Tulane Cancer Center Members: F
Faculty Membership Application and Membership Definitions

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A B C D E F G H I J K L M N O P Q R S T U V W X Y Z

Flemington, Fortgang, Friedlander, Franklin

Erik K. Flemington, Ph.D.
Associate Professor of Pathology
TCC Program Member
(504) 988-1167
1430 Tulane Ave., Box SL-79, New Orleans, LA 70112-2699
eflemin@tulane.edu
Laboratory homepage
Homepage on the Pathology website:
http://www.som.tulane.edu/departments/pathology/faculty/Fleming/Fleming.html

Biographical Narrative:
Dr. Flemington received his B.S. degree in Chemical Engineering from Michigan Technological University. He carried out his doctoral studies in Dr. Prescott Deininger's laboratory and received a Ph.D. in Biochemistry and Molecular Biology from the Louisiana State University in New Orleans in 1987. His post-doctoral work was carried out in Dr. Sam Speck's laboratory at the Dana Farber Cancer Institute in Boston where he investigated the transcriptional mechanisms involved in the Epstein Barr virus (EBV) reactivation switch. In 1991, Dr. Flemington was appointed as an Instructor of Pathology at Harvard University and in 1995, he was appointed as Assistant Professor in the department of Medicine at Harvard Medical School. In 2000, he joined the Tulane Cancer Center as an Associate Professor in the department of Pathology where he continues his work investigating transcriptional control mechanisms involved in cell cycle regulation and his work on mechanisms governing the interplay between EBV lytic replication and the cell cycle.

There are currently two major efforts in Dr. Flemington's laboratory. First, Dr. Flemington is continuing a long-standing interest in cell cycle regulation during the lytic replication phase of the human DNA tumor virus, Epstein Barr virus (EBV). His lab previously discovered that although the EBV latency associated gene expression program promotes cell cycle progression and tumorgenesis, the lytic replication cycle actively blocks cell cycle progression and consequently, has anti-tumorgenic properties. Dr. Flemington's lab is currently addressing the mechanisms utilized by EBV to block cell cycle progression during lytic replication. His lab is also carrying out screening of chemical libraries to identify new compounds that activate the EBV lytic cycle in an attempt to identify new anti-tumor candidates. The other major effort ongoing in Dr. Flemington's lab is fundamental cell cycle control studies. This effort focuses on the transcription factor, E2F, which plays a key role in regulating cell cycle progression. His recent studies have shown that a new 450 kdal E2F interacting protein, referred to as TRRAP, inhibits E2F mediated G1-S phase transition. As such, TRRAP may play a tumor suppressor like role in vivo. His lab is currently addressing the mechanisms through which the interaction between TRRAP and E2F influences E2F activity and cell cycle progression.

Selected Publications:

• Rodriguez A, Flemington EK. Transfection mediated cell cycle signaling. Anal Biochem 272: 171-181 (1999)
• Rodriguez A, Armstrong M, Dwyer D, Flemington EK. Genetic dissection of cell growth arrest functions mediated by the Epstein-Barr virus lytic gene product, Zta. J Virol 73: 9029-9038 (1999)
• Campanero MR, Armstrong M, Flemington EK. Distinct cellular factors regulate the c-myb promoter through its E2F element. Mol Cell Biol 19: 8442-8450 (1999)
• Campanero MR, Armstrong M, Flemington EK. CpG methylation as a novel mechanism for the regulation of E2F activity. Proc Natl Acad Sci USA 97: 6481-8486 (2000)
• Rodriguez A, Jung EJ, Flemington EK. Cell cycle analysis of Epstein Barr virus infected cells following treatment with lytic cycle inducing agents. J Virol 75: 4482-4489 (2001)
• Flemington EK Herpesviral lytic replication and the cell cycle: Arresting new developments. J Virol 75: 4475-4481 (2001)
• Rodriguez A, Jung EJ, Yin Q, Cayrol, C, Flemington EK. Role of c-myc regulation in Zta mediated induction of the cyclin dependent kinase inhibitors, p21 and p27, and cell growth arrest. Virology 284:159-169 (2001)
• Ryu, H, Lee, J, Olofsson, BA, Mwidau, A, Deodoglu, A, Escudero, M, Flemington EK, Azizkhan-Clifford, J, Ferrante, RJ, Ratan, RR. Histone deacetylase inhibitors prevent oxidative neuronal death independent of expanded polyglutamine repeats via an Sp1-dependent pathway. Proc Natl Acad Sci 100:4281-4285 (2003)
• Lin, Z, Yin, Q, Flemington EK. Identification of a Negative Regulatory Element in the Epstein-Barr virus (EBV) Zta Transactivation Domain that is Regulated by the Cell Cycle Control Factors, c-Myc and E2F1. J Virol 78:11962-11971 (2004)

Ilana S. Fortgang, M.D.
Assistant Professor of Pediatrics, Section of Gastroenterology
TCC Contributing Member
(504) 988-0297
1430 Tulane Ave., Box SL-37, New Orleans, LA 70112-2699
fortgang@tulane.edu

Biographical Narrative:
Ulcerative colitis and Crohn disease are the inflammatory bowel diseases (IBD) characterized by repeated bouts of acute intestinal mucosal injury and epithelial cell destruction. Patients with IBD harbor an increased risk of colon cancer and develop this malignancy at much younger ages than do those in the general population. Although the precise etiology of IBD is not yet known, it is appreciated that susceptible individuals respond in a dysregulated manner to enteric luminal antigens. This reaction is significant for a pathological influx of inflammatory cells to the damaged tissue, resulting in a predominant and enduring surge of proinflammatory cytokines, including tumor necrosis factor (TNF). As well, and despite its name, increased levels of TNF have been found in the setting of numerous carcinomas. The goal of Dr. Fortgang's current research is to define the specific role of tumor necrosis factor receptors (TNFRs) in neoplastic transformation associated with chronic inflammation. Specific emphasis is to be placed on elucidating the downstream pathways activated over the course of tumorigenesis. The overall hypothesis is that loss of TNFR1 but not of TNF or TNFR2 confers increased vulnerability to invasive carcinoma. Her team will explore the discrete roles of TNF and TNFRs and their signal transduction pathways utilizing the well-characterized AOM/DSS model of chronic colitis and tumorigenesis. These studies have potential direct relevance to the treatment of human cancers because they will identify novel therapeutic targets and define their mechanisms of regulation, crucial steps in the process of determining and designing small molecules to modulate activity in vivo.

Selected Publications:

• Fortgang I, Srivastav S, Baskin GB, Schumacher PM, Levy LS. Retrospective analysis of clinical and laboratory factors associated with lymphoma in simian AIDS. Leukemia & Lymphoma, 45:161-169, 2004.
• Bellows C, Belafsky P, Fortgang IS, Beech DJ. Melanoma in African-Americans: trends in biological behavior and clinical characteristics over two decades. J. Surg Oncology Suppl., 78(1): 10-16, 2001.
• Fortgang IS, Baskin GB, Ruff K, Levy LS. Pathobiology of simian-AIDS-associated lymphoma: the Tulane Regional Primate Research Center (TNPRC) experience. Recent Res Devel Virol, 2(2001): 455-470, 2001.
• Fortgang IS, Rege T, Baskin GB, Murphy-Corb M, Levy LS. Variation in simian immunodeficiency virus env V1 region in simian AIDS-associated lymphoma. AIDS Res and Hum Retroviruses, 17: 459-465, 2001.
• Fortgang IS, Didier PJ, Levy LS. B-cell leukemia in a rhesus macaque (Macaca mulatta) infected with simian immunodeficiency virus. Leukemia and Lymphoma, 37: 657-662, 2000.
• Habis A, Baskin G, Simpson L, Fortgang I, Murphey-Corb M, Levy LS. Rhesus lymphocryptovirus infection during the progressions of SAIDS and SAIDS-associated lymphoma in the rhesus macaque. AIDS Res and Hum Retroviruses, 16: 163-171, 2000.

Paul L. Friedlander, M.D.
Clinical Associate Professor of Otolaryngology
TCC Associate Member
(504) 988-1028
1430 Tulane Ave., Box SL-59, New Orleans, LA 70112-2699
pfriedla@tulane.edu

Biographical Narrative:

Dr. Friedlander received his B.S. in biology from Georgetown University and his M.D. from LSU (New Orleans). Following medical school, he completed a two-year general surgery residency at George Washington University, an otolaryngology residency at LSU (New Orleans), and a head and neck surgical oncology fellowship at Memorial Sloan-Kettering Cancer Center. In 1997, he joined the faculty at LSU, where the majority of his effort was in translational research in head and neck cancers. He established the head and neck tumor bank there, which was responsible for collecting clinical information and samples on 250 patients with head and neck cancers. He also participated in translaitonal research involving the use of modified adenoviruses in targeting head and neck cancer as well as immunomodulation of head and neck cancer using the CD40 ligand protein. He is currently investigating the possible role of the Hepatitis C virus as a cofactor in the development of head and neck cancer.

Selected Publications:

• Nobles J, Hagan J, Wold C, Fazekas-May M, Gilbert J, Friedlander PL. Outcome analysis of patients with squamous cell carcinoma of the head and neck and hepatitis C. Laryngoscope, 115(10):1882-86, 2005.
• Nobles J, Wold C, Fazekas-May MA, Friedlander PL. The incidence and epidemiology of hepatitis C virus (HCV) in patients with squamous cell carcinoma of the head and neck (SCCHN). Laryngoscope, 114 (112): 2119-22, 2004.
• Lanson NA, Friedlander PL, Schwarzenberger P, Kolls JK, Wang G. Replication of an adenoviral vector controlled by the human telomerase reverse transcriptase promotor causing tumor-selective tumorlysis. Cancer Research, 63(22): 7936-41, 2003.
• Friedlander PL, Delaune CL, Abadie J, Toups M, LaCour J, Marrero L, Zhong Q, Kolls J. Immunoprotective effect of CD40 ligand gene therapy in malignant mesothelioma and squamous cell carcinoma. American Journal of Respiratory Cell and Molecular Biology, 29(3): 321-330, 2003.
• Lalonde ES, Beyers G, Friedlander PL, Kolls J. Efficacy of transfection rates on head and neck squamous cell cancer by a novel adenovirus: an in vitro and in vivo study. Head and Neck, 24(12): 1038-1046, 2002.

David S. Franklin, Ph.D.
Associate Professor of Biochemistry
TCC Program Member
(504) 988-8868, (504) 988-2739 Fax
1430 Tulane Ave., Box SL-43, New Orleans, LA 70112-2699
franklin@tulane.edu

Biographical Narrative:

Dr. Franklin received his Ph.D. in 1994 from Louisiana State University Medical Center (now LSUHSC). His research interests involve the human cancer syndrome multiple endocrine neoplasia (MEN). Using both tissue culture and in vivo mouse model systems, his lab studies the tumor suppressor MEN1 and proto-oncogene RET, whose mutations predispose patients to develop MEN tumors. Specifically, how do the MEN1 and RET gene products mediate normal cell cycle regulation? What are the effects of MEN tumor-specific mutations on the normal processes? In addition, the Franklin lab is involved in assessing the potential use of the Reishi mushroom as a complementary and alternative medicine in mouse models for breast and colon cancer.

Selected Publications:

• Joshi PP, Kulkarni MV, Yu BK, Smith KR, Norton DL, Van Veelen W, Hoppener JWM, Franklin DS. Simultaneous down regulation of CDK inhibitors p18INK4c and p27KIP1 is required for MEN2A-RET mediated mitogenesis. Oncogene, 26:554-570, 2007.
• Paris M, Wang WH, Franklin DS, Andrisani OM. The homeodomain transcription factor Phox2a, via cAMP-mediated activation, induces p27KIP1 transcription, coordinating neural progenitor cell cycle exit and differentiation. Mol Cell Biol, 26(23): 8826-8839, 2006.
• Damo LA, Snyder PW, Franklin DS. Tumorigenesis in p27/p53- and p18/p53-double null mice: functional collaboration between the pRb and p53 pathways. Mol Carcinogenesis, 42:109, 2005.
• Yuan Y, Shen H, Franklin DS, Scadden DT, Cheng, T. In vivo self-renewing divisions of hematopoietic stem cells are increased in the absence of the early G1-phase inhibitor, p18 INK4C. Nature Cell Biol, 6(5): 436-442, 2004.
• Myers TK, Andreuzza S, Franklin DS. p18 INK4c and p27KIP1 are required for cell cycle arrest of differentiated myotubes. Exp Cell Res, 300(2): 365-378, 2004.

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