Affiliation: Texas Medical Center
- Dietary pectin and calcium inhibit colonic proliferation in vivo by differing mechanismsS Umar
Division of Gastroenterology, Hepatology and Nutrition, Department of Internal Medicine, The University of Texas Medical School, Houston, Texas, USA
Cell Prolif 36:361-75. 2003..TMCH is thus a diet-sensitive model for examining the effect of specific nutrients on molecular characteristics of the pre-neoplastic colonic epithelium...
- Murine colonic mucosa hyperproliferation. I. Elevated CFTR expression and enhanced cAMP-dependent Cl(-) secretionS Umar
Department of Integrative Biology, Pharmacology and Physiology, Division of Gastroenterology, Hepatology and Nutrition, The University of Texas Health Science Center at Houston, Medical School, Houston 77030, USA
Am J Physiol Gastrointest Liver Physiol 278:G753-64. 2000..This novel mode of CFTR regulation may explain why high endogenous levels of cellular CFTR mRNA and protein within the TMCH epithelium were not matched with larger increases in transmucosal CFTR Cl(-) current...
- Increased beta-catenin expression and nuclear translocation accompany cellular hyperproliferation in vivoJ H Sellin
Department of Internal Medicine, The University of Texas Medical School-Houston, 77030, USA
Cancer Res 61:2899-906. 2001..These findings predict that an oncogenic signaling mechanism related to non-E-cadherin-bound beta-catenin is active in hyperproliferating native colonocytes and is similar to that recorded during the early stages of colon carcinogenesis...
- Activation of NF-kappaB is required for mediating proliferative and antiapoptotic effects of progastrin on proximal colonic crypts of mice, in vivoS Umar
Department of Internal Medicine, University of Texas Medical Branch, Galveston, TX 77555 1043, USA
Oncogene 27:5599-611. 2008..Thus, downregulation of NF-kappaB may significantly reduce the increased risk of colon carcinogenesis in response to PG...
- Utility of a bacterial infection model to study epithelial-mesenchymal transition, mesenchymal-epithelial transition or tumorigenesisP Chandrakesan
Division of Gastroenterology, Department of Internal Medicine, Oklahoma City, OK, USA
Oncogene 33:2639-54. 2014..The TMCH model, therefore, provides an excellent template to study how alterations in intestinal stem cells promote trans-differentiation, crypt regeneration or colon carcinogenesis following bacterial infection. ..
- Increased nuclear translocation of catalytically active PKC-zeta during mouse colonocyte hyperproliferationS Umar
Department of Integrative Biology, Pharmacology, and Physiology, University of Texas Health Science Center at Houston, Medical School, 77030, USA
Am J Physiol Gastrointest Liver Physiol 279:G223-37. 2000..These results suggest separate cellular and nuclear roles, respectively, for PKC-zeta in quiescent and mitotically active colonocytes. PKM-zeta may specifically act as a modulator of proliferation during TMCH...