Visualizar Tese - Instituto de Biociências - Unesp
Visualizar Tese - Instituto de Biociências - Unesp Visualizar Tese - Instituto de Biociências - Unesp
studies using in vivo models are needed to assess the rate of response to drugs that inhibit cellgrowth and proliferation in ULs.In conclusion, the integrative analysis of genomic and transcriptomic data provided acomprehensive and biologically meaningful insight into tumorigenesis of ULs revealinggenomic amplifications translated by up-regulation of modulators. To our knowledge, this isthe first study using a large series of ULs evaluated by integrative genomic and transcriptomicanalysis. The findings indicate genes that could be targets for development of specifictherapies related to extracellular matrix and cell proliferation related to Uterine Leiomyomas.15
REFERENCES[1] Baird DD, Dunson DB (2003) Why is parity protective for uterine fibroids? Epidemology14: 247-250.[2] Mantovani MS, Barbieri Neto J, Philbert PMP (1999) Multiple uterine leiomyomas:Cytogenetic analysis. Gynecol Oncol 72: 71–75.[3] Cook H, Ezzati M, Segars JH et al. (2010) The impact of uterine leiomyomas onreproductive outcomes. Minerva Ginecol 62: 225-236.[4] Flake GP, Andersen J, Dixon D (2003) Etiology and pathogenesis of uterine leiomyomas:a review. Environ Health Perspect 111: 1037-1054.[5] Ishikawa H, Ishi K, Serna VA et al. (2010) Progesterone is essential for maintenance andgrowth of uterine leiomyoma. Endocrinology 151:2433-2442.[6] Sozen I and Arici A (2002) Interactions of cytokines, growth factors, and the extracellularmatrix in the cellular biology of uterine leiomyomata. Fertil Steril 78: 1-12.[7] Marsh EE, Lin Z, Yin P, Milad M et al. (2008) Differential expression of microRNAspecies in human uterine leiomyoma versus normal myometrium. Fertil Steril 89: 1771-1776.[8] Bonatz G, Frahm SO, Andreas S et al. (1998) Telomere shortening in uterine leiomyomas.Am J Obstet Gynecol 179: 591-596.[9] Malik M, Norian J, McCarthy-Keith D et al. (2010) Why leiomyomas are called fibroids:the central role of extracellular matrix in symptomatic women. Semin Reprod Med 28: 169–179.[10] Canevari RA, Pontes A, Rogatto SR (2005) Microallelotyping Defines Novel Regions ofLoss of Heterozygosity in Uterine Leiomyomas. Mol Carcinog 42: 177–182.[11] Canevari, RA and Rogatto SR (2007) Uterine Leiomyoma: Updates in Cytogenetics andMolecular Analysis. Asian Journal of Cancer 6: 15-28.[12] El-Gharib MN and Elsobky ES (2010) Cytogenetic aberrations and the development ofuterine leiomyomata. J Obstet Gynaecol Res 36: 101–107.[13] Arslan AA, Gold LI, Mittal K et al. (2005) Gene expression studies provide clues to thepathogenesis of uterine leiomyoma: new evidence and a systematic review. HumanReproduction 20: 852-863.[14] Quade BJ, Wang TY, Sornberger K et al. (2004) Molecular pathogenesis of uterinesmooth muscle tumors from transcriptional profiling. Genes Chrom Cancer 40: 97–108.[15] Vanharanta S, Wortham NC, Laiho P et al. (2005) 7q deletion mapping and expressionprofiling in uterine fibroids. Oncogene 24: 6545-6554.[16] Hodge JC, Park PJ, Dreyfuss JM et al. (2009) Identifying the molecular signature of theinterstitial deletion 7q subgroup of uterine leiomyomata using a paired analysis. Genes ChromCancer 48: 865–885.[17] Akavia UD, Litvin O, Kim J et al. (2010) An integrated approach to uncover drivers ofcancer. Cell 143: 1005–1017.[18] Staaf J, Jönsson G, Ringnér M et al. (2010) High-resolution genomic and expressionanalyses of copy number alterations in HER2-amplified breast cancer. Breast CancerResearch, 12: R25.16
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REFERENCES[1] Baird DD, Dunson DB (2003) Why is parity protective for uterine fibroids? Epi<strong>de</strong>mology14: 247-250.[2] Mantovani MS, Barbieri Neto J, Philbert PMP (1999) Multiple uterine leiomyomas:Cytogenetic analysis. Gynecol Oncol 72: 71–75.[3] Cook H, Ezzati M, Segars JH et al. (2010) The impact of uterine leiomyomas onreproductive outcomes. Minerva Ginecol 62: 225-236.[4] Flake GP, An<strong>de</strong>rsen J, Dixon D (2003) Etiology and pathogenesis of uterine leiomyomas:a review. Environ Health Perspect 111: 1037-1054.[5] Ishikawa H, Ishi K, Serna VA et al. (2010) Progesterone is essential for maintenance andgrowth of uterine leiomyoma. Endocrinology 151:2433-2442.[6] Sozen I and Arici A (2002) Interactions of cytokines, growth factors, and the extracellularmatrix in the cellular biology of uterine leiomyomata. Fertil Steril 78: 1-12.[7] Marsh EE, Lin Z, Yin P, Milad M et al. (2008) Differential expression of microRNAspecies in human uterine leiomyoma versus normal myometrium. Fertil Steril 89: 1771-1776.[8] Bonatz G, Frahm SO, Andreas S et al. (1998) Telomere shortening in uterine leiomyomas.Am J Obstet Gynecol 179: 591-596.[9] Malik M, Norian J, McCarthy-Keith D et al. (2010) Why leiomyomas are called fibroids:the central role of extracellular matrix in symptomatic women. Semin Reprod Med 28: 169–179.[10] Canevari RA, Pontes A, Rogatto SR (2005) Microallelotyping Defines Novel Regions ofLoss of Heterozygosity in Uterine Leiomyomas. Mol Carcinog 42: 177–182.[11] Canevari, RA and Rogatto SR (2007) Uterine Leiomyoma: Updates in Cytogenetics andMolecular Analysis. Asian Journal of Cancer 6: 15-28.[12] El-Gharib MN and Elsobky ES (2010) Cytogenetic aberrations and the <strong>de</strong>velopment ofuterine leiomyomata. J Obstet Gynaecol Res 36: 101–107.[13] Arslan AA, Gold LI, Mittal K et al. (2005) Gene expression studies provi<strong>de</strong> clues to thepathogenesis of uterine leiomyoma: new evi<strong>de</strong>nce and a systematic review. HumanReproduction 20: 852-863.[14] Qua<strong>de</strong> BJ, Wang TY, Sornberger K et al. (2004) Molecular pathogenesis of uterinesmooth muscle tumors from transcriptional profiling. Genes Chrom Cancer 40: 97–108.[15] Vanharanta S, Wortham NC, Laiho P et al. (2005) 7q <strong>de</strong>letion mapping and expressionprofiling in uterine fibroids. Oncogene 24: 6545-6554.[16] Hodge JC, Park PJ, Dreyfuss JM et al. (2009) I<strong>de</strong>ntifying the molecular signature of theinterstitial <strong>de</strong>letion 7q subgroup of uterine leiomyomata using a paired analysis. Genes ChromCancer 48: 865–885.[17] Akavia UD, Litvin O, Kim J et al. (2010) An integrated approach to uncover drivers ofcancer. Cell 143: 1005–1017.[18] Staaf J, Jönsson G, Ringnér M et al. (2010) High-resolution genomic and expressionanalyses of copy number alterations in HER2-amplified breast cancer. Breast CancerResearch, 12: R25.16