ArticleProceedings of the National Academy of Sciences of the United States of America1992
Suppression of deregulated c-MYC expression in human colon carcinoma cells by chromosome 5 transfer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 30 citations in OpenAlex.
- Transcriptional and Post-Transcriptional Regulation of Thrombospondin-1 Expression: A Computational Model.PLoS computational biology · 2017Article
- Beta-catenin--a linchpin in colorectal carcinogenesis?The American journal of pathology · 2002Review
- MYC oncogenes and human neoplastic disease.Oncogene · 1999Review
- Raf-1 kinase, epidermal growth factor receptors, and mutant Ras proteins in colonic carcinomas.Digestive diseases and sciences · 1996Article
- Difference in allelic expression of genes probably associated with tumor progression in murine fibrosarcomas and cell lines.Japanese journal of cancer research : Gann · 1994Article
- Over-expression of the c-myc proto-oncogene in colorectal carcinoma.British journal of cancer · 1993Article
- Identification of a colon mucosa gene that is down-regulated in colon adenomas and adenocarcinomas.Proceedings of the National Academy of Sciences of the United States of America · 1993Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Two-thirds of sporadic colon carcinomas express elevated levels of the c-MYC protooncogene. In addition, most colon carcinoma cell lines show constitutive elevated expression (10- to 40-fold over normal) of MYC RNA and protein that is not modulated in response to a mitogenic stimulus. Indirect immunofluorescence has been used to detect c-MYC protein in such cell lines, in hybrid cells resulting from fusions of such lines with cells that regulate MYC normally, and in carcinoma cells to which a normal copy of chromosome 5 has been transferred by microcell fusion. The deregulated expression of c-MYC is suppressed by fusion with a cell that regulates MYC normally. In addition, transfer of chromosome 5 by microcell fusion results in suppression of deregulated expression. Suppressed cells are no longer tumorigenic in nude mice. Loss of the transferred chromosome results in reexpression of the tumorigenic phenotype and in constitutive elevated expression of MYC. These data indicate that function of a tumor-suppressor gene on chromosome 5 is necessary for the regulated expression of MYC in at least some colon cells. Loss of this suppressor results in deregulated MYC expression and is a necessary, but most likely not sufficient, event for the expression of the tumorigenic phenotype in a subset of colon carcinomas.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.