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Title: Evidence that the familial adenomatous polyposis gene is involved in a subset of colon cancers with a complementable defect in c-myc regulation

Abstract

Human colorectal carcinomas frequently express elevated levels of c-myc mRNA in the absence of a gross genetic change at the c-myc locus. To test the hypothesis that these tumors are defective in a gene function necessary for the regulation of c-myc expression, the authors fused an osteosarcoma cell line that exhibits normal c-myc regulation with two colon carcinoma cell lines that express deregulated levels of c-myc mRNA. Since rates of c-myc mRNA turnover in the colon carcinoma cells were found to be comparable to those in normal cells, increased message stability cannot account for the increased steady-state levels of transcripts. These finding suggest that loss of function of a trans-acting regulator is responsible for the deregulation of c-myc expression in a major fraction of colorectal carcinomas. Analysis of restriction fragment length polymorphisms in tumor/normal tissue pairs from patients with primary colorectal lesions indicated that deregulation of c-myc expression in the tumors is correlated with frequent loss of alleles of syntenic markers on chromosome 5q. Chromosome 5q is the region known to contain the gene for familial adenomatous polyposis, an inherited predisposition to colon cancer. These findings, together with the arlier finding that the colonic distribution of tumors exhibiting deregulated c-mycmore » expression is similar to that reported for familial polyposis, provide evidence that loss of function of the familial adenomatous polyposis gene is involved in a subset of colorectal cancers in which c-myc expression is deregulated.« less

Authors:
; ;  [1]
  1. Fox Chase Cancer Center, Philadelphia, PA (USA)
Publication Date:
OSTI Identifier:
5159972
Resource Type:
Journal Article
Journal Name:
Proceedings of the National Academy of Sciences of the United States of America; (USA)
Additional Journal Information:
Journal Volume: 86:11; Journal ID: ISSN 0027-8424
Country of Publication:
United States
Language:
English
Subject:
59 BASIC BIOLOGICAL SCIENCES; CARCINOGENESIS; MOLECULAR BIOLOGY; MESSENGER-RNA; AUTORADIOGRAPHY; TUMOR CELLS; GENE REGULATION; CARCINOMAS; DNA; DNA HYBRIDIZATION; ETIOLOGY; GENES; HYBRIDIZATION; LARGE INTESTINE; MAN; OSTEOSARCOMAS; PHOSPHORUS 32; RECTUM; ANIMAL CELLS; ANIMALS; BETA DECAY RADIOISOTOPES; BETA-MINUS DECAY RADIOISOTOPES; BODY; DAYS LIVING RADIOISOTOPES; DIGESTIVE SYSTEM; DISEASES; GASTROINTESTINAL TRACT; INTESTINES; ISOTOPES; LIGHT NUCLEI; MAMMALS; NEOPLASMS; NUCLEI; NUCLEIC ACIDS; ODD-ODD NUCLEI; ORGANIC COMPOUNDS; ORGANS; PATHOGENESIS; PHOSPHORUS ISOTOPES; PRIMATES; RADIOISOTOPES; RNA; SARCOMAS; SKELETAL DISEASES; VERTEBRATES; 550401* - Genetics- Tracer Techniques

Citation Formats

Erisman, M D, Scott, J K, and Astrin, S M. Evidence that the familial adenomatous polyposis gene is involved in a subset of colon cancers with a complementable defect in c-myc regulation. United States: N. p., 1989. Web. doi:10.1073/pnas.86.11.4264.
Erisman, M D, Scott, J K, & Astrin, S M. Evidence that the familial adenomatous polyposis gene is involved in a subset of colon cancers with a complementable defect in c-myc regulation. United States. doi:10.1073/pnas.86.11.4264.
Erisman, M D, Scott, J K, and Astrin, S M. Thu . "Evidence that the familial adenomatous polyposis gene is involved in a subset of colon cancers with a complementable defect in c-myc regulation". United States. doi:10.1073/pnas.86.11.4264.
@article{osti_5159972,
title = {Evidence that the familial adenomatous polyposis gene is involved in a subset of colon cancers with a complementable defect in c-myc regulation},
author = {Erisman, M D and Scott, J K and Astrin, S M},
abstractNote = {Human colorectal carcinomas frequently express elevated levels of c-myc mRNA in the absence of a gross genetic change at the c-myc locus. To test the hypothesis that these tumors are defective in a gene function necessary for the regulation of c-myc expression, the authors fused an osteosarcoma cell line that exhibits normal c-myc regulation with two colon carcinoma cell lines that express deregulated levels of c-myc mRNA. Since rates of c-myc mRNA turnover in the colon carcinoma cells were found to be comparable to those in normal cells, increased message stability cannot account for the increased steady-state levels of transcripts. These finding suggest that loss of function of a trans-acting regulator is responsible for the deregulation of c-myc expression in a major fraction of colorectal carcinomas. Analysis of restriction fragment length polymorphisms in tumor/normal tissue pairs from patients with primary colorectal lesions indicated that deregulation of c-myc expression in the tumors is correlated with frequent loss of alleles of syntenic markers on chromosome 5q. Chromosome 5q is the region known to contain the gene for familial adenomatous polyposis, an inherited predisposition to colon cancer. These findings, together with the arlier finding that the colonic distribution of tumors exhibiting deregulated c-myc expression is similar to that reported for familial polyposis, provide evidence that loss of function of the familial adenomatous polyposis gene is involved in a subset of colorectal cancers in which c-myc expression is deregulated.},
doi = {10.1073/pnas.86.11.4264},
journal = {Proceedings of the National Academy of Sciences of the United States of America; (USA)},
issn = {0027-8424},
number = ,
volume = 86:11,
place = {United States},
year = {1989},
month = {6}
}