The DOI matches its Crossref record; 84 of the 84 references it cites were found in a registry or an index.
p53 Mutations in Human Cancers
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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In the citing paper
“Sequencing of commonly mutated exons 5 through 9 (39) of the p53 gene by using DNA isolated from the frozen tumors did not reveal any mutations.”
From Ink4a / Arf tumor suppressor does not modulate the degenerative conditions or tumor spectrum of the telomerase-deficient mouse (2007) · cites this paper as [39]
In the citing paper
“loss of TP53 provides a selective advantage for neoplastic growth18.”
From Role of TP53 mutations in the origin and evolution of therapy-related acute myeloid leukaemia (2015) · cites this paper as [18]
Citations
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Cited by
Sorted by citations
Free radicals and antioxidants in normal physiological functions and human disease
Valko, M., Leibfritz, D., Moncol, J., Cronin, M. T. D., Mazur, M., & Telser, J. (2007) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2006.07.001 · Cited by 14,269
WAF1, a potential mediator of p53 tumor suppression
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Self-citationFree radicals, metals and antioxidants in oxidative stress-induced cancer
Valko, M., Rhodes, C. J., Moncol, J., Izakovic, M., & Mazur, M. (2006) · Chemico-Biological Interactions · doi:10.1016/j.cbi.2005.12.009 · Cited by 6,680
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Metadata
- Authors
- Hollstein, M., Sidransky, D., Vogelstein, B., & Harris, C. C.
- Affiliations
- National Institutes of Health (US)
- Johns Hopkins University (US)
- Venue
- Science
- Published
- 1991-07-05
- Volume
- 253
- Issue
- 5015
- Pages
- 49-53
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- 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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