplace or the environmentand having a familyhistory of lung cancer havealso been found to contributeto an increased risk for gettingthe disease.LocalizedRegionalDistant16100Invasive Lung Cancer – White PopulationStage Distribution 1973 – 2009 Metropolitan DetroitInvasive Lung Cancer – African-American PopulationStage Distribution 1973 – 2009 Metropolitan Detroit1001008080PERCENTAGE604020PERCENTAGE604020197519801985 1990 1995 2000 2005197519801985 1990 1995 2000 2005YEAR DIAGNOSED - 3 YEAR MOVING AVERAGEYEAR DIAGNOSED - 3 YEAR MOVING AVERAGE5-Year Relative Survival Rates for Lung Cancer –100 White Population by Stage, 1973 – 2009 Metropolitan Detroit5-Year Relative Survival Rates for Lung Cancer –African-American Population by Stage, 1973 – 2009 Metropolitan Detroit1001008080PERCENTAGE604020PERCENTAGE604020197519801985 1990 1995 2000 2005197519801985 1990 1995 2000 2005YEAR DIAGNOSED - 3 YEAR MOVING AVERAGEYEAR DIAGNOSED - 3 YEAR MOVING AVERAGE

Survival Analysis of Colorectal Cancer by StageThe five-year survival rate forcolorectal cancer has graduallyincreased over the past 31 yearsfor the general population.Currently, the five-year relativesurvival rate for local stagecancer is over 90% compared to73% in 1973. At distant stage,the five-year relative survivalrate is over 10% compared to4% in 1973. This improvedsurvival has been linked to improvedearly detection practicesincluding the increased use ofscreening sigmoidoscopy.Age, family history, and dietare risk factors in developingcolorectal cancer. The symptomsof colorectal cancer may mimicsome other conditions such ashemorrhoids or inflammatorybowel disease. It is best to consultwith a physician to determinethe correct cause of thesymptoms. Screening typicallybegins at age 50 for the generalpopulation. If there is familyhistory of the disease, a patientneeds to confer with their physicianto discuss when screeningshould begin.LocalizedRegionalDistant100Invasive Colorectal Cancer – White PopulationStage Distribution 1973 – 2009 Metropolitan DetroitInvasive Colorectal Cancer – African-American PopulationStage Distribution 1973 – 2009 Metropolitan Detroit1780 100100PERCENTAGE PERCENTAGE60806040402020PERCENTAGE806040201985 1990 1995 2000197519801985 1990 1995 2000 2005197519801985 1990 1995 2000 2005YEAR DIAGNOSED - 3 YEAR MOVING AVERAGEYEAR DIAGNOSED - 3 YEAR MOVING AVERAGE5-Year Relative Survival Rates for Colorectal Cancer –100 White Population by Stage, 1973 – 2009 Metropolitan Detroit5-Year Relative Survival Rates for Colorectal Cancer –African-American Population by Stage, 1973 – 2009 Metropolitan Detroit80100100PERCENTAGE PERCENTAGE60806040204020PERCENTAGE80604020197519801985 1990 1995 2000 2005197519801985 1990 1995 2000 2005YEAR DIAGNOSED - 3 YEAR MOVING AVERAGEYEAR DIAGNOSED - 3 YEAR MOVING AVERAGE

Cancer Research at MDCSSThe Young Women’s Health History Study -Breast Cancer Risk Factors in Young Women 19Risk Factors for Ovarian Cancer inAfrican-American Women 2018Patterns of Care Study 21Genetic Pathways of Inflammation and Riskof Lung Cancer and Chronic ObstructivePulmonary Disease 22

The Young Women’s Health History Study -Breast Cancer Risk Factors in Young WomenEllen Velie, PhD (Principal Investigator), Kendra Schwartz, MD, MSPHEach year in the United States, about 44,000 women are newlydiagnosed with breast cancer before 50 years of age (SEER) 1 . Tumorsin these young women are more likely to be aggressive with a worseprognosis, but their causes remain poorly understood 2 .500Age-Adjusted Incidence of Invasive Female Breast Cancerin Women (50+), SEER-9, 1992 – 2009In the United States, White women are more likely to develop breastcancer after age 50 (figure 1), but among the youngest women,under age 40, African American women are more likely to developbreast cancer (figure 2) 3 . African American and poorer women alsoappear more likely to develop tumors with the worst prognosis 3,4 .In addition, compared to similarly aged White women, African-American women have higher death rates from breast cancer (figure3). In young African-American, under 40 years of age, only about 42%of breast cancers are diagnosed at the local stage, before the cancerhas spread beyond the breast, whereas in young White women 48%are diagnosed before the cancer has spread 5 . Screening is not usuallyrecommended before age 40 because current screening modalities donot work well for young women. It’s therefore particularly importantwe understand the causes of breast cancer in young women, in orderto prevent the development of the disease.Ellen Velie, PhD at Michigan State University, with Co-Investigators,Kendra Schwartz, MD, MSPH at Wayne State University (WSU)and Ann Hamilton, PhD at the University of Southern California(USC), assisted by Westat, a research corporation, are conductingthe “Young Women’s Health History Study”, funded by the NationalCancer Institute, to evaluate risk factors for breast cancer in youngwomen. The study is being conducted in a socioeconomically diversepopulation of African-American and White women in MetropolitanDetroit and Los Angeles County. The study’s objectives are toexamine whether potentially modifiable lifestyle factors measuredover a woman’s lifetime, related genetic factors, as well as the socialconditions that influence lifestyle factors, explain why some youngwomen develop specific types of breast cancer. Researchers plan toenroll 4,000 young women – both those who have had breast cancerand those who have had not, to compare these two groups of women.The “Young Women’s Health History Study” began recruitment ofparticipants in December of 2011. Young women randomly selectedfor this study are encouraged to participate. Whether or not womenhave had breast cancer, their story will give researchers a fullerpicture of women’s lives. Unfortunately, due to the studies’ scientificmethodology, women who are not contacted cannot volunteerthemselves. For questions regarding this research, please visit thestudy web-site, http://ywhhs.org/. In the metropolitan Detroit areayou can also contact the study toll-free phone number: 1-(877)-679-9687 and either Dr. Kendra Schwartz or the Study ProjectCoordinator, Ms. Kathy Cross will get back with you.Reference:1. Howlader N, Noone AM, Krapcho M, Neyman N, Aminou R, Altekruse SF, KosaryCL, Ruhl J, Tatalovich Z, Cho H, Mariotto A, Eisner MP, Lewis DR, Chen HS, FeuerEJ, Cronin KA (eds). SEER Cancer Statistics Review, 1975-2009 (Vintage 2009Populations), National Cancer Institute. Bethesda, MD, http://seer.cancer.gov/csr/1975_2009_pops09/, based on November 2011 SEER data submission, postedto the SEER web site, April 2012.2. Brinton LA, Sherman ME, Carreon JD, Anderson WF. Recent trends in breastcancer among younger women in the United States. J Natl Cancer Inst. 2008 Nov19;100 (22):1643-8. Epub 2008 Nov 11.3. Andaya AA, Enewold L, Horner MJ, Jatoi I, Shriver CD, Zhu K. Socioeconomicdisparities and breast cancer hormone receptor status. Cancer Causes Control2012 23: 951-958.400RATE PER 100,000RATE PER 100,000400300RATE PER 100,000300201612865432101992199219951995White19982001YEAR OF DIAGNOSIS19982001YEAR OF DIAGNOSIS20042004African-American2007Age-Adjusted Incidence of Invasive Female Breast Cancerin Women (

Risk Factors for Ovarian Cancer in African-American WomenInvestigator: Michele L. Cote, PhD20Ovarian cancer is diagnosed in more than22,000 women in the United States each year,making it the 9th most commonly diagnosedcancer in women. (Jemal et al, 2009) Incidencerates are higher among white women thanAfrican-American women (14.1/100,000 and10.1/100,000, respectively), and incidencerates have been declining over time. (Altekruse,et al, 2010) The decrease in incidencetrends from 1975 to 2005 is much higher among white women(-2.7%) than African-Americans (-0.4%). The median age at diagnosisis younger among African-Americans compared to whites (61versus 64 years). (Altekruse, et al, 2010)Ovarian cancer survival is poor, with an overall 5-year survival of43.9% for white women and 38.8% for African-American women.Although ovarian cancer accounts for 3% of cancer diagnosesamong women, it is the fifth most common cause of cancer mortalityaccounting for 6% of cancer deaths. The high mortality is largelyattributable to late detection, with 79% of the cancers diagnosed inregional or distant stages, when there is already spread beyond thepelvis. (Altekruse, et al, 2010)Ovarian cancer mortality statistics are even grimmer for African-American women. The ratio of mortality to incidence rates is 74%for African-Americans compared to 65% for whites. (SEER) It hasbeen noted that five-year survival rates for white women increasedfrom 36% to 45% from the period 1975-77 to 1996-2004, whereas5-year survival for African-Americans has decreased, droppingfrom 43% in 1975-77 to 38% in 1996-2004. (SEER) Thus, despiteimprovements in surgical techniques and chemotherapy 5-yearsurvival has not improved for African-American women after adiagnosis of ovarian cancer.Risk factors for ovarian cancer have been explored primarily inwhite women. In the few studies that have included African-American women, reproductive factors such as a greater number ofpregnancies, oral contraceptive use and tubal ligation are associatedwith reduced risk of ovarian cancer in both races (John 1993, Ness2000, and Mooreman 2008). These analyses have all been limitedby the small number of African-Americans included in the studies.Thus, there is a need to further investigate ovarian cancer risk factorsamong African-American women, including known genetic riskfactors (i.e. BRCA mutations) and other less-common exposures.Joining eight other institutions and led by investigators at DukeUniversity, Dr. Michele Cote and researchers at the MetropolitanDetroit Cancer Surveillance System (MDCSS) of Wayne State Universityhave embarked upon a study of ovarian cancer in African-American women. During the course of the 5 year study, investigatorsplan to interview and obtain blood specimens from 1,000African-American women with ovarian cancer and 1,000 healthywomen. Medical record release and yearly follow up will also berequested of the women with ovarian cancer. MDCSS hopes tocontribute about 13% of the study subjects. The goal of the studyis to examine epidemiologic and genetic risk factors for ovariancancer among African-American women.RATE PER 100,000RATE PER 100,00025201510525201510519751975References:Age-Adjusted Incidence of MalignantOvarian Cancer by Race, SEER-9, 1973 – 20091980WhiteYEAR OF DIAGNOSIS20001985 1990 1995 2000 2005African-AmericanAge-Adjusted Incidence-based Mortality fromMalignant Ovarian Cancer, 1973 – 20091980YEAR OF DEATH20001985 1990 1995 2000 20051. Altekruse SF, Kosary CL, Krapcho M, Neyman N, Aminou R, Waldron W, RuhlJ, Howlader N, Tatalovich Z, Cho H, Mariotto A, Eisner MP, Lewis DR, CroninK, Chen HS, Feuer EJ, Stinchcomb DG, Edwards BK (eds). SEER Cancer StatisticsReview, 1975-2007, National Cancer Institute. Bethesda, MD, http://seer.cancer.gov/csr/1975_2007/, based on November 2009 SEER data submission, posted tothe SEER web site, 2010.2. Jemal A, Siegel R, Ward E, Hao Y, Xu J, Thun MJ. Cancer statistics, 2009. CACancer J Clin. 2009 Jul-Aug;59(4):225-49.3. John EM, Whittemore AS, Harris R, Itnyre J Characteristics relating to ovariancancer risk: collaborative analysis of seven U.S. case-control studies. Epithelialovarian cancer in black women. Collaborative Ovarian Cancer Group.J Natl CancerInst. 1993 Jan 20;85(2):142-7.4. Moorman PG, Palmieri RT, Akushevich L, Berchuck A, Schildkraut JM Am JEpidemiol. Ovarian cancer risk factors in African-American and white women.2009 Sep 1;170(5):598-606.5. Ness RB, Grisso JA, Cottreau C, Klapper J, Vergona R, Wheeler JE, Morgan M,Schlesselman JJ. Factors related to inflammation of the ovarian epithelium andrisk of ovarian cancer. Epidemiology. 2000 Mar;11(2):111-7.

Patterns of Care StudyIkuko Kato (Principal Investigator), PhD, Patricia Arballo-Spong, BS, Ann S. Bankowski, MSW, Kari A. Borden, RHIT, CTRSEER Patterns ofCare (POC) Studieshave been funded bythe National CancerInstitute in order toassess the incorporationof state-of-theartcancer treatmentsinto clinical practiceand the extent towhich cancer patientsreceive such treatments.These studies are designed to describe, characterize, andcompare practice patterns and treatments provided for cancer indifferent geographic areas of the United States. The MetropolitanDetroit Cancer Surveillance System (MDCSS) has participated inPOC studies to provide representative samples from metropolitanDetroit since 1997, when this study was integrated into the SEERprogram. The results of POC studies have been summarized byNCI staff and disseminated in scientific journals and professionalmeetings; and used to develop educational or training opportunitiesto improve the use of state-of-the-art cancer therapy in communitypractice through collaboration with professional organizations.Each year three to four types of cancer are selected for this study.Table 1 lists cancers studied in years 1997 to 2010. These pertainto patients diagnosed in years 1995 -2008, i.e., 2 years behindthe years of the survey, to allow for sufficient time to capture allcare that patients received during the initial course of treatment.Choices of cancers reflect the introduction of new treatment methods,therapeutics, diagnostic tests, predictive and prognostic markersfor particular cancer sites, as well as special research interests.Examples include use of less invasive surgeries such a laparoscopicresection and cryosurgery, radioimmunotherapy, new monoclonalantibodies and antiangiogenic agents, active surveillance for prostatecancer, and HER2 and Oncotype tests for breast cancer. Somecancers have been chosen more than once during this period toexamine chronological trends.For the past 10 years, approximately 340 cases per year have beenincluded from the MDCSS in this study. These samples are randomlyselected by a computer program at a time point when the numberof selected cancer cases reach 95% of the projected number of casesfor a given year. There are two major components in POC studies:(1) re-abstracting medical records in more detail beyond regularabstracts required for SEER and (2) physicians’ surveys. The formerincludes individual chemo-, immuno-, hormona-therapeutic agents,in addition to other new treatments/tests/markers of interest.SEER abstracting staff complete these tasks at all facilities where apatient received diagnosis and treatments. Typically, multiple medicalrecord abstracts are required per patient. The physicians’ surveyis mailed to a follow-up physician identified through the MDCSS.This is a very crucial part of the study because private physiciansprovide a large proportion of treatment received by cancer patients,particularly adjuvant chemotherapy, hormonal therapy andimmunotherapy, on an outpatient basis, while the current SEERprogram is focused primarily on collection of treatment data fromhospitals, radiation oncology facilities and larger clinics. Thus, ourability to assess the extent to which such therapies are provided, thecharacteristics of patients and providers in relation to treatmentsrendered and the efficacy of those treatments depends upon the useof supplemental data collection efforts such as the POC Study.Year of SurveySince 2005, we have formed a strong POC study team within theMDCSS, which includes Patricia Arballo-Spong, SEER Project Coordinator;Ann Bankowski, Research Assistant; Kari Borden, AbstractingSupervisor and Dr. Ikuko Kato as the Principal Investigator.Through this teamwork we have implemented several improvementsin this study; e.g., development of an efficient database totrack the progress of each record and to search alternative follow-upphysicians, and electronic data submission and data security. Weare very proud that we have contributed high quality data to thisSEER-supported study.Finally, we can not thank enough, all physicians who respondedto a survey over these years despite their extremely busy workschedules. Through the end of 2009, the POC studies produced 28publications, including Annual Report to the Nation on the statusof Cancer (1). These publications can be accessed online at http://healthservices.cancer.gov/surveys/poc/Reference:Table 1 - Cancers selected for SEERPatterns of Care (POC) Studies, 1997 – 2010Cancer Sites/Types1997 Bladder, Breast, Colorectal, Melanoma1998 Childhood Cancer, Non-Small Cell Lung, Ovarian, Melanoma1999 Childhood Brain Stem, DCIS Breast, Cervical, Head and Neck2000 Chronic Lymphocyctic Leukemia, Pancreas, Prostate, Corpus Uteri2001 Vulva, Testicular, Non-Hodgkin’s Lymphoma (NHL), Multiple Myeloma2002 Breast, Cervical, Colorectal2003 Cervical, Lower Esophageal/Gastric, Melanoma2004 Ovarian, Prostate, Sarcoma2005 B-Cell Lymphoma, Bladder, Chronic Myelogenous Leukemia, Multiple Myeloma2006 Node negative, ER positive female Breast, Male Breast, Head and Neck, Kidney2007 Breast, Colorectal, Non-Small Cell Lung2008 Glioblastoma, Thyroid, Cancers in Adolescent and Young Adult2009 Small Cell Lung, Acute Myeloid Leukemia, Multiple Myeloma, Liver2010 Prostate, NHL, Chronic Lymphocytic Leukemia, Gastrointestinal Stromal Tumors1. Edwards BK, Brown ML, Wingo PA, Howe HL, Ward E, Ries LA, Schrag D,Jamison PM, Jemal A, Wu XC, Friedman C, Harlan L, Warren J, AndersonRN, Pickle LW. Annual report to the nation on the status of cancer, 1975-2002,featuring population-based trends in cancer treatment. J Natl Cancer Inst 2005Oct 5;97(19):1407-27.21

Genetic Pathways of Inflammation and Risk of Lung Cancerand Chronic Obstructive Pulmonary DiseaseInvestigator: Ann G. Schwartz, PhD, MPH22Lung cancer is the leading cause of cancer deaths and chronic obstructivepulmonary disease (COPD) is the fourth leading cause ofall adult deaths in the United States. COPD is a heterogeneous setof diseases, including emphysema and chronic bronchitis. Lungcancer and COPD together account for substantial deaths andmorbidity. Five year survival following a lung cancer diagnosis isonly 15%. African-Americans are hardest hit by lung cancer, havingboth the highest rates of new lung cancers and lung cancer deathsthan any other racial or ethnic group. Smoking contributes to bothCOPD and lung cancer. About 15% of smokers will develop at leastone of these diseases. About 85-90% of all lung cancers and COPDdiagnoses are attributable to cigarette smoking. Having COPDalso contributes to the risk of getting lung cancer. After beingdiagnosed with COPD, the risk of subsequently developing lungcancer increases about 2-fold, even among people who have neversmoked. This risk seems to be most closely associated with a historyof emphysema. While low dose CT has recently been shown to bean accepted screening method for lung cancer, population screeningis not yet under way. Without screening, lung cancer is identifiedin late stages and it is often too late for surgical treatment. Neitherlung cancer, nor COPD are particularly responsive to treatment.Therefore it is vitally important to understand the underlyingsusceptibility to lung cancer and COPD, in order to understand thecarcinogenic process and to identify those persons at highest risk ofgetting these diseases. Once we understand who is at greatest riskof getting lung cancer and COPD, those at risk can be targeted forscreening and prevention interventions.It has been shown that a family history of COPD increases risk oflung cancer, even after accounting for familial clustering of smoking.This suggests a common underlying genetic contribution tothese two diseases. The biologic mechanisms linking COPD andlung cancer are not known, but chronic inflammation of lung tissueis likely to play a role. Both lung cancer and COPD develop in a lungenvironment battling chronic inflammation, which is developedover a lifetime from cigarette smoke exposure. This environmentis conducive to genetic damage, cancer initiation and progression.We do not yet know which specific genetic inflammatory mediatorseither jointly or independently promote COPD and tumor development.Although biologic responses to tobacco smoke underlie bothCOPD and lung cancer, the inflammatory processes leadingto COPD and those associated with lung cancer may be different.This is suggested by the absence of COPD features in some lung cancerpatients and the absence of lung cancer in some COPD patients.Which inflammation-producing genetic pathways are activatedand/or suppressed is likely to determine the course of diseasedevelopment among smokers. However, no comprehensive studyevaluating multiple genetic markers of inflammation in smokerswith lung cancer compared to smokers with COPD and smokerswithout either disease has ever been conducted. In addition,African-Americans, who are more likely to develop lung cancer butare less often diagnosed with COPD than Whites, have historicallynot been included in large numbers in studies of genetic variation ininflammation-related genes. This study, called the “InHALE Study”,RATE PER 100,000100806040201975Age-Adjusted Incidence Rates ofLung & Bronchus Cancers, SEER-9, 1973 – 20091980White20001985 1990 1995 2000 2005YEAR OF DIAGNOSISAfrican-AmericanSource: Surveillance, Epidemiology, and End Results (SEER) Program (www.seer.cancer.gov) SEER*StatDatabase: Incidence - SEER 9 Regs Research Data, Nov 2010 Sub (1973-2008) - Linked To County Attributes - Total U.S., 1969-2009 Counties, National Cancer Institute, DC-CPS, Surveillance Research Program, Cancer Statistics Branch, released April 2011 (updated 10/28/2011),based on the November 2010 submission.Note: Rates are per 100,000 and age-adjusted to the 2000 US Std Population (19 age groups - Census P25-1130) standard.will investigate the hypotheses that genetic variation in inflammation-relatedgenes contributes to the development of lung cancerand that this association varies by the presence or absence of COPD,and by race.To study the underlying inflammatory mechanisms linking COPDand lung cancer, we will evaluate single nucleotide polymorphisms(SNPs) in inflammatory pathway genes. Our goal is to develop agenetic profile that predicts susceptibility to lung cancer with andwithout COPD in response to tobacco exposure. Our study will expandon previous work by incorporating COPD phenotyping usingCT diagnosis of emphysema and spirometry to evaluate lung function.There has not been a study of these pathway genes in African-Americans, a group that is less likely to report COPD, smokes fewercigarettes, but sadly, is more likely to be diagnosed and die of lungcancer than Whites. We will invite patients from two large, urbanhealth systems, Karmanos Cancer Institute (KCI) and Henry FordHealth System (HFHS), to participate in this important study. Wewill recruit 2050 lung cancer cases and 2050 smokers with andwithout COPD. We hope to equally include African-Americans andWhites in this study, so we can better understand why African-Americans are harder hit with lung cancer and design better preventionstrategies for everyone. All study participants will be invited to

complete a risk factor questionnaire, undergo CTs and spirometry,provide a blood and saliva sample, and when available a tissueblock, so that we can investigate the genetic variation contributingto inflammation and thereby potentially identify a way to preventor reduce inflammation that may contribute to development ofCOPD and lung cancer. No other large study has been done thatincludes detailed phenotyping of lung cancer and COPD and jointlyevaluates inflammatory genes in germline DNA and target tissuein the same individuals. This work will lead to a better understandingof the inflammatory process in lung carcinogenesis, provideavenues for the identification of a high risk group for intervention,and provide insight into possible treatment options.InHALE, as well as all studies conducted through the MDCSS,follows strict confidentiality guidelines during all aspects of theresearch study. Independent Institutional Review Boards (IRB) thatprotect human rights during research oversee the study, both atKCI (overseen by the Wayne State University IRB) and Henry FordHealth System. Each participant will be given a consent form thatdescribes all aspects of the study and who they can contact with anyquestions. In this way, each participant is fully informed about thestudy and how the study will be conducted, before deciding if theywish to participate. All confidential data is maintained in lockedfiles and there is only limited access to computerized data. Paperrecords that contain identifiers are kept separate from the riskfactor questionnaires. The risk factor questionnaires are identifiedonly by a unique ID number, to hide the study participant’sidentity and to keep the information they provide confidential.The interview will include questions about health history includinghistory of other lung diseases and inflammatory conditions, use ofanti-inflammatory drugs, such as aspirin, smoking history, passivesmoking history, height, weight, occupation, and exposure history.Blood and other biological samples will also be labeled with only aunique ID number.This 5 year study into the genetic inflammatory pathways underlyingdevelopment of COPD and lung cancer is now enrolling patientsat both the Karmanos Cancer Institute and the Henry Ford HealthGene content for the custom,focused SNP array (640 genes total, ~ 6700 SNPS).System. Should your physician invite you to participate in thisimportant research, please consider saying “Yes.” The physician willthen put you in contact with the study interviewers. They will beavailable during normal clinic appointments to meet with you. Thisstudy will also enroll people who do not have lung cancer, but who dosmoke, for comparison purposes. You may see our study brochureshanded out at your church, area health fairs or cancer awarenessprograms; you may also hear or see ads for the “InHALE Study”.Together, we hope to prevent future lung cancers and COPD.References:1. SEER Cancer Statistics Review, 1975-2006. 2009. http://SEER.cancer.gov/csr.Accessed June 1, 2009.2. Mathers CD, Loncar D. Projections of global mortality and burden of disease from2002 to 2030. PLoS Med. Nov 2006;3(11):e442. PMID: 171320523 Sethi JM, Rochester CL. Smoking and chronic obstructive pulmonary disease.Clinics in chest medicine. Mar 2000;21(1):67-86, viii. PMID: 107630904. CDC. Cigarette smoking among adults--United States, 2002. Morbidity andMortality Weekly Report. 2004;53(20):428-431. PMID:5. Mannino DM, Aguayo SM, Petty TL, Redd SC. Low lung function and incidentlung cancer in the United States: data From the First National Health andNutrition Examination Survey follow-up. Archives of internal medicine. Jun 232003;163(12):1475-1480. PMID: 128240986. Schabath MB, Delclos GL, Martynowicz MM, et al. Opposing effects ofemphysema, hay fever, and select genetic variants on lung cancer risk. Am JEpidemiol. Mar 1 2005;161(5):412-422. PMID: 157184777. Littman AJ, Thornquist MD, White E, Jackson LA, Goodman GE, Vaughan TL.Prior lung disease and risk of lung cancer in a large prospective study. CancerCauses Control. Oct 2004;15(8):819-827. PMID: 154569958. Turner MC, Chen Y, Krewski D, Calle EE, Thun MJ. Chronic obstructivepulmonary disease is associated with lung cancer mortality in a prospective studyof never smokers. American journal of respiratory and critical care medicine.Aug 1 2007;176(3):285-290. PMID: 1747861523Inflammation(243 genes)COPD(84 genes)Lung Cancer(358 genes)9. Mayne ST, Buenconsejo J, Janerich DT. Familial cancer history and lung cancer riskin United States nonsmoking men and women. Cancer Epidemiol Biomarkers Prev.Dec 1999;8(12):1065-1069. PMID: 1061333810. Wu AH, Yu MC, Thomas DC, Pike MC, Henderson BE. Personal and family historyof lung disease as risk factors for adenocarcinoma of the lung. Cancer Res. Dec 151988;48(24 Pt 1):7279-7284. PMID: 319149811. Schwartz AG, Ruckdeschel JC. Familial lung cancer: genetic susceptibility andrelationship to chronic obstructive pulmonary disease. American journal ofrespiratory and critical care medicine. Jan 1 2006;173(1):16-22. PMID: 1614144512. Gohagan J, Marcus P, Fagerstrom R, Pinsky P, Kramer B, Prorok P. Baseline findingsof a randomized feasibility trial of lung cancer screening with spiral CT scan vschest radiograph: the Lung Screening Study of the National Cancer Institute. Chest.Jul 2004;126(1):114-121. PMID: 15249451

The Epidemiology Research CoreDirector: Kendra Schwartz, MD, MSPH; Co-Director: Fawn D. Vigneau, JD, MPH;Project Coordinator: Patricia Arballo-Spong; Administrator: Sharon Moton24Wayne State University(WSU) and Karmanos CancerInstitute (KCI) house theMetropolitan Detroit CancerSurveillance System (MDCSS)and the EpidemiologyResearch Core (ERC). TheMDCSS is a National CancerInstitute (NCI)-funded,population-based Surveillance Epidemiology and End Results(SEER) cancer registry. The MDCSS collects cancer data for themetropolitan Detroit area (Wayne, Oakland and Macomb counties)population of nearly four million residents. Data are collected fromapproximately 60 different hospitals, clinics, pathology laboratoriesand radiation therapy facilities in the area (Figure 1).Figure 1. MDCSS/Detroit SEER – Participating FacilitiesThe MDCSS receives SEER contractual funding for the conduct ofcancer case-finding, medical record abstraction for SEER-requiredinformation, vital status follow-up, and the provision of data backto the contributing facilities for clinical and accreditation purposes.NCI contractual funding for the MDCSS covers only basic registryoperations. The ERC was developed to support population-basedcancer research. The services of the ERC represent populationbasedresearch activities that are outside the scope of the MDCSS/SEER cancer registry data collection. The ERC does this byaccessing metropolitan Detroit cancer case data for research,epidemiology consulting and collaboration with researchersconducting investigations in cancer prevention, etiology, treatmentand outcomes. The ERC benefits cancer research in metropolitanDetroit by centralizing access to SEER data and standardizingpatient, physician and hospital interactions for population-basedresearch purposes.SEER data are complex and require knowledge of and expertisewith the data management system for manipulation. Furthermore,strict confidentiality measures must be maintained. The ERCmaintains patient and provider confidentiality by performingall patient, physician and hospital contact for the conduct ofpopulation-based research in-house. ERC faculty and staff haveextensive expertise in using both local and national SEER data andprovide the necessary support for access and utilization of thesedata for population-based investigations of cancer prevention,etiology, treatment and outcomes. Specifically, the EpidemiologyResearch Core provides:• Consultation. Consultation and collaborative research expertise focusedon study design, proposal development, IRB applications, and interpretationof population-based local and national SEER data.• Rapid Case Ascertainment. Rapid identification and ascertainment ofeligible study participants, requiring review of all pathology reportsindicating a cancer diagnosis at approximately 60 metropolitan areahospitals, clinics, pathology laboratories and radiation therapy facilitiesand rapid collection of patient demographic information. This speeds upcase identification for population-based studies, with most cases identifiedwithin one to two months of diagnosis.• Control Identification. Identification of population-based control groupsfor case-control study designs via random digit dialing, Centers for Medicaidand Medicare Services (CMS) records, Department of Motor Vehicles (DMV)records, and other mechanisms.• Research Support and Training. Liaison for WSU IRB, regulatorytraining of epidemiology study staff, oversight and research support forepidemiology studies.• Collection and Abstraction of Medical Records. Collection of medicalrecords and abstracting of study-specific data which are not available in theMDCSS registry.• Biospecimen Collection. Collection of biologic specimens, includingblood, buccal cells and tumor blocks, from study participants and/ordiagnosing hospitals.• Database Query. Response to requests for population-based datarequiring query of the MDCSS and/or the national SEER Limited-Use datafiles for descriptive analyses.• Database Linkage. Linkage of outside data sources to MDCSS data for thecollection of patient demographics, treatment and survival data.Current projects utilizing ERC services include:• Inflammation Pathways and COPD in the Developmentof Lung Cancer• Life Course Energy Balance and Breast Cancer Risk in Black/White Women Under 50• Patient and Provider Influences on Disparities in ColorectalCancer Care• The Epidemiology of Ovarian Cancer in African-American WomenResearchers wishing to utilize Metropolitan Detroit SEER data can contact:Kendra L. Schwartz, MD, MSPHDirector, Epidemiology Research Corekensch@med.wayne.eduFawn D. Vigneau, JD, MPHCo-Director, Epidemiology Research Corevigneauf@med.wayne.eduPrices for use of ERC services are listed on our web-site:https://research1.karmanos.org/research/Home2/Researchers2/CoreFacilities/EpidemiologyResearch/ServicesFees.aspx

List of Studies Conducted at theMetropolitan Detroit Cancer Surveillance SystemThe Metropolitan Detroit Cancer Surveillance System participates ina number of collaborative research projects. A brief description of asample of these projects conducted during the past 2 years follows.Inflammation Pathways and COPD in theDevelopment of Lung CancerA. SchwartzThe biologic mechanisms linking COPD and lung cancer areunknown, but chronic inflammation is likely to play a role. Thisstudy will evaluate SNPs and copy number variation in genesin inflammatory pathways. The study will expand on previouswork by incorporating COPD phenotyping using CT diagnosis ofemphysema and pulmonary function testing (PFT). It also willexpand on the panel of genes beyond those few already evaluated,will incorporate copy number variation as well as non-synonymousand functional SNPs, and will include a large African-Americanpopulation. There has not been a study of these pathway genesin African-Americans, a group that is less likely to report COPD,smokes fewer cigarettes, but is more likely to be diagnosed withlung cancer than whites. It is hypothesized that genetic variationin inflammation-related genes contributes to the development oflung cancer and this association varies by the presence or absenceof COPD, and by race. The goal is to develop a genetic profile basedon SNPs and copy number variation in inflammation pathway genesthat predicts susceptibility to lung cancer with and without COPDin response to tobacco exposure.foundation to conduct studies of other cancers in African-Americanwomen in the future. We will expand the examination of geneticassociation to a more comprehensive genome-wide associationstudy once data collection is complete.Dr. Cote commenced rapid case ascertainment in December 2010for the Metropolitan Detroit site of the multi-site study. Thenational collaboration will attempt to enroll 1,000 cases and 1,000controls at nine sites across the U.S. The Detroit site startedBiospecimen Collection in October, 2011 and will collect blood andtissue on 35 cases annually.A Genome Wide Study of Lung Cancerin Never SmokersA. Schwartz/O. GorlovaThis study will identify genetic architecture of the predispositionto lung cancer in never smokers.Genetic Susceptibility for Lung Cancer inAfrican-AmericansA. Schwartz/C. AmosThe aim of this work is to validate novel genetic variants identifiedin genome-wide association studies in African-American lungcancer cases and age, race and gender-matched controls identifiedfrom our existing study populations.25Transdisciplinary Research in Cancerof the Lung (TRICL)A. Schwartz/C. AmosThis study integrates data from multiple genome-wide associationstudies in lung cancer and carries these findings forward tocharacterize mechanisms by which the identified genes influencelung cancer risk. We will use results from extended epidemiologicalstudies to develop refined risk models to predict lung cancer riskand to validate the results using data from cohort studies.The Epidemiology of Ovarian Cancer inAfrican-American WomenA. Schwartz/M. CoteTo address the lack of knowledge regarding ovarian cancer amongAfrican-American women, investigators at nine institutions inareas with relatively large numbers of African-Americans in thepopulation (North Carolina, South Carolina, Georgia, Alabama,New Orleans, New Jersey, Ohio, Illinois, and Detroit) will conducta population-based, case-control study to assess etiologic riskfactors for African-Americans. Further, we will obtain treatmentand outcome information to evaluate prognostic factors inovarian cancer cases. We anticipate that this study will provide aPancreatic Cancer Genetic Epidemiology ConsortiumA. Schwartz/G. PetersenThis project establishes the PACGENE Consortium of sixinstitutions throughout the Unites States and Canada whosepurpose is to identify and recruit kindreds with familial pancreaticcancer for gene discovery research. Family history and risk factorinformation will be collected from participating family members,along with DNA specimens for a 10-cM genome screen for linkageand subsequent fine mapping of selected chromosomal regions. Dr.Schwartz is the PI of a subcontract to the Mayo Clinic, where the PIof the Consortium is Dr. Gloria Petersen.Genetic Epidemiology of Lung Cancer IA. SchwartzThis study is designed to create a family registry and searchfor lung cancer genes in high risk lung cancer families.A supplemental study will identify additional lung cancer caseswith family histories for a future GWAS.

List of Studies Conducted at theMetropolitan Detroit Cancer Surveillance System (cont.)Genetic Epidemiology of Lung CancerA. SchwartzThis study is a case-control study of lung cancer in African-Americans that will use admixture mapping to identify genes forlung cancer. This grant has been continuously funded since 1999and also focused on familial aggregation and candidate gene studiesin early onset and never smoking lung cancer cases.A supplement is focused on reconsenting participants for use oftheir biospecimens in an NCI-directed GWAS in African-Americans.Disparity in Quality of Breast Cancer Treatmentand Effects on OutcomeK. Schwartz/J. GriggsIn this research study we will investigate the relationship betweenthe quality of breast cancer adjuvant treatment and disease-freeand overall survival; determine whether racial, socioeconomic,and weight-based disparities exist in the quality of breast canceradjuvant treatment and timing of treatments; and verify thatdisparities in outcomes exist.26Life Course Energy Balance and Breast Cancer Riskin Black/White Women Under 50K. Schwartz/E. VelieBreast cancer in younger women (under age 50) is poorlyunderstood and understudied. Moreover, it is associated with aworse prognosis than breast cancer in older women. Potentiallymodifiable risk factors related to energy balance over the life course(e.g. growth and puberty patterns, body mass, insulin resistance,diet and physical activity) have been implicated in the etiology ofbreast cancer in younger women. The overall objective of this studyis to investigate, in a socioeconomically diverse population of Blackand White women, whether life course energy balance pathways areassociated with breast cancer risk. The study will also investigatethe association of energy balance with the different breast cancermolecular subtypes. Dr. Kendra Schwartz is the local PI for thisNational Cancer Institute funded study.Racial, Ethnic and SES Disparities in Qualityof Breast Cancer Systemic TherapyK. Schwartz/J. GriggsThe study will conduct a medical record review and tests onpreviously removed breast cancer tumor tissue to explore thequality of adjuvant chemotherapy and hormonal therapy as well asvariations based on race and ethnicity. It is a companion study to“Racial/Ethnic Disparities in Work and QOL Outcomes in Survivorsof Breast Cancer” for patients who were initially diagnosed withinvasive breast cancer without distant metastasis.Racial/Ethnic Disparities in Work and QOL Outcomesin Survivors of Breast CancerK. Schwartz/S. HawleyThe study will re-survey female breast cancer patients four yearsafter diagnosis to explore employment changes, quality of liferatings, decisions about adjuvant therapy, and variations inexperience based on race and ethnicity. This is a follow-up studydesigned specifically for patients who enrolled in “Health SystemFactors and Patient Outcomes in Breast Cancer.”Health System Factors and Patient Outcomesin Breast CancerK. Schwartz/S. KatzThis study measures the impact of the breast cancer experienceon women, addressing topics such as barriers to diagnosis andtreatment, coordination of care and employment difficultiesrelated to treatment.Prostate Cancer Treatment Decision Making -ACS Mentored Research AwardK. Schwartz/J. XuThis study uses both qualitative and quantitative methods tobetter understand racial/ethnic disparities in prostate cancerdecision treatment. A structured interview will be conducted withrecently diagnosed prostate cancer patients, prior to treatment.This information will be used in creating a culturally sensitivecomprehensive instrument to determine factors associated withprostate cancer treatment choice, which will then be pilot tested asa mailed questionnaire to recently diagnosed prostate cancer casesidentified through SEER.Patient and Provider Influences on Disparities inColorectal Cancer CareI. KatoThe investigators seek to examine whether racial disparities in useof chemotherapy for stage III colorectal cancer are primarily dueto socioeconomic, psychosocial and patient-provider relationshipfactors. The project will be conducted in collaboration with theAtlanta SEER registry under leadership of Dr. Morris at theUniversity of Michigan.

Analysis of Cancer Rates and Trends Using CensusTract Variables from Multiple RegistriesI. KatoDespite the growing recognition of the magnitude andpersistence of health disparities, few indicators for socioeconomicstatus (SES) are available in most of the US public healthsurveillance databases to date. Using the data from four SEERregistries, Detroit, Hawaii, Utah and Seattle-Puget, that have along history of high quality cancer registration and excellentcensus tract coverage, we intend to develop common objective andtransferrable census tract SES variables across multi-decennialdata from 1970 to 2000 and examine long-term chronologicaltrends in cancer survival for selected cancer sites according tothose census tract variables. This investigation may help identifyspecific SES groups in the community which require more intensiveintervention in reducing disparities.Oxidative Stress, Antioxidants and RacialDisparities in Prostate CancerC. BockThis study will examine three genes in the oxidative stress pathwayalong with intake of three antioxidants to determine whethervariation in the genes modifies prostate cancer risk associated withintake of each of the antioxidants.Genetic Susceptibility to Cancers of the Prostateand Urinary BladderJ. Beebe-DimmerThe overall goal of this research is to estimate the effects ofgenetic factors on risk of prostate and bladder cancers in twoestablished studies.SEER Patterns of Care StudyI. KatoThe SEER Patterns of Care (POC) Study annually examinestreatment patterns in the U.S. for rotating cancer sites.The 2012 POC study will collect data on metastatic melanoma,mesothelioma, oligodendroglioma/astrocytoma, neuroblastoma,and ovarian cancer diagnosed in the year 2011.27Exploring Common Linkage Regions inLung Cancer and COPDM. CoteThe overall goal of this research plan is to investigate theimportance of chromosome 6 on lung cancer and COPDdevelopment.A Genome Wide Admixture Scan of MultipleMyeloma in African-AmericansJ. Zonder/C. BockAfrican-Americans experience the highest risk of multiple myelomain the world. The reason for the higher risk is not known, but thereis evidence that genetic factors might contribute. The purpose ofthis research study is to identify the causes of multiple myelomain African-Americans, especially genetic risk factors, which wehope, will lead to better treatments and prevention. We expectthat about 2,000 patients will participate in this study. Patients arebeing recruited from California, Alabama, New Jersey, Louisiana,Detroit, Atlanta, Houston, Baltimore and Chicago. This study isbeing led by Wendy Cozen, DO, MPH.

Metropolitan Detroit CancerSurveillance System/SEER Publications 2010-201228In PressBecker N, Falster MO, Vajdic CM, de Sanjose S, Martinez-Maza O, BracciPM, Melbye M, Smedby KE, Engels EA, Turner J, Vineis P, CostantiniAS, Holly EA, Spinelli JJ, La Vecchia C, Zheng T, Chiu BCH, Montella M,Cocco P, Maynadie M, Foretova L, Staines A, Brennan P, Davis S, SeversonR, Cerhan JR, Breen EC, Birmann B, Cozen W, Grulich AE, NewtonR. Self-reported history of infections and the risk of non-hodgkinlymphoma: an InterLymph pooled analysis. Int J Cancer. In press.Keegan TH, Lichtensztajn DY, Kato I, Kent EE, Wu XC, West MM, HamiltonAS, Zebrack B, Bellizzi KM, Smith AW, and the AYAHSCG. Unmetadolescent and young adult cancer survivors information and serviceneeds: a population-based cancer registry study. J Cancer Surviv. In press.Parsons HM, Harlan LC, Lynch CF, Hamilton AS, Wu XC, Kato I, SchwartzSM, Smith AW, Keel G, Keegan TH. Impact of Cancer on Work andEducation Among Adolescent and Young Adult Cancer Survivors. J ClinOncol. In press.Schwartz AG, Schwartz K, Harris J. USA, Michigan, Metropolitan Detroit.In Cancer Incidence in Five Continents, Volume IX: IARC ScientificPublication. In press.Simon MS, Lamerato L, Krajenta R, Booza JR, Ruterbusch JJ, Kunz S,Schwartz K. Racial Differences in the Use of Adjuvant Chemotherapy forBreast Cancer in a Large Urban Integrated Health System. InternationalJournal of Breast Cancer. In press.Wang SS, Hartge P, Cerhan J, Cozen W, Davis S, Severson R, Chatterjee N,Yeager M, Chanock S, Rothman N. Immune gene polymorphisms and riskof non-Hodgkin lymphoma in the NCI-SEER case control study. J ClinOncol. In press.Wang SS, Purdue M, Cerhan JR, Zheng T, Menashe I, Armstrong B, Lan Q,Hartge P, Kricker A, Zhang Y, Morton LM, Valdjic C, Holford T, SeversonRK, Grulich A, Leaderer B, Davis S, Zahm S, Cozen W, Yeager M, ChanockSJ, Chatterjee N, Rothman N. Common Genetic Variations in the TumorNecrosis Factor (TNF) and TNF Receptor Superfamilies and NuclearFactor Kappa Beta Transcription Factors and Risk of Non-HodgkinLymphoma. PLoS ONE. In press.Wang S, Levin A, Smolinski S, Vigneau F, Levin N, Tainsky M. BreastCancer and Other Neoplasia in Women with Neurofibromatosis Type 1:A Retrospective Review of Cases in the Detroit Metropolitan Area. Am JMed Genet Part A. In press.2012Al-Sukhni W, Joe S, Lionel AC, Zwingerman N, Zogopoulos G, MarshallCR, Borgida A, Holter S, Gropper A, Moore S, Bondy M, Klein AP,Petersen GM, Rabe KG, Schwartz AG, Syngal S, Scherer SW, GallingerS. Identification of germline genomic copy number variation in familialpancreatic cancer. Hum Genet. 2012. [Epub ahead of print]Beebe-Dimmer JL, Cetin K, Shahinian V, Morgenstern H, Yee C, SchwartzKL, Acquavella J. Timing of androgen deprivation therapy use andfracture risk among elderly men with prostate cancer in the UnitedStates. Pharmacoepidemiol Drug Saf. 2012;21(1):70-8.Bellizzi KM, Smith A, Schmidt S, Keegan TH, Zebrack B, Lynch CF, DeapenD, Shnorhavorian M, Tompkins BJ, Simon M, and the A, Young AdultHealth O, Patient Experience Study Collaborative G. Positive and negativepsychosocial impact of being diagnosed with cancer as an adolescent oryoung adult. Cancer. 2012. [Epub ahead of print]Boleij A, Roelofs R, Danne C, Bellais S, Dramsi S, Kato I, Tjalsma H.Selective Antibody Response to Streptococcus gallolyticus Pilus Proteinsin Colorectal Cancer Patients. Cancer Prev Res (Phila). 2012;5(2):260-5.Chen LS, Saccone NL, Culverhouse RC, Bracci PM, Chen CH, Dueker N, HanY, Huang H, Jin G, Kohno T, Ma JZ, Przybeck TR, Sanders AR, SmithJA, Sung YJ, Wenzlaff AS, Wu C, Yoon D, Chen YT, Cheng YC, Cho YS,David SP, Duan J, Eaton CB, Furberg H, Goate AM, Gu D, Hansen HM,Hartz S, Hu Z, Kim YJ, Kittner SJ, Levinson DF, Mosley TH, Payne TJ,Rao DC, Rice JP, Rice TK, Schwantes-An TH, Shete SS, Shi J, Spitz MR,Sun YV, Tsai FJ, Wang JC, Wrensch MR, Xian H, Gejman PV, He J, HuntSC, Kardia SL, Li MD, Lin D, Mitchell BD, Park T, Schwartz AG, Shen H,Wiencke JK, Wu JY, Yokota J, Amos CI, Bierut LJ. Smoking and geneticrisk variation across populations of European, Asian, and African-American ancestry--a meta-analysis of chromosome 15q25. GenetEpidemiol. 2012;36(4):340-51. PMC3387741.Cote ML, Kam A, Chang CY, Raskin L, Reding KW, Cho KR, Gruber SB,Ali-Fehmi R. A pilot study of microsatellite instability and endometrialcancer survival in white and African-American women. Int J GynecolPathol. 2012;31(1):66-72.Cote ML, Liu M, Bonassi S, Neri M, Schwartz AG, Christiani DC, SpitzMR, Muscat JE, Rennert G, Aben KK, Andrew AS, Bencko V, BickebollerH, Boffetta P, Brennan P, Brenner H, Duell EJ, Fabianova E, Field JK,Foretova L, Friis S, Harris CC, Holcatova I, Hong YC, Isla D, Janout V,Kiemeney LA, Kiyohara C, Lan Q, Lazarus P, Lissowska J, Le MarchandL, Mates D, Matsuo K, Mayordomo JI, McLaughlin JR, Morgenstern H,Mueller H, Orlow I, Park BJ, Pinchev M, Raji OY, Rennert HS, Rudnai P,Seow A, Stucker I, Szeszenia-Dabrowska N, Dawn Teare M, Tjonnelan A,Ugolini D, van der Heijden HF, Wichmann E, Wiencke JK, Woll PJ, YangP, Zaridze D, Zhang ZF, Etzel CJ, Hung RJ. Increased risk of lung cancerin individuals with a family history of the disease: A pooled analysis fromthe International Lung Cancer Consortium. Eur J Cancer. 2012. [Epubahead of print]Cote ML, Colt JS, Schwartz KL, Wacholder S, Ruterbusch JJ, Davis F,Purdue M, Graubard BI, Chow WH. Cigarette smoking and renal cellcarcinoma risk among black and white Americans: effect modificationby hypertension and obesity. Cancer Epidemiol Biomarkers Prev.2012;21(5):770-9. PMC3348421.Djuric Z, Severson RK, Kato I. Association of dietary quercetin withreduced risk of proximal colon cancer. Nutr Cancer. 2012;64(3):351-60.PMC3329181.Jacobs KB, Yeager M, Zhou W, Wacholder S, Wang Z, Rodriguez-Santiago B,Hutchinson A, Deng X, Liu C, Horner MJ, Cullen M, Epstein CG, BurdettL, Dean MC, Chatterjee N, Sampson J, Chung CC, Kovaks J, Gapstur SM,Stevens VL, Teras LT, Gaudet MM, Albanes D, Weinstein SJ, Virtamo J,Taylor PR, Freedman ND, Abnet CC, Goldstein AM, Hu N, Yu K, YuanJM, Liao L, Ding T, Qiao YL, Gao YT, Koh WP, Xiang YB, Tang ZZ, FanJH, Aldrich MC, Amos C, Blot WJ, Bock CH, Gillanders EM, Harris CC,Haiman CA, Henderson BE, Kolonel LN, Le Marchand L, McNeill LH,Rybicki BA, Schwartz AG, Signorello LB, Spitz MR, Wiencke JK, WrenschM, Wu X, Zanetti KA, Ziegler RG, Figueroa JD, Garcia-Closas M, MalatsN, Marenne G, Prokunina-Olsson L, Baris D, Schwenn M, Johnson A,Landi MT, Goldin L, Consonni D, Bertazzi PA, Rotunno M, RajaramanP, Andersson U, Freeman LE, Berg CD, Buring JE, Butler MA, Carreon T,Feychting M, Ahlbom A, Gaziano JM, Giles GG, Hallmans G, HankinsonSE, Hartge P, Henriksson R, Inskip PD, Johansen C, Landgren A, McKean-Cowdin R, Michaud DS, Melin BS, Peters U, Ruder AM, Sesso HD, SeveriG, Shu XO, Visvanathan K, White E, Wolk A, Zeleniuch-Jacquotte A,Zheng W, Silverman DT, Kogevinas M, Gonzalez JR, Villa O, Li D, DuellEJ, Risch HA, Olson SH, Kooperberg C, Wolpin BM, Jiao L, Hassan M,Wheeler W, Arslan AA, Bueno-de-Mesquita HB, Fuchs CS, GallingerS, Gross MD, Holly EA, Klein AP, Lacroix A, Mandelson MT, Petersen

G, Boutron-Ruault MC, Bracci PM, Canzian F, Chang K, Cotterchio M,Giovannucci EL, Goggins M, Bolton JA, Jenab M, Khaw KT, KroghV, Kurtz RC, McWilliams RR, Mendelsohn JB, Rabe KG, Riboli E,Tjonneland A, Tobias GS, Trichopoulos D, Elena JW, Yu H, AmundadottirL, Stolzenberg-Solomon RZ, Kraft P, Schumacher F, Stram D, SavageSA, Mirabello L, Andrulis IL, Wunder JS, Garcia AP, Sierrasesumaga L,Barkauskas DA, Gorlick RG, Purdue M, Chow WH, Moore LE, SchwartzKL, Davis FG, Hsing AW, Berndt SI, Black A, Wentzensen N, Brinton LA,Lissowska J, Peplonska B, McGlynn KA, Cook MB, Graubard BI, Kratz CP,Greene MH, Erickson RL, Hunter DJ, Thomas G, Hoover RN, Real FX,Fraumeni JF, Jr., Caporaso NE, Tucker M, Rothman N, Perez-Jurado LA,Chanock SJ. Detectable clonal mosaicism and its relationship to agingand cancer. Nat Genet. 2012;44(6):651-8. PMC3372921.Mina N, Soubani AO, Cote ML, Suwan T, Wenzlaff AS, Jhajhria S, SamarahH, Schwartz AG. The relationship between chronic obstructive pulmonarydisease and lung cancer in African-American patients. Clin Lung Cancer.2012;13(2):149-56.Patel MK, Cote ML, Ali-Fehmi R, Buekers T, Munkarah AR, Elshaikh MA.Trends in the utilization of adjuvant vaginal cuff brachytherapy and/orexternal beam radiation treatment in stage I and II endometrial cancer: asurveillance, epidemiology, and end-results study. Int J Radiat Oncol BiolPhys. 2012;83(1):178-84.Roberts NJ, Jiao Y, Yu J, Kopelovich L, Petersen GM, Bondy ML, GallingerS, Schwartz AG, Syngal S, Cote ML, Axilbund J, Schulick R, Ali SZ,Eshleman JR, Velculescu VE, Goggins M, Vogelstein B, PapadopoulosN, Hruban RH, Kinzler KW, Klein AP. ATM mutations in patients withhereditary pancreatic cancer. Cancer Discov. 2012;2(1):41-6.Rosenberger A, Bickeboller H, McCormack V, Brenner DR, Duell EJ,Tjonneland A, Friis S, Muscat JE, Yang P, Wichmann HE, Heinrich J,Szeszenia-Dabrowska N, Lissowska J, Zaridze D, Rudnai P, FabianovaE, Janout V, Bencko V, Brennan P, Mates D, Schwartz AG, Cote ML,Zhang ZF, Morgenstern H, Oh SS, Field JK, Raji O, McLaughlin JR,Wiencke J, LeMarchand L, Neri M, Bonassi S, Andrew AS, Lan Q, Hu W,Orlow I, Park BJ, Boffetta P, Hung RJ. Asthma and lung cancer risk: asystematic investigation by the International Lung Cancer Consortium.Carcinogenesis. 2012;33(3):587-97. PMC3291861.Schwartz AG. Genetic epidemiology of cigarette smoke-induced lungdisease. Proc Am Thorac Soc. 2012;9(2):22-6. PMC3359114.Semaan A, Ali-Fehmi R, Munkarah AR, Bandyopadhyay S, Morris RT, RizkS, Mert I, Ruterbusch JJ, Cote ML. Clinical/pathologic features andpatient outcome in early onset endometrial carcinoma: A populationbased analysis and an institutional perspective from the Detroitmetropolitan area, Michigan. Gynecol Oncol. 2012;124(2):265-9.Sethi S, Ali-Fehmi R, Franceschi S, Struijk L, van Doorn LJ, Quint W,Albashiti B, Ibrahim M, Kato I. Characteristics and survival of head andneck cancer by HPV status: a cancer registry-based study. Int J Cancer.2012;131(5):1179-86. PMC3319485.Seward S, Ali-Fehmi R, Munkarah AR, Semaan A, Al-Wahab ZR, ElshaikhMA, Cote ML, Morris RT, Bandyopadhyay S. Outcomes of patients withuterine serous carcinoma using the revised FIGO staging system. Int JGynecol Cancer. 2012;22(3):452-6.Wu X, Scelo G, Purdue MP, Rothman N, Johansson M, Ye Y, Wang Z,Zelenika D, Moore LE, Wood CG, Prokhortchouk E, Gaborieau V,Jacobs KB, Chow WH, Toro JR, Zaridze D, Lin J, Lubinski J, TrubickaJ, Szeszenia-Dabrowska N, Lissowska J, Rudnai P, Fabianova E, MatesD, Jinga V, Bencko V, Slamova A, Holcatova I, Navratilova M, Janout V,Boffetta P, Colt JS, Davis FG, Schwartz KL, Banks RE, Selby PJ, HarndenP, Berg CD, Hsing AW, Grubb RL, 3rd, Boeing H, Vineis P, Clavel-ChapelonF, Palli D, Tumino R, Krogh V, Panico S, Duell EJ, Quiros JR, SanchezMJ, Navarro C, Ardanaz E, Dorronsoro M, Khaw KT, Allen NE, Buenode-MesquitaHB, Peeters PH, Trichopoulos D, Linseisen J, LjungbergB, Overvad K, Tjonneland A, Romieu I, Riboli E, Stevens VL, Thun MJ,Diver WR, Gapstur SM, Pharoah PD, Easton DF, Albanes D, Virtamo J,Vatten L, Hveem K, Fletcher T, Koppova K, Cussenot O, Cancel-Tassin G,Benhamou S, Hildebrandt MA, Pu X, Foglio M, Lechner D, HutchinsonA, Yeager M, Fraumeni JF, Jr., Lathrop M, Skryabin KG, McKay JD, GuJ, Brennan P, Chanock SJ. A genome-wide association study identifies anovel susceptibility locus for renal cell carcinoma on 12p11.23. Hum MolGenet. 2012;21(2):456-62. PMC3276284.2011Alderman AK, Hawley ST, Morrow M, Salem B, Hamilton A, Graff JJ,Katz S. Receipt of delayed breast reconstruction after mastectomy:do women revisit the decision? Ann Surg Oncol. 2011;18(6):1748-56.PMC3174852.Beebe-Dimmer J, Morgenstern H, Cetin K, Yee C, Bartoces M, Shahinian V,Fryzek J, Acquavella J, Schwartz KL. Androgen deprivation therapy andcataract incidence among elderly prostate cancer patients in the UnitedStates. Ann Epidemiol. 2011;21(3):156-63.Boffetta P, Jayaprakash V, Yang P, Asomaning K, Muscat JE, Schwartz AG,Zhang ZF, Le Marchand L, Cote ML, Stoddard SM, Morgenstern H, HungRJ, Christiani DC. Tobacco smoking as a risk factor of bronchioloalveolarcarcinoma of the lung: pooled analysis of seven case-control studies in theInternational Lung Cancer Consortium (ILCCO). Cancer Causes Control.2011;22(1):73-9. PMC3002160.Chang CM, Wang SS, Dave BJ, Jain S, Vasef MA, Weisenburger DD, CozenW, Davis S, Severson RK, Lynch CF, Rothman N, Cerhan JR, Hartge P,Morton LM. Risk factors for non-Hodgkin lymphoma subtypes definedby histology and t(14;18) in a population-based case-control study. Int JCancer. 2011;129(4):938-47. PMC3125462.Colt JS, Schwartz K, Graubard BI, Davis F, Ruterbusch J, DiGaetano R,Purdue M, Rothman N, Wacholder S, Chow WH. Hypertension and riskof renal cell carcinoma among white and black Americans. Epidemiology.2011;22(6):797-804. PMC3188386.Cote ML, Haddad R, Edwards DJ, Atikukke G, Gadgeel S, Soubani AO,Lonardo F, Bepler G, Schwartz AG, Ethier SP. Frequency and type ofepidermal growth factor receptor mutations in African-Americanswith non-small cell lung cancer. J Thorac Oncol. 2011;6(3):627-30.PMC3057407.Daniel CR, Schwartz KL, Colt JS, Dong LM, Ruterbusch JJ, Purdue MP,Cross AJ, Rothman N, Davis FG, Wacholder S, Graubard BI, Chow WH,Sinha R. Meat-cooking mutagens and risk of renal cell carcinoma. Br JCancer. 2011;105(7):1096-104. PMC3185955.Filson CP, Miller DC, Colt JS, Ruterbusch J, Linehan WM, Chow WH,Schwartz K. Surgical approach and the use of lymphadenectomy andadrenalectomy among patients undergoing radical nephrectomy for renalcell carcinoma. Urol Oncol. 2011. PMC3123686. [Epub ahead of print]Gold LS, Stewart PA, Milliken K, Purdue M, Severson R, Seixas N, BlairA, Hartge P, Davis S, De Roos AJ. The relationship between multiplemyeloma and occupational exposure to six chlorinated solvents. OccupEnviron Med. 2011;68(6):391-9. PMC3094509.Harlan LC, Lynch CF, Keegan TH, Hamilton AS, Wu XC, Kato I, West MM,Cress RD, Schwartz SM, Smith AW, Deapen D, Stringer SM, Potosky AL,Group AHSC. Recruitment and follow-up of adolescent and young adult29

Metropolitan Detroit CancerSurveillance System/SEER Publications 2010-2012 (continued)30cancer survivors: the AYA HOPE Study. J Cancer Surviv. 2011;5(3):305-14. PMC3159756.Hinch AG, Tandon A, Patterson N, Song Y, Rohland N, Palmer CD, Chen GK,Wang K, Buxbaum SG, Akylbekova EL, Aldrich MC, Ambrosone CB, AmosC, Bandera EV, Berndt SI, Bernstein L, Blot WJ, Bock CH, Boerwinkle E,Cai Q, Caporaso N, Casey G, Cupples LA, Deming SL, Diver WR, Divers J,Fornage M, Gillanders EM, Glessner J, Harris CC, Hu JJ, Ingles SA, IsaacsW, John EM, Kao WH, Keating B, Kittles RA, Kolonel LN, Larkin E, LeMarchand L, McNeill LH, Millikan RC, Murphy A, Musani S, Neslund-Dudas C, Nyante S, Papanicolaou GJ, Press MF, Psaty BM, Reiner AP, RichSS, Rodriguez-Gil JL, Rotter JI, Rybicki BA, Schwartz AG, Signorello LB,Spitz M, Strom SS, Thun MJ, Tucker MA, Wang Z, Wiencke JK, WitteJS, Wrensch M, Wu X, Yamamura Y, Zanetti KA, Zheng W, Ziegler RG,Zhu X, Redline S, Hirschhorn JN, Henderson BE, Taylor HA, Jr., PriceAL, Hakonarson H, Chanock SJ, Haiman CA, Wilson JG, Reich D, MyersSR. The landscape of recombination in African-Americans. Nature.2011;476(7359):170-5. PMC3154982.Hofmann JN, Baccarelli A, Schwartz K, Davis FG, Ruterbusch JJ, Hoxha M,McCarthy BJ, Savage SA, Wacholder S, Rothman N, Graubard BI, Colt JS,Chow WH, Purdue MP. Risk of renal cell carcinoma in relation to bloodtelomere length in a population-based case-control study. Br J Cancer.2011;105(11):1772-5. PMC3242602.Lan Q, Wang SS, Menashe I, Armstrong B, Zhang Y, Hartge P, PurdueMP, Holford TR, Morton LM, Kricker A, Cerhan JR, Grulich A, CozenW, Zahm SH, Yeager M, Vajdic CM, Schenk M, Leaderer B, Yuenger J,Severson RK, Chatterjee N, Chanock SJ, Zheng T, Rothman N. Geneticvariation in Th1/Th2 pathway genes and risk of non-Hodgkin lymphoma:a pooled analysis of three population-based case-control studies. Br JHaematol. 2011;153(3):341-50. PMC3075370.Lu Y, Abdou AM, Cerhan JR, Morton LM, Severson RK, Davis S, CozenW, Rothman N, Bernstein L, Chanock S, Hartge P, Wang SS. Humanleukocyte antigen class I and II alleles and overall survival in diffuselarge B-cell lymphoma and follicular lymphoma. ScientificWorldJournal.2011;11:2062-70. PMC3217596.Mujahid MS, Janz NK, Hawley ST, Griggs JJ, Hamilton AS, Graff J, KatzSJ. Racial/ethnic differences in job loss for women with breast cancer. JCancer Surviv. 2011;5(1):102-11. PMC3040347.Neklason DW, Done MW, Sargent NR, Schwartz AG, Anton-Culver H,Griffin CA, Ahnen DJ, Schildkraut JM, Tomlinson GE, Strong LC, MillerAR, Stopfer JE, Burt RW. Activating mutation in MET oncogene infamilial colorectal cancer. BMC Cancer. 2011;11:424. PMC3202244.Peterson L, Soliman A, Ruterbusch JJ, Smith N, Schwartz K. Comparisonof exposures among Arab American and non-Hispanic White femalethyroid cancer cases in metropolitan Detroit. J Immigr Minor Health.2011;13(6):1033-40.Purdue MP, Bakke B, Stewart P, De Roos AJ, Schenk M, Lynch CF, BernsteinL, Morton LM, Cerhan JR, Severson RK, Cozen W, Davis S, RothmanN, Hartge P, Colt JS. A case-control study of occupational exposure totrichloroethylene and non-Hodgkin lymphoma. Environ Health Perspect.2011;119(2):232-8.Purdue MP, Johansson M, Zelenika D, Toro JR, Scelo G, Moore LE,Prokhortchouk E, Wu X, Kiemeney LA, Gaborieau V, Jacobs KB, ChowWH, Zaridze D, Matveev V, Lubinski J, Trubicka J, Szeszenia-DabrowskaN, Lissowska J, Rudnai P, Fabianova E, Bucur A, Bencko V, Foretova L,Janout V, Boffetta P, Colt JS, Davis FG, Schwartz KL, Banks RE, SelbyPJ, Harnden P, Berg CD, Hsing AW, Grubb RL, 3rd, Boeing H, Vineis P,Clavel-Chapelon F, Palli D, Tumino R, Krogh V, Panico S, Duell EJ, QuirosJR, Sanchez MJ, Navarro C, Ardanaz E, Dorronsoro M, Khaw KT, AllenNE, Bueno-de-Mesquita HB, Peeters PH, Trichopoulos D, Linseisen J,Ljungberg B, Overvad K, Tjonneland A, Romieu I, Riboli E, MukeriaA, Shangina O, Stevens VL, Thun MJ, Diver WR, Gapstur SM, PharoahPD, Easton DF, Albanes D, Weinstein SJ, Virtamo J, Vatten L, HveemK, Njolstad I, Tell GS, Stoltenberg C, Kumar R, Koppova K, Cussenot O,Benhamou S, Oosterwijk E, Vermeulen SH, Aben KK, van der Marel SL,Ye Y, Wood CG, Pu X, Mazur AM, Boulygina ES, Chekanov NN, FoglioM, Lechner D, Gut I, Heath S, Blanche H, Hutchinson A, Thomas G,Wang Z, Yeager M, Fraumeni JF, Jr., Skryabin KG, McKay JD, RothmanN, Chanock SJ, Lathrop M, Brennan P. Genome-wide association studyof renal cell carcinoma identifies two susceptibility loci on 2p21 and11q13.3. Nat Genet. 2011;43(1):60-5. PMC3049257.Purdue MP, Colt JS, Graubard B, Davis F, Ruterbusch JJ, Digaetano R,Karami S, Wacholder S, Schwartz K, Chow WH. A case-control study ofreproductive factors and renal cell carcinoma among black and whitewomen in the United States. Cancer Causes Control. 2011;22(11):1537-44.Reinersman JM, Johnson ML, Riely GJ, Chitale DA, Nicastri AD, SoffGA, Schwartz AG, Sima CS, Ayalew G, Lau C, Zakowski MF, Rusch VW,Ladanyi M, Kris MG. Frequency of EGFR and KRAS mutations in lungadenocarcinomas in African-Americans. J Thorac Oncol. 2011;6(1):28-31.Schwartz AG, Wenzlaff AS, Bock CH, Ruterbusch JJ, Chen W, Cote ML,Artis AS, Van Dyke AL, Land SJ, Harris CC, Pine SR, Spitz MR, Amos CI,Levin AM, McKeigue PM. Admixture mapping of lung cancer in 1812African-Americans. Carcinogenesis. 2011;32(3):312-7. PMC3047238.Smedby KE, Foo JN, Skibola CF, Darabi H, Conde L, Hjalgrim H, Kumar V,Chang ET, Rothman N, Cerhan JR, Brooks-Wilson AR, Rehnberg E, IrwanID, Ryder LP, Brown PN, Bracci PM, Agana L, Riby J, Cozen W, Davis S,Hartge P, Morton LM, Severson RK, Wang SS, Slager SL, FredericksenZS, Novak AJ, Kay NE, Habermann TM, Armstrong B, Kricker A, MillikenS, Purdue MP, Vajdic CM, Boyle P, Lan Q, Zahm SH, Zhang Y, Zheng T,Leach S, Spinelli JJ, Smith MT, Chanock SJ, Padyukov L, Alfredsson L,Klareskog L, Glimelius B, Melbye M, Liu ET, Adami HO, HumphreysK, Liu J. GWAS of follicular lymphoma reveals allelic heterogeneity at6p21.32 and suggests shared genetic susceptibility with diffuse largeB-cell lymphoma. PLoS Genet. 2011;7(4):e1001378. PMC3080853.Wang SS, Menashe I, Cerhan JR, Cozen W, Severson RK, Davis S,Hutchinson A, Rothman N, Chanock SJ, Bernstein L, Hartge P, MortonLM. Variations in chromosomes 9 and 6p21.3 with risk of non-Hodgkinlymphoma. Cancer Epidemiol Biomarkers Prev. 2011;20(1):42-9.Wang SS, Lu Y, Rothman N, Abdou AM, Cerhan JR, De Roos A, Davis S,Severson RK, Cozen W, Chanock SJ, Bernstein L, Morton LM, HartgeP. Variation in effects of non-Hodgkin lymphoma risk factors accordingto the human leukocyte antigen (HLA)-DRB1*01:01 allele and ancestralhaplotype 8.1. PLoS One. 2011;6(11):e26949. PMC3212525.Wheeler DC, De Roos AJ, Cerhan JR, Morton LM, Severson R, Cozen W,Ward MH. Spatial-temporal analysis of non-Hodgkin lymphoma inthe NCI-SEER NHL case-control study. Environ Health. 2011;10:63.PMC3148953.2010Amos CI, Pinney SM, Li Y, Kupert E, Lee J, de Andrade MA, Yang P,Schwartz AG, Fain PR, Gazdar A, Minna J, Wiest JS, Zeng D, RothschildH, Mandal D, You M, Coons T, Gaba C, Bailey-Wilson JE, Anderson MW.A susceptibility locus on chromosome 6q greatly increases lung cancerrisk among light and never smokers. Cancer Res. 2010;70(6):2359-67.PMC2855643.

Boleij A, Roelofs R, Schaeps RM, Schulin T, Glaser P, Swinkels DW, KatoI, Tjalsma H. Increased exposure to bacterial antigen RpL7/L12 inearly stage colorectal cancer patients. Cancer. 2010;116(17):4014-22.PMC2930125.Cetin K, Beebe-Dimmer JL, Fryzek JP, Markus R, Carducci MA. Recenttime trends in the epidemiology of stage IV prostate cancer in the UnitedStates: analysis of data from the Surveillance, Epidemiology, and EndResults Program. Urology. 2010;75(6):1396-404.De Roos AJ, Davis S, Colt JS, Blair A, Airola M, Severson RK, Cozen W,Cerhan JR, Hartge P, Nuckols JR, Ward MH. Residential proximity toindustrial facilities and risk of non-Hodgkin lymphoma. Environ Res.2010;110(1):70-8. PMC2795078.Dombi GW, Rosbolt JP, Severson RK. Neural network analysis ofemployment history as a risk factor for prostate cancer. Comput BiolMed. 2010;40(9):751-7.Fang S, Pinney SM, Bailey-Wilson JE, de Andrade MA, Li Y, Kupert E, YouM, Schwartz AG, Yang P, Anderson MW, Amos CI. Ordered subset analysisidentifies loci influencing lung cancer risk on chromosomes 6q and 12q.Cancer Epidemiol Biomarkers Prev. 2010;19(12):3157-66.Geyer SM, Morton LM, Habermann TM, Allmer C, Davis S, Cozen W,Severson RK, Lynch CF, Wang SS, Maurer MJ, Hartge P, Cerhan JR.Smoking, alcohol use, obesity, and overall survival from non-Hodgkinlymphoma: a population-based study. Cancer. 2010;116(12):2993-3000.PMC2889918.Gold LS, Milliken K, Stewart P, Purdue M, Severson R, Seixas N, Blair A,Davis S, Hartge P, De Roos AJ. Occupation and multiple myeloma: anoccupation and industry analysis. Am J Ind Med. 2010;53(8):768-79.Grulich AE, Vajdic CM, Falster MO, Kane E, Smedby KE, Bracci PM, deSanjose S, Becker N, Turner J, Martinez-Maza O, Melbye M, Engels EA,Vineis P, Costantini AS, Holly EA, Spinelli JJ, La Vecchia C, Zheng T, ChiuBC, Franceschi S, Cocco P, Maynadie M, Foretova L, Staines A, Brennan P,Davis S, Severson RK, Cerhan JR, Breen EC, Birmann B, Cozen W. Birthorder and risk of non-hodgkin lymphoma--true association or bias? Am JEpidemiol. 2010;172(6):621-30. PMC2950815.Jagsi R, Abrahamse P, Morrow M, Hawley ST, Griggs JJ, Graff JJ, HamiltonAS, Katz SJ. Patterns and correlates of adjuvant radiotherapy receiptafter lumpectomy and after mastectomy for breast cancer. J Clin Oncol.2010;28(14):2396-403.Kakarala M, Rozek L, Cote M, Liyanage S, Brenner DE. Breast cancerhistology and receptor status characterization in Asian Indian andPakistani women in the U.S.--a SEER analysis. BMC Cancer. 2010;10:191.PMC2873947.Karami S, Schwartz K, Purdue MP, Davis FG, Ruterbusch JJ, Munuo SS,Wacholder S, Graubard BI, Colt JS, Chow WH. Family history of cancerand renal cell cancer risk in Whites and African-Americans. Br J Cancer.2010;102(11):1676-80. PMC2883149.Kato I, Land S, Majumdar AP, Barnholtz-Sloan J, Severson RK. Functionalpolymorphisms to modulate luminal lipid exposure and risk of colorectalcancer. Cancer Epidemiol. 2010;34(3):291-7. 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Affiliations and AcknowledgementsSTATE OF MICHIGAN32The cancer statistics collected and disseminated here could not havebeen presented without the untiring work of the cancer registrar,editing, follow-up and management teams of the MetropolitanDetroit Cancer Surveillance System. Nor could this work have beenpresented without the collaboration of each of the facilities on thefollowing page and the entities listed here.Special thanks go to the Michigan Department of CommunityHealth for their ongoing assistance, and also to the many physicianswho support our efforts to ensure complete cancer reporting fortri-county residents. Finally, we would like to acknowledge thecancer patients and their families. It is to you we dedicate this work.The Metropolitan Detroit Cancer Surveillance System is funded by:The Division of Cancer Prevention and ControlNational Cancer InstituteDepartment of Health and Human ServicesSEER Contract # HHSN261201000028CControl # NO1-PC-00028

Metropolitan Detroit Cancer Surveillance SystemParticipating InstitutionsThe following hospitals, pathology laboratories and radiationoncology treatment facilities are participants in the MetropolitanDetroit Cancer Surveillance System. Their collaboration makespossible Detroit area population-based cancer reporting.Hospitals and Associated Path Labs, Radiation Facilities and ClinicsBotsford General HospitalChildren’s Hospital of MichiganCrittenton HospitalDetroit Receiving HospitalDoctors Hospital of MichiganGarden City HospitalHarper HospitalHenry Ford HospitalHenry Ford – WarrenHenry Ford – MacombHenry Ford Wyandotte HospitalHuron Valley-Sinai HospitalHutzel HospitalJohn D. Dingell Dept. of VeteransAdministration Medical CenterKarmanos Cancer CenterMcLaren Hospital – MacombMcLaren Hospital – OaklandMichigan Orthopedic SpecialtyHospitalOakwood HospitalOakwood Annapolis HospitalOakwood Heritage HospitalOakwood Southshore MedicalCenterProvidence HospitalSt. John Detroit Riverview HospitalSt. John Hospital and MedicalCenterSt. John Macomb Hospital CenterSt. John Northshore HospitalSt. John Oakland HospitalSt. Joseph Mercy HospitalAnn Arbor*St. Joseph Mercy Hospital OaklandSt. Mary HospitalSinai-Grace HospitalSoutheast Michigan SurgicalHospitalUniversity Health CenterUniversity Hospital Ann Arbor*Veterans Administration MedicalCenter – Ann Arbor*William Beaumont Hospital –Grosse PointeWilliam Beaumont Hospital –Royal OakWilliam Beaumont Hospital –Troy33Independent Pathology LaboratoriesAmeripath Institute of UrologyDetroit Bio-Medical LaboratoriesMedical Diagnostic LabPinkus LaboratoryBeaumont Reference LaboratoryDianon SystemsMichigan Institute of UrologyPlus DiagnosticsBio-Reference LaboratoryGenoptix LaboratoryMidwest Skin PathologyQuest Diagnostics, Inc.Bostwick LaboratoriesHilbrich Dermatology Lab, PLCNovice Dermatopathology LabSt. John Oral PathologyContemporary Imaging AssociatesHospital Consolidated LaboratoriesOakwood Medical LaboratoryDermatopathology AssociatesLaboratory Corporation of AmericaOppenheimer Urologic ReferenceLaboratoryIndependent Radiation Oncology Facilities21st Century OncologyDownriver Center for OncologyRadiation Therapy Associates*Hospital not located in the tri-county area.

Appendix AMichigan Public Health Code and HIPAA (Excerpts)Michigan Act 368 of 1978 and HIPAA Law and Federal Rules (Excerpts);Public Law 104-191; 104th Congress; August 21, 199634333.2619 Cancer registry; establishment; purpose; reports; records;rules; medical or department examination or supervision notrequired; contracts; evaluation of reports; publication of summaryreports; commencement of reporting; effective date of section.Sec. 2619.(1) The department shall establish a registry to record casesof cancer and other specified tumorous and precancerousdiseases that occur in the state, and to recordinformation concerning these cases as the departmentconsiders necessary and appropriate in order to conductepidemiologic surveys of cancer and cancer-relateddiseases in the state.(2) Each diagnosed case of cancer and other specifiedtumorous and precancerous diseases shall be reported tothe department pursuant to subsection (4), or reportedto a cancer reporting registry if the cancer reportingregistry meets standards established pursuant tosubsection (4) to ensure the accuracy and completeness ofthe reported information. A person or facility required toreport a diagnosis pursuant to subsection (4) may elect toreport the diagnosis to the state through an existing cancerregistry only if the registry meets minimum reportingstandards established by the department.(3) The department shall maintain comprehensive recordsof all reports submitted pursuant to this section. These reportsshall be subject to the same requirements of confidentiality asprovided in section 2631 for data or records concerning medicalresearch projects.(4) The director shall promulgate rules which provide forall of the following:(a) A list of tumorous and precancerous diseases other thancancer to be reported pursuant to subsection (2).(b) The quality and manner in which the cases and otherinformation described in subsection (1) are reportedto the department.(c) The terms and conditions under which records disclosing thename and medical condition of a specific individual and keptpursuant to this section are released by the department.(5) This section does not compel an individual to submitto medical or department examination or supervision.(6) The department may contract for the collection andanalysis of, and research related to, the epidemiologicdata required under this section.(7) Within 2 years after the effective date of this section, thedepartment shall begin evaluating the reports collectedpursuant to subsection (2). The department shall publishand make available to the public reports summarizing theinformation collected. The first summary report shall bepublished not later than 180 days after the end of the first2 full calendar years after the effective date of this section.Subsequent annual summary reports shall be made on a fullcalendar year basis and published not later than 180 days afterthe end of each calendar year.(8) Reporting pursuant to subsection (2) shall begin the nextcalendar year after the effective date of this section.(9) This section shall take effect July 1, 1984.History: Add. 1984, Act 82, Eff. July 1, 1984Popular Name: Act 368333.2621 Comprehensive policy for conduct and support ofresearch and demonstration activities; conducting and supportingdemonstration projects and scientific evaluations.Sec. 2621.(1) The department shall establish a comprehensive policypursuant to and consistent with section 2611(2) for theconduct and support of research and demonstration activitiesrelated to the department’s responsibility for the health careneeds of the people of this state.(2) The department shall conduct research and demonstrationactivities related to the department’s responsibility for theenvironmental, preventive, and personal health needs of thecommunities and people of this state, including:(a) The causes, effects, and methods of prevention of illness.(b) The determinants of health, including behavior relatedto health.(c) The accessibility, acceptability, availability, organization,distribution, utilization, quality, and financing of healthcare, especially those services for the medically needy.(3) The department may conduct and support demonstrationprojects to carry out subsection (2).(4) The department shall conduct or support the conduct ofscientific evaluations of the effectiveness, efficiency, andrelevance of programs conducted or supported by thedepartment.History: 1978, Act 368, Eff. Sept. 30, 1978Popular Name: Act 368

333.2631 Data concerning medical research project;confidentiality; use.Sec. 2631.The information, records of interviews, written reports,statements, notes, memoranda, or other data or recordsfurnished to, procured by, or voluntarily shared with thedepartment in the conduct of a medical research project,or a person, agency, or organization which has been designatedin advance by the department as a medical research projectwhich regularly furnishes statistical or summary data withrespect to that project to the department for the purpose ofreducing the morbidity or mortality from any cause or conditionof health are confidential and shall be used solely for statistical,scientific, and medical research purposes relating to the causeor condition of health.History: 1978, Act 368, Eff. Sept. 30, 1978Popular Name: Act 368333.2632 Data concerning medical research project; inadmissibleas evidence; exhibition or disclosure.Sec. 2632.The information, records, reports, statements, notes,memoranda, or other data described in section 2631 are notadmissible as evidence in an action in a court or before anyother tribunal, board, agency, or person. Furnishing the datato the department in the conduct of a medical research projector to a designated medical research project does not result inthe loss of any privilege which the data may otherwise havemaking them inadmissible as evidence. The information, records,reports, notes, memoranda, or other data shall not be exhibitednor their contents disclosed in any way, in whole or in part, bythe department or its representative, or by any other person,agency, or organization, except as is necessary for the purposeof furthering the medical research project to which they relateconsistent with section 2637 and the rules promulgated undersection 2678. A person participating in a designated medicalresearch project shall not disclose the information obtainedexcept in strict conformity with the research project.History: 1978, Act 368, Eff. Sept. 30, 1978Popular Name: Act 368333.2633 Data concerning medical research projects; liability forfurnishing.Sec. 2633.The furnishing of information, records, reports, statements,notes, memoranda, or other data to the department, eithervoluntarily or as required by this code, or to a person, agency, ororganization designated as a medical research project does notsubject a physician, hospital, sanatorium, rest home, nursinghome, or other person or agency furnishing the information,records, reports, statements, notes, memoranda, or other datato liability in an action for damages or other relief, and is notconsidered to be the willful betrayal of a professional secret or theviolation of a confidential relationship.History: 1978, Act 368, Eff. Sept. 30, 1978 ;-- Am. 1988, Act 122,Eff. Mar. 30, 1989Popular Name: Act 368• • •SEC. 1178. EFFECT ON STATE LAW(b) PUBLIC HEALTH.--Nothing in this part shall beconstrued to invalidate or limit the authority, power, orprocedures established under any law providing for thereporting of disease or injury, child abuse, birth, or death,public health surveillance, or public health investigationor intervention.(c) STATE REGULATORY REPORTING.--Nothing in thispart shall limit the ability of a State to require a healthplan to report, or to provide access to, information formanagement audits, financial audits, program monitoringand evaluation, facility licensure or certification, orindividual licensure or certification.• • •35Rendered 6/7/2005 16:58:30Michigan Compiled Laws© 2005 Legislative Council, State of MichiganCourtesy of www.legislature.mi.govSource: http://aspe.hhs.gov/admnsimp/pl104191.htm (emphasis added)

Metropolitan Detroit Cancer Surveillance SystemEpidemiology Section | 4100 John R Street MM04EP | Detroit, MI 48201For Additional Information:Telephone: (313) 578-4231Fax: (313) 578-4306http://seer.cancer.gov/registries/detroit.html36Prepared ByRon Shore, MPHBiostatistical ProgrammerPatricia Arballo-Spong, BSSEER Project CoordinatorFawn D. Vigneau, JD, MPHCo-Director, Epidemiology Research CoreKendra Schwartz, MD, MSPHDirector, Epidemiology Research CoreAnn G. Schwartz, PhD, MPHDirector, Metropolitan Detroit Cancer Surveillance SystemContributing AuthorsMichele L. Cote, PhDIkuko Kato, MD, PhD, Patricia Arballo-Spong, BS,Ann S. Bankowski, MSW, Kari A. Borden, RHIT, CTREllen M. Velie, PhD, Kendra Schwartz, MD, MSPHAnn G. Schwartz, PhD, MPHPatricia Arballo-Spong, BSAnn S. Bankowski, MSWKari A. Borden, RHIT, CTRLeadership TeamAnn G. Schwartz, PhD, MPHDirector, Metropolitan Detroit Cancer Surveillance SystemSEER Principal InvestigatorKendra Schwartz, MD, MSPHSEER Co-InvestigatorDirector, Epidemiology Research CoreFawn D. Vigneau, JD, MPHCo-Director, Epidemiology Research CorePatricia Arballo-Spong, BSSEER Project CoordinatorWilliam O. Quarshie, MSBiostatisticianSharon Moton, BSAdministratorJoanne Harris, CTRChief of Cancer SurveillanceNancy L. Lozon, BS, CTRManager Cancer Surveillance - Office OperationsPatrick Nicolin, BA, CTRManager Cancer Surveillance - Quality Control and Field OperationsRichard Pense, BSDirector, Basic and Population Science SystemsInhee Han, BSSenior Applications AnalystGloria Kwiatkowski, BSSenior Applications AnalystPublished December 2012