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Selective radiosensitization of drug-resistant MutS homologue-2 (MSH2) mismatch repair-deficient cells by halogenated thymidine (dThd) analogues: Msh2 mediates dThd analogue DNA levels and the differential cytotoxicity and cell cycle effects of the dThd analogues and 6-thioguanine.
Author: BerryS E, DavisT W, HwangH S, KinsellaT J, SchuppJ E, de WindN
Original Abstract of the Article :
Mismatch repair (MMR) deficiency, which underlies hereditary nonpolyposis colorectal cancer, has recently been linked to a number of sporadic human cancers as well. Deficiency in this repair process renders cells resistant to many clinically active chemotherapy agents. As a result, it is of relevanc...See full text at original site
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引用元:
https://pubmed.ncbi.nlm.nih.gov/11059773
データ提供:米国国立医学図書館(NLM)
Mismatch Repair Deficiency: A Challenge in Cancer Treatment
Cancer research is an expansive desert, where scientists seek to unravel the complexities of tumorigenesis and develop effective treatments. This study, published in the field of Cancer Therapy, investigates the role of mismatch repair (MMR) deficiency in chemoresistance, a major obstacle in cancer treatment. The researchers explored the potential of halogenated thymidine analogues to selectively target MMR-deficient cells for radiosensitization, a strategy that could enhance the effectiveness of radiation therapy.
Halogenated Thymidine Analogues: A Potential Weapon Against Chemoresistance
The study found that MMR deficiency, particularly in the absence of the MSH2 gene, renders cells resistant to many chemotherapeutic agents. However, the halogenated thymidine analogues, IdUrd and BrdUrd, selectively target these MMR-deficient cells, increasing their sensitivity to radiation. This selective radiosensitization could be a powerful tool to overcome chemoresistance and improve treatment outcomes for patients with MMR-deficient cancers.
A New Oasis in the Desert of Chemoresistance
The study's findings offer a glimmer of hope in the desert of chemoresistance, suggesting that halogenated thymidine analogues could be a promising strategy to enhance the effectiveness of radiation therapy for MMR-deficient cancers. This discovery represents a significant step towards personalized cancer treatment, tailoring therapies to the specific genetic profile of individual tumors.
Dr. Camel's Conclusion
This study, like a hidden oasis in the vast desert of cancer research, reveals a potential strategy to overcome chemoresistance, a major challenge in cancer treatment. The researchers' findings suggest that halogenated thymidine analogues could be a valuable weapon in the fight against MMR-deficient cancers, potentially enhancing the effectiveness of radiation therapy and improving outcomes for patients.
Date :
- Date Completed 2000-11-08
- Date Revised 2015-11-19
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