Pomila Singh, Ph.D., Professor

  • Affiliations: Department of Neuroscience & Cell Biology, Department of Biochemistry & Molecular Biology, Sealy Cancer Center and Internal Medicine
  • Route: 1043, 10.104 Medical Research Building (MRB)
  • Tel: (409) 772-4842
  • Fax: (409) 772-3222
  • posingh@utmb.edu

Pomila Singh, Ph.D.

General Information

                                • Dr. Singh's laboratory is conducting research in the area of hormones and growth factors as it relates to colon carcinogenesis. As of 2007, her laboratory has published more than 118 papers and Dr. Singh has trained several postdoctoral fellows and graduate students. Her laboratory is currently funded by two R01 grants from the NIH to investigate the role of growth factors (such as progastrin peptides and IGFs) and chemo preventative agents (such as curcumin) on the proliferation and apoptosis of normal and cancerous intestinal epithelial cells, using either in vitro cellular models or transgenic mouse models. Her laboratory has additionally examined the role of the growth factors and their receptors on colon carcinogenesis, in the presence or absence of infectious agents, using either animal models or human samples. Transcriptional regulation of specific genes is also being examined. Dr. Singh has been awarded two patents and her laboratory has submitted an additional patent. Dr. Singh is heavily involved in teaching medical students and graduate students in the Cell Biology and Human Biologic Chemistry and genetic programs. She continues to serve on several study sections for the NIH and the VA, and is currently serving as a member of the Research Policy Committee for the AGA Institute. She has received several awards and was named the Edna Seisenheimer Professor of Cancer Studies in 2000. She is an active member of the American Gastroenterological Association (AGA) and American Association of Cancer Research (AACR). The AGA Institute recently named her a Senior AGA Fellow.

Publications

                                • Cobb S, Wood T, Ceci J, Varro A, Velasco M, Singh P. Intestinal expression of progastrin significantly increases colon carcinogenesis in transgenic mice in response to AOM.Cancer 100,1311-1323, 2004.

                                  Shen Q, Singh P. Identification of a novel SP3 binding site in the promoter of human IGFBP4 gene: role of SP3 and AP-1 in regulating promoter activity in CaCo2 cells. Oncogene, 23, 2454-2464, 2004.

                                  Rengifo-Cam W, Singh P. Role of progastrins and gastrins and their receptors in GI and pancreatic cancers: targets for treatment. Current Pharmaceutical Design 10, 2345-23358, 2004.

                                  Cowey S, Quast M, Belalcazar LM, Wei J, Deng X, Given R, Singh P. Abdominal obesity, insulin resistance and colon carcinogenesis are increased in mutant mice lacking gastrin gene expression. Cancer, 103/12, 2643-2653, 2005.

                                  Singh P, Wu H, Clark C, Owlia, A. Annexin II binds progastrin and gastrin like peptides, and mediates growth factor effects of autocrine and exogenous gastrins on colon cancer and intestinal epithelial cells. Oncogene, Vol. 26, No. 3, 425-440, 2007.

                                  Li Q, Deng X, Singh, P, Significant increase in the aggressive behavior of transgenic mice over- expressing peripheral progastrin peptides: associated changes in CCK2 and serotonin receptors in the CNS. Neuropharmacology. 32, (8), 1813-1821, 2007.

                                  Rengifo-Cam W, Umar S, Sarkar S, Singh P, Anti-apoptotic effects of progastrin on pancreatic cancer cells are mediated by sustained activation of NFkBp65, Cancer Research. 67 (15), 2007.

                                  Singh P. Role of Annexin-II in GI cancers: interaction with progastrins. Cancer Lett. 252,19-35, 2007.

                                  Umar. S, Sarkar. S, Cowey. S, Singh. P, Activation of NF-κB is required for mediating proliferative and anti-apoptotic effects of progastrin on proximal colonic crypts of mice, in vivo.  Oncogene (In press).