Stephanie L. Cobb, Ph.D.

Affiliations: 
2003 University of Texas Medical Branch, Galveston, TX 
Area:
Cell Biology, Oncology
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"Stephanie Cobb"

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Pomila Singh grad student 2003 UTMB
 (The effects of amidated and non-amidated gastrins on colon carcinogenesis: Use of knockout and transgenic mouse models.)
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Publications

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Cobb S, Wood T, Ceci J, et al. (2004) Intestinal expression of mutant and wild-type progastrin significantly increases colon carcinogenesis in response to azoxymethane in transgenic mice. Cancer. 100: 1311-23
Singh P, Lu X, Cobb S, et al. (2003) Progastrin1-80 stimulates growth of intestinal epithelial cells in vitro via high-affinity binding sites. American Journal of Physiology. Gastrointestinal and Liver Physiology. 284: G328-39
Cobb S, Velasco M, Singh P. (2003) ProgastrinI-80 is a potent anti-apoptotic factor for clonic epithelial cells in vivo Gastroenterology. 124: A461-A462
Cobb S, Ceci J, Wood T, et al. (2003) Progastrin expression in the colon promotes colonic tumor development in transgenic mice Gastroenterology. 124: A304
Cobb S, Wood T, Tessarollo L, et al. (2002) Deletion of functional gastrin gene markedly increases colon carcinogenesis in response to azoxymethane in mice. Gastroenterology. 123: 516-30
Cobb S, Given R, Velasco M, et al. (2001) Loss of functional gastrin gene results in significantly increasing the incidence of pre-neoplastic and neoplastic changes in the colonic mucosa of mice in response to azoxymethane (AOM) Gastroenterology. 120: A164
Cobb S, Owlia A, Lu XB, et al. (2001) Full-length, unprocessed, progastrin peptide (PG) exerts proliferative effects on colonic mucosa of mice via high affinity binding sites, that are specific for gastrin-like peptides with negligible affinity for cholecystokinin Gastroenterology. 120: A39
Singh P, Cobb S, Velasco M, et al. (2000) Mice targeted for gastrin gene disruption are more susceptible to colon carcinogenesis in response to the chemical carcinogin, azoxymethane (AOM) Regulatory Peptides. 94: 44
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