RSVPs are being accepted now! Reserve your spot at the symposium by October 2nd!
DEADLINE APPROACHING: Submit posters for the symposium poster session!
Posters should honor the life and/or career of Dr. Hal Moses and may be submitted by academic and administrative departments, laboratories, student groups, family members, friends, and past and present colleagues.
See guidelines below. Be creative and have fun!
- Posters may not be larger than 4' x 4'. and the minimum font size is 40 pt.
- Posters will be printed for you free-of-charge and will be hung on the morning of the symposium.
- Posters will be compiled, miniaturized, and printed for a keepsake book that will be presented to Dr. Moses at the symposium.
- If you have any questions, please reach out to Kim Dahlman (firstname.lastname@example.org).
- Submit posters using this REDCap submission portal.
Poster submission deadline: September 22, 2017
October 11, 2017
Vanderbilt Student Life Center Ballroom
310 25th Avenue South
Nashville, TN 37240
Tentative Symposium Agenda for October 11th:
|7:45 AM||Doors open; Continental Breakfast available; - RSVP HERE|
|8:10 AM||Welcome by Jennifer A. Pietenpol, Ph.D., emcee|
|8:20 AM||Speaker: Edward B. Leof, Ph.D.|
|9:00 AM||Speaker: Robert J. Coffey, Jr., M.D.|
|9:25 AM||Speaker: Rik Derynck, Dr. Sc.|
|10:00 AM||BREAK | View Poster Presentation|
|10:35 AM||Speaker: Dan Beauchamp, M.D.|
|11:00 AM||Speaker: Sanford Markowitz, M.D., Ph.D.|
|11:35 AM||LUNCH - RSVP HERE|
|12:35 PM||Speaker: Rosa Serra, PhD|
|1:05 PM||Speaker: Neil Bhowmick, Ph.D.|
|1:25 PM||Speaker: Jennifer A. Pietenpol, Ph.D.|
|1:45 PM||BREAK | View Poster Presentation|
|2:25 PM||Guest of Honor, Harold L. Moses, MD|
Questions? Contact Megan Smallwood.
Guest Speakers (in order of appearance)
Jennifer A. Pietenpol, Ph.D., is the Director of the Vanderbilt-Ingram Cancer Center, the Benjamin F. Byrd, Jr. Professor of Molecular Oncology, and Professor of Biochemistry, Cancer Biology and Otolaryngology. Dr. Pietenpol’s research focuses on breast cancer and the p53 family signaling network—the most frequently targeted network for mutation in human tumors. Recently, Dr. Pietenpol has integrated her research expertise in tumor suppressor genes and molecular genetics with bioinformatic analysis of high dimensional genomic data sets to molecularly subtype difficult-to-treat, triple negative breast cancer. Her results are being translated to clinical trials and alignment of patients to appropriate, molecularly targeted therapy. Her research has impacted many areas of science and medicine, and she has translated her discoveries into clinical impact for breast cancer patients. Dr. Pietenpol’s research is funded by the National Cancer Institute, the Susan G. Komen for the Cure Foundation, and the Department of Defense Breast Cancer Program.
After graduating from Carleton with honors in biology and as a member of Sigma Xi, Dr. Pietenpol earned her Ph.D. in cell biology at Vanderbilt University School of Medicine in 1990. She continued her postgraduate training at Johns Hopkins Oncology Center (now Sidney Kimmel Comprehensive Cancer Center) before returning to Vanderbilt in 1995 as an assistant professor of biochemistry. She achieved the rank of full professor in 2002. Dr. Pietenpol has served as associate editor or on the editorial board for numerous biomedical research journals. She has authored or co-authored over 120 articles published in peer-reviewed scientific literature.
Edward B. Leof, Ph.D., is a consultant in the Division of Pulmonary and Critical Care Medicine and Department of Biochemistry and Molecular Biology at the Mayo Clinic in Rochester, Minnesota, where he previously served as the Associate Director for Basic Sciences in the Mayo Clinic Cancer Center. He joined the Mayo staff in 1992 following 7 years as an Assistant/Associate Professor of Cell Biology at Vanderbilt University School of Medicine. He holds the academic rank of Professor and is the Erivan K. Haub Family Professor of Cancer Research in addition to being the co-leader of the Immunity & Fibrosis Platform in the Mayo Clinic Center for Biomedical Discovery as well as a volunteer EMT. Dr. Leof earned his Ph.D. at the University of North Carolina, Chapel Hill and completed a postdoctoral fellowship at the Mayo Clinic prior to joining the Vanderbilt faculty. Dr. Leof’s research interests focus on understanding the role of the multifunctional cytokine, transforming growth factor beta (TGF-β) in normal tissue homeostasis and disease, with a particular focus on organ fibrosis.
Current studies include: characterizing the cellular machinery and receptor elements mediating TGF-β receptor downregulation, recycling, and polarized epithelial cell trafficking determining the mechanism and role of mitochondrial TGF-β receptor localization addressing the role of a metabolic regulatory network in profibrotic TGF-β signaling.
Dr. Leof has been a permanent, as well as ad hoc, reviewer for numerous national and international study sections and is currently a recipient of an NIH MERIT Award from the National Institutes of General Medical Sciences.
|Robert J. Coffey, Jr., M.D. - The focus of research within the Coffey lab is the study of the role of the EGF receptor (EGFR) and its ligands in GI neoplasia. The lab has a particular interest in the trafficking of EGFR ligands in polarizing colonic epithelial cells. Naked2 has been identified as a critical regulator of basolateral trafficking of TGF-alpha, a major EGFR ligand. Naked2 is a known antagonist of Wnt-beta-catenin signaling so Naked2 provides a point of convergence between EGFR and Wnt signaling. This work has led to the identification of a new mode of EGFR ligand signaling via exosomes and the development of FAVS (fluorescent-activated vesicle sorting) to isolate and characterize cellular organelles. The lab has recently found that Lrig1, an inducible negative regulator of the EGFR, marks proliferative and quiescent intestinal stem cells, and acts as a tumor suppressor.|
|Rik Derynck, Dr. Sc. grew up in Belgium, and received his Dr. Sc. degree at the University of Ghent, Belgium, for the cDNA cloning and expression of fibroblast interferon (interferon-b). This provided the basis for the clinical evaluation and use of this interferon, which now has a $2B/year market. In 1981, he moved to Genentech in South San Francisco, where he initiated a research program aimed at the molecular characterization of the newly discovered “transforming growth factor” activity. This led to the cDNA cloning of TGF-a and TGF-b1, which are now seen as prototypes for their respective families of growth and differentiation factors. In 1991, he moved to the University of California at San Francisco, where he is Professor in the Departments of Cell and Tissue Biology, and Anatomy, and Co-Director of UCSF’s Center of Regeneration Medicine and Stem Cell Research. Besides a 15-year long research program aimed at understanding the roles of TGF-a in cancer and normal development, he has been studying the roles of TGF-b in mesenchymal differentiation and discovered that TGF-b induces epithelial-mesenchymal transdifferentiation. During the last 20+ years, his lab has been focusing primarily on the characterization of TGF-b signaling mechanisms through activation of its receptors, Smads and non-Smad pathways, and the roles of the TGF-b-activated pathways in epithelial plasticity and epithelial-mesenchymal transition. His research has greatly impacted our understanding of TGF-β family signaling mechanisms, with many mechanistic and conceptual advances (and reagents) originating from his lab, and has helped to provide the basis for therapeutic approaches based on inhibition of TGF-β signaling.|
|R. Daniel Beauchamp, M.D., is the John Clinton Foshee Distinguished Professor of Surgery, Chairman of the Section of Surgical Sciences, and Surgeon-in-Chief of Vanderbilt University Hospital and has held these positions since July 2001 and on the faculty at Vanderbilt since December 1994. He holds joint appointments as professor in the departments of Cell and Developmental Biology and Cancer Biology. He also serves as Deputy Director of the Vanderbilt-Ingram Cancer Center. Dr. Beauchamp has two active R01 grants from NIH, and leads one of the main projects in the GI Cancer SPORE. Dr. Beauchamp's primary area of research interest has been in colorectal carcinogenesis, the biology of cancer cell invasion and metastasis, and in the identification of novel molecular biomarkers and therapeutic targets in colorectal and other alimentary tract malignancies. His work applies DNA microarray and proteomic technology to identify novel biomarkers and therapeutic targets in human colorectal cancer samples. He also uses molecular genetics, chemical biology and cell biological approaches to examine mechanistic questions in cancer biology in both cell culture and mouse models. In addition to the basic cancer research Dr. Beauchamp works in collaboration with his Medical Oncology and Radiation Oncology colleagues to accrue cancer patients to approved clinical trials. He has trained and mentored numerous junior faculty members, physician scientist fellows, medical students, graduate students and post-doctoral fellows in his laboratory. He is one of the few surgeon members of the ASCI.|
|Sanford Markowitz, M.D., Ph.D., is a medical oncologist and cancer researcher and is the Markowitz-Ingalls Professors of Cancer Genetics and Distinguished University Professor at Case Western Reserve University. Markowitz’s contributions include: discovering genetic inactivation of two tumor suppressor genes, TGF-ß RII and 15-PGDH; showing RII mutations explain how cancers develop in DNA repair deficient cells (Lynch syndrome); developing 15-PGDH inhibitor drugs as therapeutics for tissue regeneration; and pioneering molecular tests of stool DNA for early colon cancer detection. Markowitz serves as Principal Investigator of the Case GI Cancers SPORE, as head of the Cancer Genetics Program at the Case Comprehensive Cancer Center, and as a physician at University Hospitals Seidman Cancer Center. Markowitz received his B.A. in chemistry and physics (summa cum laude) from Harvard University, and his M.D. and Ph.D. (in cell biology) from Yale University. He performed residency in internal medicine at the University of Chicago followed by fellowship in medical oncology at the National Cancer Institute. Recognition of Dr. Markowitz’s contributions include his being an NCI Outstanding Investigator awardee and his election as a member of the American Society of Clinical Investigation and the Association of American Physicians. He has served on numerous scientific advisory boards that include the Board of Scientific Counselors of the National Cancer Institute, and the external advisory boards of: the National Colon Cancer Research Alliance founded by Ms. Katie Couric, the Dana Farber/Harvard Cancer Center, the Abramson Family Cancer Research Center of the University of Pennsylvania, and the Human Oncology and Pathogenesis Program at Memorial Sloan-Kettering Cancer Center.|
Rosa Serra, Ph.D., is a Professor in the Department of Cell, Developmental, and Integrative Biology at the University of Alabama at Birmingham. She received her B.S. degree in Biology from St. Louis University in 1986 and her Ph.D. degree in Molecular and Cellular Biology from The Pennsylvania State University, College of Medicine in 1992. Dr. Serra pursued her postdoctoral fellowship in the laboratory of Dr. Harold Moses at Vanderbilt University where she studied the role of TGF-ß in development and cancer focusing on lung, mammary gland, and the skeleton. In 1995, she continued at Vanderbilt as a Research Assistant Professor in Cell Biology. In 1999, Dr. Serra was appointed to the faculty of Molecular and Cellular Physiology at the University of Cincinnati, College of Medicine. Dr. Serra joined the faculty at UAB in 2002 and was promoted to Full Professor in 2008. Dr. Serra has served continuously on several study sections for the past 15 years including as a charter member of the Skeletal Biology and Regeneration and the Skeletal Biology Development and Disease study sections. Dr. Serra was the Associate Director of the Cell Molecular and Developmental Biology graduate program from 2008 to 2011 and the Director of the Cancer Biology graduate program from 2011 to 2014. She was awarded the Deans award for excellence in mentorship in 2011. Dr. Serra is currently an Associate Director in the Comprehensive Arthritis, Musculoskeletal, Bone, and Autoimmunity Center and the Interim Director for the Global Center for Craniofacial, Oral, and Dental Biology at UAB.
Neil Bhowmick, PhD, obtained his B.S. in Microbiology at University of Florida, and went on to earn a Ph.D. at University of Georgia working on the structure and the function of the luteinizing hormone and endothelin G-protein coupled receptors. Under Dr. Harold Moses’ mentorship as a postdoctoral fellow at Vanderbilt University, Dr. Bhowmick defined mechanisms of epithelial-mesenchymal transdifferentiation downstream of TGF-ß and revealed a role for stromal fibroblasts in cancer initiation. Consequently, he started his laboratory studying stromal-epithelial interactions to identify mechanisms cancer initiation and progression to test targets for diagnostics and therapy at the Department of Urology in Vanderbilt University. Dr. Bhowmick's subsequent move to Cedars-Sinai Medical Center in Los Angeles led to our findings on the role of stromal fibroblasts in therapeutic resistance. Of recent, his lab has identified epigenetic, genomic, and metabolic changes in the stromal fibroblastic cells that can potentiate cancer epithelia progression. Further, they have helped define the nature of stromal heterogeneity that defines cancer associated fibroblasts. With a multidisciplinary approach, they have been able to leverage these findings for the development of a point-of-care device for the use in multiple disease states (inclusive of cardiac infarction, cerebral spinal fluid leakage, and cancers) and interventional clinical trials for prostate cancer patients.
|Harold L. Moses, MD - Accumulating data indicate that the stroma can play a critical role in cancer initiation and progression. TGF-beta signaling in both epithelial and stromal cells appears to be a key regulator of the stromal microenvironment. There is now compelling evidence from transgenic mouse studies and analyses of mutations in human carcinomas indicating that the TGF-beta signal transduction pathway is tumor suppressive. Studies of human tumors have demonstrated inactivating mutations in human tumors of genes encoding proteins involved in TGF-beta signal transduction, including DPC4/Smad4, Smad2, and the type I and type II TGF-beta receptor (TßRI and TßRII, respectively). However, there is some evidence that TGF-beta signaling can promote tumor progression in the later stages. In order to examine the roles of TGF-beta signaling in cancer more closely, we have generated mice with loxP sites flanking exon 2 of the type II receptor gene, Tgfbr2, and crossed them with mice expressing Cre driven by different epithelial specific promoters. Loss of TGF-beta signaling in six different epithelial cells gave a minimal phenotype. However, when challenged with oncogene expression or tumor suppressor gene impairment, there was rapid development of invasive and metastatic carcinomas supporting the hypothesis that epithelial cell autonomous TGF-beta signaling is tumor suppressive in both early and late stages of carcinogenesis. One mechanism appears to be enhanced expression of chemokines by Tgfbr2 null carcinoma cells with resultant recruitment of bone marrow derived cells that express abundant TGF-beta and MMPs in the tumor microenvironment and promote invasion and metastasis.
In contrast to the epithelial cell knockouts that gave a minimal phenotype, knockout of Tgfbr2 in stromal fibroblasts gave a striking epithelial phenotype in the mammary gland, prostate and forestomach, including epithelial pre-neoplasia and invasive carcinomas. One mechanism identified was paracrine stimulation of carcinoma cells by HGF, MSP and TGF-alpha. Another mechanism appeared to be over expression of chemokines by the knockout fibroblasts with recruitment of bone marrow derived cells. Thus, TGF-beta signaling in fibroblasts modulates the growth and oncogenic potential of adjacent epithelia in selected tissues. The data indicate that TGF-beta signaling is a major regulator of chemokine secretion and resultant bone marrow cell infiltration and that targeting pathways that inhibit bone marrow cell differentiation or chemokine receptors may be useful in both therapy and prevention of cancer.