Cited by 8,018Cancer-related Molecular PathwaysCancer Genomics and DiagnosticsGenetic factors in colorectal cancer

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p53 Mutations in Human Cancers

Hollstein, Monica, Sidransky, David, Vogelstein, Bert, Harris, Curtis C.·1991·Science

DOI 10.1126/science.1905840

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Abstract

Mutations in the evolutionarily conserved codons of the p53 tumor suppressor gene are common in diverse types of human cancer. The p53 mutational spectrum differs among cancers of the colon, lung, esophagus, breast, liver, brain, reticuloendothelial tissues, and hemopoietic tissues. Analysis of these mutations can provide clues to the etiology of these diverse tumors and to the function of specific regions of p53. Transitions predominate in colon, brain, and lymphoid malignancies, whereas G:C to T:A transversions are the most frequent substitutions observed in cancers of the lung and liver. Mutations at A:T base pairs are seen more frequently in esophageal carcinomas than in other solid tumors. Most transitions in colorectal carcinomas, brain tumors, leukemias, and lymphomas are at CpG dinucleotide mutational hot spots. G to T transversions in lung, breast, and esophageal carcinomas are dispersed among numerous codons. In liver tumors in persons from geographic areas in which both aflatoxin B 1 and hepatitis B virus are cancer risk factors, most mutations are at one nucleotide pair of codon 249. These differences may reflect the etiological contributions of both exogenous and endogenous factors to human carcinogenesis.

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Authors: Hollstein, M., Sidransky, D., Vogelstein, B., & Harris, C. C.
Affiliations: National Institutes of Health (US)
Johns Hopkins University (US)
ORCID: Sidransky, David
Vogelstein, Bert
Harris, Curtis C.
Venue: Science
Publisher: American Association for the Advancement of Science (AAAS)
Published: 1991-07-05
Volume: 253
Issue: 5015
Pages: 49-53
ISSN: 0036-8075 (ISSN-L)
1095-9203
DOI: 10.1126/science.1905840
OpenAlex: W2042316019
Cited by: 8,018
References: 84
Citations by year: 2026: 24 · 2025: 53 · 2024: 69 · 2023: 98 · 2022: 114 · 2021: 124 · 2020: 120 · 2019: 121 · 2018: 123 · 2017: 144 · 2016: 152 · 2015: 172 · 2014: 222 · 2013: 208 · 2012: 214
FWCI: 182.58
Type: journal article
Language: en
Open access: closed
Locations: Science (publishedVersion)
PubMed (publishedVersion)
Funders: National Cancer Institute (CA 09071, CA43460, T32CA009071)
Topics: Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
Keywords: p53, TP53 mutation, tumor suppressor, mutation spectrum, transitions and transversions, colorectal cancer, lung cancer, esophageal cancer, breast cancer, liver cancer, brain tumors, leukemia, lymphoma, aflatoxin B1, hepatitis B virus, carcinogenesis
MeSH terms: Amino Acid Sequence, Animals, Haplorhini, Base Sequence, Chickens, DNA Mutational Analysis, Humans, Molecular Sequence Data, Mutation, Neoplasms, Sequence Homology, Nucleic Acid, Trout, Xenopus, Genes, p53, Mice, Rats

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

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p53 Mutations in Human Cancers

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