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유전체항상성연구단
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A novel chemotherapeutic agent to treat tumors with DNA mismatch repair deficiencies

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dc.contributor.authorZhang Y.-
dc.contributor.authorFox J.T.-
dc.contributor.authorYoung-Un Park-
dc.contributor.authorElliott G.-
dc.contributor.authorRai G.-
dc.contributor.authorCai M.-
dc.contributor.authorSakamuru S.-
dc.contributor.authorHuang R.-
dc.contributor.authorXia M.-
dc.contributor.authorLee K.-
dc.contributor.authorJeon M.H.-
dc.contributor.authorBijoy P. Mathew-
dc.contributor.authorPark H.D.-
dc.contributor.authorEdelmann W.-
dc.contributor.authorPark C.Y.-
dc.contributor.authorSung You Hong-
dc.contributor.authorMaloney D.-
dc.contributor.authorKyungjae Myung-
dc.date.available2016-09-01T02:34:18Z-
dc.date.created2016-08-19-
dc.date.issued2016-07-
dc.identifier.issn0008-5472-
dc.identifier.urihttps://pr.ibs.re.kr/handle/8788114/2760-
dc.description.abstractImpairing the division of cancer cells with genotoxic small molecules has been a primary goal to develop chemotherapeutic agents. However, DNA mismatch repair (MMR)-deficient cancer cells are resistant to most conventional chemotherapeutic agents. Here we have identified baicalein as a small molecule that selectively kills MutSa-deficient cancer cells. Baicalein binds preferentially to mismatched DNA and induces a DNA damage response in a MMR-dependent manner. In MutSa-proficient cells, baicalein binds to MutSa to dissociate CHK2 from MutSa leading to S-phase arrest and cell survival. In contrast, continued replication in the presence of baicalein in MutSa-deficient cells results in a high number of DNA double-strand breaks and ultimately leads to apoptosis. Consistently, baicalein specifically shrinks MutSa-deficient xenograft tumors and inhibits the growth of AOM-DSS-induced colon tumors in colon-specific MSH2 knockout mice. Collectively, baicalein offers the potential of an improved treatment option for patients with tumors with a DNA MMR deficiency. ©2016 American Association for Cancer Research-
dc.description.uri1-
dc.language영어-
dc.publisherAMER ASSOC CANCER RESEARCH-
dc.subjectLynch Syndrome, Baicalein, DNA mismatch repair, Modulation of DNA repair-
dc.titleA novel chemotherapeutic agent to treat tumors with DNA mismatch repair deficiencies-
dc.typeArticle-
dc.type.rimsART-
dc.identifier.wosid000381111400016-
dc.identifier.scopusid2-s2.0-84978419126-
dc.identifier.rimsid56306ko
dc.date.tcdate2018-10-01-
dc.contributor.affiliatedAuthorYoung-Un Park-
dc.contributor.affiliatedAuthorBijoy P. Mathew-
dc.contributor.affiliatedAuthorSung You Hong-
dc.contributor.affiliatedAuthorKyungjae Myung-
dc.identifier.doi10.1158/0008-5472.CAN-15-2974-
dc.identifier.bibliographicCitationCANCER RESEARCH, v.76, no.14, pp.4183 - 4191-
dc.citation.titleCANCER RESEARCH-
dc.citation.volume76-
dc.citation.number14-
dc.citation.startPage4183-
dc.citation.endPage4191-
dc.date.scptcdate2018-10-01-
dc.description.wostc3-
dc.description.scptc3-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.subject.keywordPlusCOLORECTAL-CANCER-
dc.subject.keywordPlusDAMAGE RESPONSE-
dc.subject.keywordPlusLYNCH SYNDROME-
dc.subject.keywordPlusBAICALEIN-
dc.subject.keywordPlusCELLS-
dc.subject.keywordPlusMSH2-
dc.subject.keywordPlusSUSCEPTIBILITY-
dc.subject.keywordPlusSCUTELLARIA-
dc.subject.keywordPlusMECHANISMS-
dc.subject.keywordPlusSTABILITY-
Appears in Collections:
Center for Genomic Integrity(유전체 항상성 연구단) > 1. Journal Papers (저널논문)
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