ArticleProceedings of the National Academy of Sciences of the United States of America2001
Tolerance of human MSH2+/- lymphoblastoid cells to the methylating agent temozolomide.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- Genetic Variability in Cisplatin Metabolism in Kidney Injury in Patients With Head and Neck Squamous Cell Carcinoma Undergoing Definitive Chemoradiotherapy.Head & neck · 2025Article
- Nonrepair functions of DNA mismatch repair proteins: new avenues for precision oncology.Trends in cancer · 2025Review
- Homopolymer switches mediate adaptive mutability in mismatch repair-deficient colorectal cancer.Nature genetics · 2024Article
- Genetic variability in cisplatin metabolic pathways and outcome of locally advanced head and neck squamous cell carcinoma patients.Scientific reports · 2023Article
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- Checkpoint Inhibitor Immunotherapy to Treat Temozolomide-Associated Hypermutation in Advanced Atypical Carcinoid Tumor of the Lung.JCO precision oncology · 2022Article
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- Temozolomide-associated hypermutation in gliomas.Neuro-oncology · 2018Review
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- Azathioprine induction of tumors with microsatellite instability: risk evaluation using a mouse model.Oncotarget · 2015Article
- Minor Changes in Expression of the Mismatch Repair Protein MSH2 Exert a Major Impact on Glioblastoma Response to Temozolomide.Cancer research · 2015Article
- The molecular origin of the MMR-dependent apoptosis pathway from dynamics analysis of MutSα-DNA complexes.Journal of biomolecular structure & dynamics · 2012Article
- The Correlation between Microsatellite Instability and the Features of Sporadic Colorectal Cancer in the North Part of Iran.Gastroenterology research and practice · 2012Article
- Detection of DNA mismatch repair proteins in fresh human blood lymphocytes--towards a novel method for hereditary non-polyposis colorectal cancer (Lynch syndrome) screening.Journal of experimental & clinical cancer research : CR · 2011Article
- The protein tyrosine phosphatase receptor type R gene is an early and frequent target of silencing in human colorectal tumorigenesis.Molecular cancer · 2009Article
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- Methylation-induced G(2)/M arrest requires a full complement of the mismatch repair protein hMLH1.The EMBO journal · 2003Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Members of hereditary nonpolyposis colon cancer (HNPCC) families harboring heterozygous germline mutations in the DNA mismatch repair genes hMSH2 or hMLH1 present with tumors generally two to three decades earlier than individuals with nonfamilial sporadic colon cancer. We searched for phenotypic features that might predispose heterozygous cells from HNPCC kindreds to malignant transformation. hMSH2(+/-) lymphoblastoid cell lines were found to be on average about 4-fold more tolerant than wild-type cells to killing by the methylating agent temozolomide, a phenotype that is invariably linked with impairment of the mismatch repair system. This finding was associated with an average 2-fold decrease of the steady-state level of hMSH2 protein in hMSH2(+/-) cell lines. In contrast, hMLH1(+/-) heterozygous cells were indistinguishable from normal controls in these assays. Thus, despite the fact that HNPCC families harboring mutations in hMSH2 or hMLH1 cannot be distinguished clinically, the early stages of the carcinogenic process in hMSH2 and hMLH1 mutation carriers may be different. Should hMSH2(+/-) colonocytes and lymphoblasts harbor a similar phenotype, the increased tolerance of the former to DNA-damaging agents present in the human colon may play a key role in the initiation of the carcinogenic process.
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