Affiliation: Baylor College of Medicine
- 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...
- 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...
- 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...