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Tumor suppressor p53 (TP53) at the crossroads of the exposome and the cancer genome.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Schetter, Aaron J. Harris, Curtis C. |
| Copyright Year | 2012 |
| Abstract | Tumor suppressor p53 (TP53) was discovered more than two decades ago to be frequently mutated in diverse types of human cancer (1, 2), and the mutation frequency was shown to be even higher by whole-exome sequencing of the cancer genome (3, 4). In PNAS (5), Chen et al. show a dose dependency between exposure to aristolochic acid (AA), a known human carcinogen and nephrotoxin, and the TP53 mutational spectrum in the cancer genome of upper urinary tract urothelial carcinomas. AA is metabolically activated by enzymatic nitroreduction to form aristolactam-DNA (AL-DNA) adducts. These adducts are poorly removed by nucleotide excision repair, persist for many years in human tissues, and cause mutations in TP53 and other cancer-related genes, including HRAS and FGFR3. |
| File Format | PDF HTM / HTML |
| DOI | 10.1073/pnas.1205457109 |
| PubMed reference number | 22592801 |
| Journal | Medline |
| Volume Number | 109 |
| Issue Number | 21 |
| Alternate Webpage(s) | http://www.pnas.org/content/109/21/7955.full.pdf |
| Alternate Webpage(s) | https://doi.org/10.1073/pnas.1205457109 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
