ArticleProceedings of the National Academy of Sciences of the United States of America1998
Strand asymmetry of CpG transitions as indicator of G1 phase-dependent origin of multiple tumorigenic p53 mutations in stem cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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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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
12 citing papers in PubMed, 35 citations in OpenAlex.
- BRAFBMC neurology · 2021Article
- Evolutionary Forces and Codon Bias in Different Flavors of Intrinsic Disorder in the Human Proteome.Journal of molecular evolution · 2020Article
- Article
- Conserved nonsense-prone CpG sites in apoptosis-regulatory genes: conditional stop signs on the road to cell death.Evolutionary bioinformatics online · 2013Article
- Detection of TP53 R249 Mutation in Iranian Patients with Pancreatic Cancer.Journal of oncology · 2013Article
- Oncogenic potential is related to activating effect of cancer single and double somatic mutations in receptor tyrosine kinases.Human mutation · 2012Article
- Emerging insights into the molecular and cellular basis of glioblastoma.Genes & development · 2012Review
- Evidence for sequenced molecular evolution of IDH1 mutant glioblastoma from a distinct cell of origin.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2011Article
- Article
- Human lung cancer and p53: the interplay between mutagenesis and selection.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Molecular analysis of microdissected tumors and preneoplastic intraductal lesions in pancreatic carcinoma.The American journal of pathology · 2000Article
- P53 mutations in thyroid carcinoma: tidings from an old foe.Journal of endocrinological investigationReview
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
In dividing cells, expression of mutations is DNA strand symmetric. Of all mutations originating de novo in nondividing cells, only those in the transcribed (noncoding) strand are immediately expressed in mRNA and protein. In contrast, any new mutation in the nontranscribed (coding) strand remains unexpressed until the cells enter S phase and begin proliferation. This previously unrecognized difference enables us to examine the cell cycle-dependent origin of multiple tumorigenic mutations in stem cells. The human p53 gene, which acts as a gatekeeper in the control of G1 to S phase transition, was chosen for the analysis. Of all multiple mutations contained in p53 databases, we have tested in detail CpG transitions. Three features of CpG sites dictate this choice: C --> T transitions at methylated mCpG are the direct product of mC deamination and are replication-independent; it is easy to identify the strand bearing a primary mC --> T event because C --> T on the transcribed strand appears as G --> A on the nontranscribed strand; and CpG transitions are the most frequent (as both singular and multiple occurrences) tumor-related p53 mutations. The origin of double nonsilent CpG transitions in nondividing cells predicts a significant excess of the heterostrand (C --> T, G --> A) doublets over the homostrand (C --> T, C --> T and G --> A, G --> A) doublets. For p53, we found such an excess. Based on this result, along with the results of three other tests reported here, we conclude that the majority of multiple p53 mutations from human tumors occurred in quiescent stem cells.
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