IARC Database of p53 gene mutations in human tumors and cell lines: updated compilation, revised formats and new visualisation tools

Hainaut, Pierre; Hernandez, Tina; Robinson, Alan J.; Rodriguez-Tomé, Patricia; Flores, Tomas P.; Hollstein, Monica; Harris, Curtis C.; Montesano, Ruggero

doi:10.1093/nar/26.1.205

Cited by 401 publications

(274 citation statements)

References 24 publications

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“…6,7 For this reason, it is not surprising that mutations in the p53 gene are found in greater than half of all human tumors. 8,9 Activation of p53 occurs in response to various types of stress, including DNA damage, hypoxia, and oncogenes, and results in increased levels of modified protein. Activated p53 initiates signaling pathways that lead to either cell cycle arrest or apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Viral oncoapoptosis of human tumor cells

Aubert

Blaho

2003

Gene Ther

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Many cancer cells refractory to radiation treatment and chemotherapy proliferate because of loss of intrinsic programmed cell death (apoptosis) regulation. Consequently, the resolution of these cancers are many times outside the management capabilities of conventional therapeutics. We now report that replication-defective D27 herpes simplex virus (rd D27) triggers apoptosis in three representative transformed human cell lines. Susceptibility to virus-induced cell death is dependent on the abundance and distribution of modified p53 protein in the tumor cells indicating specific targeting of the treatment. Primary human and mouse fibroblast cells that produce modified p53 are resistant to rd D27 killing but not to apoptosis induced by nonviral environmental factors. These results suggest that induction of apoptosis by nonreplicating virus is a feasible genetic therapy approach for killing human cancer cells. Our findings may have important implications in designing novel virus-based anticancer strategies in appropriate animal model systems.

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Section: Introductionmentioning

confidence: 99%

Viral oncoapoptosis of human tumor cells

Aubert

Blaho

2003

Gene Ther

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“…This is within the frequency reported for breast carcinoma in other series (8, 9, 30 -34). The majority of changes reported for breast cancer have been point mutations (22), and in our series, eight of the 10 mutations (80%) involved base pair substitutions. All mutations, except two (cytology specimens 7 and 13) have been previously reported to occur in breast cancer as listed in a p53 database (22).…”

Section: Discussionmentioning

confidence: 48%

“…The majority of changes reported for breast cancer have been point mutations (22), and in our series, eight of the 10 mutations (80%) involved base pair substitutions. All mutations, except two (cytology specimens 7 and 13) have been previously reported to occur in breast cancer as listed in a p53 database (22). Silent gene changes were detected in 1.9% of patients, which is similar to the frequency (1.8%) reported by Burns et al (6).…”

Section: Discussionmentioning

confidence: 48%

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Correlation of p53 Mutations in ThinPrep-Processed Fine Needle Breast Aspirates with Surgically Resected Breast Cancers

Pollett

Bédard

et al. 2000

Modern Pathology

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Mutations of the p53 gene are one of the most common genetic changes found in cancer; their presence may be prognostic and even influence treatment for breast cancer. In this study, we investigated whether DNA could be extracted from the residual cells left in ThinPrep-processed breast fine-needle aspirates and whether p53 gene changes could be detected in the DNA. The results were then correlated with DNA extracted from the matched formalin-fixed, paraffin-embedded, surgically resected breast cancer when available. DNA was successfully extracted from 54 of 62 aspirates and all 31 surgical specimens. p53 gene mutations were detected in 10 of the 54 cytology specimens (18.5%) and consisted of base pair substitutions or deletions. Silent or intronic p53 changes were found in five additional aspirates. One of the aspirates had two gene alterations, resulting in a total of six gene changes. Five of these changes were located in introns 6 or 9 and the sixth was a silent (no amino acid change) change in exon 6. p53 Polymorphisms were detected in nine aspirates (16.3%) and were located in codon 47 (one aspirate), codon 72 (six aspirates), and codon 213 (two aspirates). All cases with surgical material available showed identical p53 mutations, alterations, and polymorphisms in the resected tumors compared with those detected in the corresponding aspirates. The results of this study show that DNA suitable for analysis of p53 gene sequence changes can be successfully extracted from ThinPrep-processed breast fine-needle aspirates, and that identical alterations are detected in both the cytology and surgical specimens.

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“…P53 is a tumor suppressor molecule mutated in 50% of all human cancers (Hainaut et al, 1998). The P53 pathway responds to a variety of intrinsic and extrinsic stress signals and when activated maintains cellular integrity by inducing cell cycle arrest, senescence or apoptosis (reviewed in (Harris and Levine, 2005)).…”

mentioning

confidence: 99%

P53 levels determine outcome during β-catenin tumor initiation and metastasis in the mammary gland and male germ cells

2006

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b-catenin, an oncogene, and P53, a tumor suppressor, are common targets of mutation in human cancers. It has been observed that P53 is often inactivated in tumors involving b-catenin activation. In an attempt to model this situation in vivo, we crossed the previously characterized MMTV-DN-b-catenin mouse with the P53 knockout mouse. Female multiparous mice that carry the MMTV-DN-bcatenin transgene and that are heterozygous for P53 (Tg DN-bCat / þ , P53 þ /À) display an increased tumor burden (2.05 vs 1.31 tumors/animal), with a generally more advanced pathology, and increased metastatic rate (39 vs 0%) relative to transgenic female mice that are wild type for P53 (Tg DN-bCat / þ , P53 þ / þ ). These differences were not due to complete loss of P53 as only one of 21 tumors demonstrated loss of heterozygosity at the P53 locus. Furthermore, no mutations were present in tumors retaining a single wild-type allele. Tg DN-bCat / þ , P53À/À male mice developed testicular teratomas and survived an average of 65 days, whereas non-Tg DN-bCat , P53À/À males survived an average of 84 days. Sixty-two percent of Tg DN-bCat , P53À/À mice developed testicular teratomas, whereas only 10% of the non-Tg DN-bCat , P53À/À mice developed these tumors. These results indicate that the level of P53 and the tissue of origin are important factors in determining outcome of cancer caused by oncogene activation.

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IARC Database of p53 gene mutations in human tumors and cell lines: updated compilation, revised formats and new visualisation tools

Cited by 401 publications

References 24 publications

Viral oncoapoptosis of human tumor cells

Viral oncoapoptosis of human tumor cells

Correlation of p53 Mutations in ThinPrep-Processed Fine Needle Breast Aspirates with Surgically Resected Breast Cancers

P53 levels determine outcome during β-catenin tumor initiation and metastasis in the mammary gland and male germ cells

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