H.M. BLIGH FACULTY - Rosalind Franklin University

Bala Chandran, M.S., Ph.D.
Professor and Chair
Room: 2.300
Telephone: 847.578.8822
E-mail: bala.chandran@rosalindfranklin.edu
H.M. BLIGH FACULTY
Bala Chandran, M.S., Ph.D.
Dr. Chandran received his M.S. from Jawaharlal Institute of Post-Graduate Medical Education and Research in
Pondicherry, India in 1974, and his Ph.D. degree on vaccinia virus immunobiology from All-India Institute of
Medical Sciences in New Delhi, India in 1979. Dr. Chandran’s postdoctoral experience includes positions at the
Cancer Research Group at McMaster University in Hamilton and the Department of Comparative and Experimental
Pathology at the University of Florida in Gainesville. An award-winning teacher, Dr. Chandran was appointed
Assistant Professor in the Department of Microbiology, Molecular Genetics and Immunology at the University of
Kansas Medical Center in 1986, and then Professor in 1996. Dr. Chandran joined the Department of Microbiology
and Immunology at Rosalind Franklin University of Medicine and Science on July 1, 2005 as Professor and Chair.
Research
Molecular biology of the herpesviruses is under study to elucidate their mechanism of pathogenesis. Kaposi’s
sarcoma associated human herpesvirus (KSHV) or HHV-8 is a new herpesvirus implicated in the etiology of AIDSrelated
Kaposi’s sarcoma, primary effusion lymphoma and multicentric Castleman’s disease. KSHV produces
several unique proteins that regulate cell cycle, signaling, angiogenesis and immune system. The molecular
events in KSHV infection of target cells are under study to understand how KSHV manipulates the host cell for a
successful infection. Studies in progress include: a) Defining the cell surface molecules recognized by KSHV and
the role of viral envelope glycoproteins in the cell surface receptor interactions; B) Signaling pathways induced
by KSHV during infection and their role in infection; C) Viral gene expression during infection; and D) Modulation
of host cell genes by KSHV. These studies provide unique opportunity of utilizing cutting edge molecular and cell
biological techniques to examine viral oncogenesis by integrating cell surface receptors, signaling molecules,
cellular processes, cell cycle regulatory molecules, transcription factors, innate immune responses and angiogenic
factors. A thorough understanding of KSHV pathogenesis from these studies will lead to novel methods to control
KSHV infection. Dr. Chandran’s research has been continuously funded by NIH and NCI. He is a member of the
Editorial boards of the Journal of Virology and Human Virology. He has served as a member in NIH, MRC (UK) ,
ACS and other grant review panels.
2005-2010 Report

H.M. BLIGH FACULTY
David N. Everly, Ph.D.
Assistant Professor
Room: 2.252
Telephone: 847.578.8653
E-mail: david.everly@rosalindfranklin.edu
David N. Everly, Ph.D.
Dr. Everly received his B.A. in Biology in 1991 from William Jewell College in Liberty, MO. He received his Ph.D. in
Cell Biology and Biophysics, and Molecular Biology and Biochemistry from the University of Missouri-Kansas City
in 1998 studying herpes simplex virus virion host shutoff. He continued his studies at UMKC from 1998-2001
as a postdoctoral fellow. In 2001 he joined the laboratory of Nancy Raab-Traub in the Linberger Comprehensive
Cancer Center at the University of North Carolina-Chapel Hill to study tumor virology and Epstein-Barr virus. He
was appointed Research Assistant Professor in 2006 in the department of Microbiology and Immunology at UNC.
Dr. Everly joined the Department of Microbiology and Immunology as an Assistant Professor at Rosalind Franklin
University of Medicine and Science in August of 2007.
Research
Epstein-Barr virus (EBV) is a ubiquitous infectious agent that infects greater than 90% of the world’s population
and is the etiologic agent of infectious mononucleosis. EBV is also a DNA tumor virus that is associated with a
number of human malignancies and efficiently transforms B-lymphocytes. Burkitt’s lymphoma and nasopharyngeal
carcinoma are highly associated with EBV, while some types of Hodgkin disease and some gastric cancers
contain EBV. EBV-infected B-cell lymphomas are a significant complication of immunosuppressed conditions,
including post-transplant and AIDS-associated lymphomas. Our laboratory studies the cellular signaling pathways
that are important for different aspects of EBV biology. First, in viral oncogenesis, we are interested in latent
membrane protein 1 (LMP1) and its role in EBV-associated cancers. LMP1, termed the EBV oncogene, is expressed
in most EBV-associated cancers, is essential for B-cell transformation, and is sufficient for rodent fibroblast
transformation. Our studies using rodent fibroblast transformation have yielded new insights into the mechanisms
of transformation by LMP1, including regulation of cell cycle proteins and definition of pathways required for
transformation. A second interest in the lab concerns signaling cascades induced by EBV infection. Binding of
viruses to their cellular receptors not only gives the virus a point of entry into the infected cell but also initiates
signaling pathways important for the establishment of an environment favorable for viral infection and survival
of the infected cell. Understanding signaling pathways and factors induced by EBV infection will define new areas
of viral pathogenesis. Each newly defined mechanism will illuminate new potential points of intervention in viral
infection and oncogenesis.
2005-2010 Report

Patricio I. Meneses, Ph.D.
Assistant Professor
Room: 2.351
Telephone: 847.578.8835
E-mail: patricio.meneses@rosalindfranklin.edu
H.M. BLIGH FACULTY
Patricio I. Meneses, Ph.D.
Dr. Meneses received his B.S from the State University of New York at Stony Brook, Stony Brook, NY in 1990,
and his Ph.D. Cornell University Medical College, New York, NY in 1999. He did his postdoctoral fellowship in the
laboratory of Dr. Peter M. Howley in the Department of Pathology at Harvard Medical School. Dr. Meneses went on
to the position of Senior Research Investigator at the University of Pennsylvania School of Medicine Department
of Neurology, and Microbiology and Immunology. He joined the Department of Microbiology and Immunology at
Rosalind Franklin University of Medicine and Science on January 1, 2006, as Assistant Professor.
Research
Cervical cancer is one of the leading causes of death in women worldwide. Papillomaviruses have been
demonstrated to be the etiologic agent associated with over 99% of cervical cancers. Our interest lies in
understanding the mechanism utilized by papillomavirus to establish a primary infection. The laboratory focuses
on the role of the papillomaviruses minor capsid L2 during infection. This work has led to the discovery that
BPV-1 and HPV16 traffic through a novel pathway that includes clathrin coated pits, caveolin-1 vesicles, and the
endoplasmic reticulum (ER). This trafficking seems to be an L2 mediated event. In part, L2 mediates this event
by its interaction with the ER cellular protein syntaxin 18 that is involved in vesicle trafficking into and out of
the ER. Our work was the first description of PV trafficking through the ER, a property shared by its papovavirus
family members SV40 and murine polyomavirus. In addition to the role of L2 in intracellular trafficking, we have
identified several novel interactions of L2 that suggest its role in 1) cellular senescence, 2) cell cycle regulation,
and 3) regulation of the innate immune response. These are potential novel properties for a capsid protein. We
have also identified a region of L2 that is highly conserved in all PV genotypes, as well as in other envelope and
nonenveloped proteins involved in viral entry, whose mutation prevents infection. This region is being explored as a
potential anti-viral target. The studies of the entry and intracellular trafficking mechanism used by papillomavirus
described by our group may be relevant to multiple non-enveloped and enveloped viruses. In addition, PVs can be
a very useful tool that can lead to a better understanding of the dynamic mechanism of basic cellular endocytosis,
intracellular trafficking, and sorting. Our laboratory has received funding from NIH/NCI, the American Cancer
Society, and the H. M. Bligh Cancer Research Laboratories.
2005-2010 Report

Neelam Sharma-Walia, Ph.D.
Research Assistant Professor
Room: 2.416,
Telephone: 847.578.3000 x 7777
E-mail: neelam.sharma-walia@rosalindfranklin.edu
H.M. BLIGH FACULTY
Neelam Sharma-Walia, Ph.D.
Dr. Sharma-Walia received her Ph.D. in Experimental Medicine and Biotechnology from the Postgraduate Institute
of Medical Education and Research, Chandigarh, India in 1998. She was appointed as Senior Demonstrator in
the Department of Experimental Medicine and Biotechnology, Postgraduate Institute of Medical Education and
Research, Chandigarh, India from 1998-2000. She worked as postdoctoral fellow in the Northwestern University
Medical School, Chicago in 2001 and in the Department of Microbiology, Molecular Genetics and Immunology at
University of Kansas Medical Center from 2002-2005. She joined the Rosalind Franklin University of Medicine and
Science in July, 2005 as a Research Assistant Professor.
Research
Our initial studies have shown that Kaposi’s sarcoma associated herpesvirus (KSHV) envelope associated
glycoproteins gB has the ability to induce the integrin-dependent pre-existing FAK-Src-PI-3K-Rho GTPase signal
pathways in host cells, and glycoprotein gpK8.1A has the potential to induce a robust ERK1/2 response in human
microvascular endothelial cells and in human foreskin fibroblast cells, which in turn may provide a very conducive
environment for the successful infection of target cells.
Our previous studies also show the upregulation of prostaglandin pathway’s major stress angiogenic protein COX-
2 and its lipid metabolite PGE2 in the endothelial cells strictly displaying viral latency and Body-cavity B-cell
lymphoma (BCBL) cells carrying multicopy viral genome. Our studies showed that KSHV induced COX-2/PGE2 play
important role in KSHV pathogenesis related events like inflammation, invasion, angiogenesis and cell survival.
Using a variety of cutting edge technologies, we are currently deciphering the role of prostaglandin pathway in
KSHV episome maintenance, chromatin remodeling, PEL/endothelial interactions. Our research also focuses on the
identification of the cellular and viral factors involved in the stability of COX-2 and continuous regulated secretion
of PGE2 in KSHV positive lymphoma cells.
2005-2010 Report

H.M. BLIGH FACULTY
Gulam Waris, Ph.D.
Assistant Professor
Room: 2.349,
Telephone: 847.578.3000 x 7774
E-mail: gulam.waris@rosalindfranklin.edu
Gulam Waris, Ph.D.
Dr. Waris received his Ph.D. degree in Biochemistry from Aligarh Muslim University, Aligarh, India in 1999. He
completed his postdoctoral fellowship on viral hepatitis B and C in the laboratory of Dr. Aleem Siddiqui at the
University of Colorado Health Sciences Center (UCHSC), Denver. Dr. Waris was appointed as an Instructor in the
Department of Microbiology at UCHSC, and later moved to Division of Infectious Diseases, Department of Medicine
at University of California, San Diego, in 2005, as Assistant Project Scientist. Dr. Waris joined the Department
of Microbiology and Immunology at Rosalind Franklin University of Medicine and Science on March 1, 2007, as
Assistant Professor.
Research
Chronic liver disease due to infection with hepatitis C virus (HCV) is a major global health problem that currently
affects 170 million people. Persistent HCV infections can progress to chronic hepatitis, liver fibrosis, cirrhosis, and
ultimately hepatocellular carcinoma. At present, antiviral therapies are limited and prophylactic vaccines are not
available, partially due to the lack of a non-primate animal model and an efficient cell culture system. Our work
combines molecular biology, genetic tools, biochemical techniques, cell biology and recently developed robust
HCV cell culture infection systems to define the molecular mechanisms of viral replication and the determinants
of the HCV-host interaction. Specifically, we focus on characterizing the ribonucleoprotein (RNP) complexes to
identify the potential anti-viral targets for therapeutic intervention. Our studies also provided the first compelling
evidence that HCV induces oxidative stress via calcium signaling and has deep impact on liver failure and
incidence of cancer. We demonstrated the molecular mechanisms of activation of several key players including
oncogenic transcription factors and proinflammatory molecules in response to oxidative stress that can be used as
a drug targets in liver oncogenesis. Our research is aimed at delineating the mechanism by which viral infection
induces 1) liver fibrosis; 2) inflammation and liver oncogenesis; 3) metabolic disorders such as steatosis and insulin
resistance; 4) Tumor angiogenesis; 5) HCV-HBV coinfection. These studies will open new avenues for antiviral
therapy.
2005-2010 Report

Chao-Lan Yu, Ph.D.
Associate Professor
Room: 2.345
Telephone: 847.578.8333
E-mail: chao-lan.yu@rosalindfranklin.edu
H.M. BLIGH FACULTY
Chao-Lan Yu, Ph.D.
Dr. Yu received his B.S. in 1985, from Taipei Medical University, Taiwan, and his Ph.D. in Microbiology and
Immunology at the University of Michigan, Ann Arbor, in 1995. He did a postdoctoral fellowship in 1995, in
the laboratory of Dr. Richard Jove in the Molecular Oncology Program of the H. Lee Moffitt Cancer Center and
Research Institute of Tampa, FL, and from 1996-99, in the lab of Dr. Steven J. Burakoff in the Department of
Pediatric Oncology at the Dana-Farber Cancer Institute of Boston, MA . From 1999-2001, he was an instructor of
Pediatrics at Harvard Medical School of Boston, and from 2001-2007, Assistant Professor of Molecular Physiology
and Biophysics at Vanderbilt University School of Medicine in Nashville, TN. Dr. Yu joined the Department of
Microbiology and Immunology as Associate Professor at Rosalind Franklin University of Medicine and Science in
April of 2007.
Research
STAT (Signal transducers and activators of transcription) was first identified as the critical intracellular signaling
component in response to many cytokines and growth factors. Our earlier studies first demonstrated their possible
involvement in cellular transformation and in human cancer (Science 269:81, 1995). These findings identified
STAT signaling as a novel molecular target for cancer therapy that is being actively pursued in both academic
institutions and pharmaceutical companies. The underlying mechanisms of constitutive STAT activation in tumor
cells, however, are complex and not fully understood. Our research currently focuses on three different areas as
outlined below.
First, the suppressors of cytokine signaling (SOCS) are critical in the negative feedback control of the STAT
pathway. We observed the loss of expression of multiple SOCS family members in cells transformed by oncogenic
Lck, a key protein tyrosine kinase in T cell signal transduction. We hypothesize that disrupted SOCS gene
expression may contribute to constitutive STAT activation in cancer cells and enforced SOCS expression may
have tumor-suppressing activity. We will explore the detailed mechanisms of how different SOCS genes are
dysregulated in cancer cells. The role of SOCS as tumor suppressor will also be thoroughly investigated in various
tumor models.
Second, cumulative evidence points to an important link between cellular metabolism and cancer. Recently, we
reported a novel finding that STAT5 specifically interacted with PDC-E2, a mitochondrial protein, in T cell leukemia.
Our studies suggest that STAT5 may be actively involved in the cross talk between the nuclear and mitochondrial
compartments. Our current effort is focusing on elucidating the molecular details and functional outcomes of
2005-2010 Report

Chao-Lan Yu, Ph.D.
PDC-E2-STAT5 interaction in both normal and tumor cells.
Third, we successfully set up an animal model to study leukemogenesis in vivo. We also established leukemia cell
lines that express green fluorescence protein for easy tracking. We will use this animal model to study tumor
suppressor genes, such as SOCS, and chemical compounds that exhibit potential tumor-suppressing activity. In
collaboration with Dr. K.-P. Chang in our Department, we will also evaluate the possibility of using photosensitive
Leishmania mutants as a vehicle in stimulating immunity against cancer cells.
In summary, results from our studies will reveal important insights into the molecular details of oncogenesis. This
knowledge has profound implications in designing novel therapeutic approaches in treating cancer. The H.M. Bligh
fund plays a very important role in the development of these exciting research projects.
2005-2010 Report

Dominik M. Duelli, Ph.D.
Assistant Professor
Department of Pathology
email: Dominik.Duelli@rosalindfranklin.edu
H.M. BLIGH FACULTY
Dominik M. Duelli, Ph.D.
Research
Our laboratory’s mission is to help reduce the incidence of cancer. We focus on the use of circulating RNAs for the
diagnosis of breast cancer and herpesvirus-associated cancers.
Our pre-clinical activities are the development of methods 1) to specifically isolate vesicles that contain
diagnostic RNAs and which are released from cancer cells into body fluids, and 2) to profile their diagnostic RNA
content with high sensitivity and specificity.
Our basic science project is the identification of the sorting machinery responsible for the selective release of
diagnostic miRNAs from cancer cells.
Our research is conducted in collaboration with RFUMS laboratories, and genetic and epidemiology laboratories
at the NIH/NCI, UCSF, Duke and IU. Project support includes the Department of Defense Breast Cancer Research
Program (BCRP), the Illinois Chapter of the American Cancer Society, the Susan G Komen for the Cure Foundation,
and start-up funds from RFUMS and support of the Bligh Research Center.
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H.M. BLIGH FACULTY
External Grants
Bala Chandran
1. P.I. NIH/NCI R01CA75911 4/1/98-7/31/13
Antigens of KSHV
2. P.I. NIH/NCI R01CA099925 7/1/04-4/30/10
Biology of HHV-8 interactions with host cells
Competitive renewal submitted
3. P.I. NIH/NCI R01 AI 4/1/05-3/31/11
Entry of HHV-8 into the target cells
Competitive renewal to be submitted
Chao-Lan Yu
1. P.I. NIH/NCI R01 CA107210 9/1/06-7/31/11
SOCS: Its Regulation and Role in Oncogenesis
Patricio I. Meneses
1. P.I. NIH/NCI K 22 CA117971 7/1/06-6/30/09
Papillomavirus infection, role of minor capsid protein L2 capsid protein L2
2. P.I. American Cancer Society of Illinois
ACS-IL # 07-34 7/1/07-6/30/08
Understanding the initial events of Papillomavirus infection
3. P.I. American Cancer Society of Illinois.
ACS-IL # 09-15 1/1/09-12/31/10
Renewal: Understanding the initial events of Papillomavirus infection
Gulam Waris
1. NIH R21 AI078532-02 5/15/09-4/30/11
Hepatitis C virus and liver fibrogenesis
2. P.I. American Cancer Society of Illinois
ACS-IL 11/1/08-10/31/09
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H.M. BLIGH FACULTY
External Grants
David Everly
1. P.I. American Cancer Society of Illinois
CS-I 7/1/08-6/30/09
Neelam Sharma- Walia
1. P.I. NIH/NCI R21 CA 128660 9/15/08-8/31/10
Role of COX-2 and PGE2 in KSHV pathogenesis
Dominik M. Duelli
1. P.I. American Cancer Society of Illinois
ACS-IL 1/1/08-12/31/08
2005-2010 Report