ArticleJournal of cancer research and clinical oncology1990
c-myc overexpression is a tumor-specific phenomenon in a subset of human colorectal carcinomas.
Article in Journal of cancer research and clinical oncology, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Small RNA Profiling of piRNAs in Colorectal Cancer Identifies Consistent Overexpression ofCancers · 2020Article
- Linking FOXO3, NCOA3, and TCF7L2 to Ras pathway phenotypes through a genome-wide forward genetic screen in human colorectal cancer cells.Genome medicine · 2018Article
- Pre-Analytical Determination of the Effect of Extended Warm or Cold Ischaemia on RNA Stability in the Human Ileum Mucosa.PloS one · 2015Article
- Epigenetics of colorectal cancer.Gastroenterology · 2012Review
- Loss of heterozygosity at the 5,10-methylenetetrahydrofolate reductase locus in human ovarian carcinomas.British journal of cancer · 1997Article
- Chromosomal localisation of two putative 11p oncosuppressor genes involved in human ovarian tumours.British journal of cancer · 1992Article
- Correlation between chromosome 5q deletions and different mechanisms of c-myc overexpression in human colorectal cancer.British journal of cancer · 1991Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcriptional activity of the c-myc proto-oncogene was examined in 25 primary human colorectal carcinomas and their corresponding normal mucosae. The purpose was to determine whether the elevated levels of c-myc expression, frequently detected in this type of tumor, might be the consequence of alterations in the cell growth rate or the effect of a real transcriptional deregulation of the gene. In about 44% of the tumors the elevated c-myc expression was consequent to the enhanced growth rate of the neoplastic tissue, as estimated by the expression of the S-phase-specific histone H3 gene. In the other 56%, c-myc overexpression did not entirely depend on the proliferative activity of the neoplastic population. In this latter group, c-myc deregulation did not reside in structural modifications of the putative regulatory regions of the gene. Therefore, c-myc overexpression, at least in a subset of colorectal cancer, seems to be consequent to alterations in transregulative phenomena exerted on the c-myc gene by other genetic loci.
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