ArticleProceedings of the National Academy of Sciences of the United States of America1999
The onset and extent of genomic instability in sporadic colorectal tumor progression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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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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Who cites it
97 citing papers in PubMed, 387 citations in OpenAlex.
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- CAR-T with License to Kill Solid Tumors in Search of a Winning Strategy.International journal of molecular sciences · 2019Review
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- Role of apurinic/apyrimidinic nucleases in the regulation of homologous recombination in myeloma: mechanisms and translational significance.Blood cancer journal · 2018Article
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- MIIP haploinsufficiency induces chromosomal instability and promotes tumour progression in colorectal cancer.The Journal of pathology · 2017Article
- Impact of RAD51C-mediated Homologous Recombination on Genomic Integrity in Barrett's Adenocarcinoma Cells.Journal of gastroenterology and hepatology research · 2017Article
- The Tumor-Associated Variant RAD51 G151D Induces a Hyper-Recombination Phenotype.PLoS genetics · 2016Article
- Emerging immunotherapies for glioblastoma.Expert opinion on emerging drugs · 2016Review
- Field cancerisation in colorectal cancer: a new frontier or pastures past?World journal of gastroenterology · 2015Review
37 more citing papers are in PubMed but not listed here.
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7 authors at 3 institutions in 2 countries.
Funding
Abstract
Cancer cell genomes contain alterations beyond known etiologic events, but their total number has been unknown at even the order of magnitude level. By sampling colorectal premalignant polyp and carcinoma cell genomes through use of the technique inter-(simple sequence repeat) PCR, we have found genomic alterations to be considerably more abundant than expected, with the mean number of genomic events per carcinoma cell totaling approximately 11,000. Colonic polyps early in the tumor progression pathway showed similar numbers of events. These results indicate that, as with certain hereditary cancer syndromes, genomic destabilization is an early step in sporadic tumor development. Together these results support the model of genomic instability being a cause rather than an effect of malignancy, facilitating vastly accelerated somatic cell evolution, with the observed orderly steps of the colon cancer progression pathway reflecting the consequences of natural selection.
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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.