TY - JOUR
T1 - Tissue-specific expression of c-Ha-ras in premalignant gastrointestinal mucosae
AU - Meltzer, Stephen J.
AU - Zhou, Dujin
AU - Weinstein, Wilfred M.
N1 - Funding Information:
’ This work was supported by the National Foundation of Ileitis and Colitis, USPHS Grant ROl-CA44688-01, NIH Grant AM 35400 (IBD Center), Grant DK17328 to the Center for Ulcer Research and Education (UCLA), The Frank C. Bressler Research Fund, Grant ACS-IN.147G from the American Cancer Society, and the University of Maryland Cancer Center.
PY - 1989/12
Y1 - 1989/12
N2 - The molecular mechanisms underlying premalignant gastrointestinal diseases, such as ulcerative colitis and Barrett's esophagus, remain unknown. For this reason, the expression of the protooncogene c-Ha-ras was studied in ulcerative colitis and Barrett's esophagus. Total cellular RNA was extracted from different regions of the gastrointestinal tract in these two diseases. Expression of c-Ha-ras was greater in proximal than in distal colon and undetectable in Barrett's esophagus. These regional differences in expression were not seen with the control gene β-actin or with the protooncogenes c-myc and p53. In order to evaluate structural factors contributing to expression, amplification and methylation of c-Ha-ras DNA were studied in these tissues by Southern and slot blotting. No amplification of c-Ha-ras or six other protooncogenes was detected. These data suggest tissue-specific regulation of c-Ha-ras expression in the gastrointestinal tract in certain premalignant disease states.
AB - The molecular mechanisms underlying premalignant gastrointestinal diseases, such as ulcerative colitis and Barrett's esophagus, remain unknown. For this reason, the expression of the protooncogene c-Ha-ras was studied in ulcerative colitis and Barrett's esophagus. Total cellular RNA was extracted from different regions of the gastrointestinal tract in these two diseases. Expression of c-Ha-ras was greater in proximal than in distal colon and undetectable in Barrett's esophagus. These regional differences in expression were not seen with the control gene β-actin or with the protooncogenes c-myc and p53. In order to evaluate structural factors contributing to expression, amplification and methylation of c-Ha-ras DNA were studied in these tissues by Southern and slot blotting. No amplification of c-Ha-ras or six other protooncogenes was detected. These data suggest tissue-specific regulation of c-Ha-ras expression in the gastrointestinal tract in certain premalignant disease states.
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U2 - 10.1016/0014-4800(89)90024-5
DO - 10.1016/0014-4800(89)90024-5
M3 - Article
C2 - 2557232
AN - SCOPUS:0024801474
SN - 0014-4800
VL - 51
SP - 264
EP - 274
JO - Experimental and Molecular Pathology
JF - Experimental and Molecular Pathology
IS - 3
ER -