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Antitumor activity of HM781-36B, an irreversible Pan-HER inhibitor, alone or in combination with cytotoxic chemotherapeutic agents in gastric cancer

DC Field Value Language
dc.contributor.authorNam, Hyun-Jin-
dc.contributor.authorKim, Hwang-Phill-
dc.contributor.authorYoon, Young-Kwang-
dc.contributor.authorHur, Hyung-Seok-
dc.contributor.authorSong, Sang-Hyun-
dc.contributor.authorKim, Maeng-Sup-
dc.contributor.authorLee, Gwan-Sun-
dc.contributor.authorHan, Sae-Won-
dc.contributor.authorIm, Seock-Ah-
dc.contributor.authorKim, Tae-You-
dc.contributor.authorOh, Do-Youn-
dc.contributor.authorBang, Yung-Jue-
dc.date.accessioned2021-01-31T11:00:35Z-
dc.date.available2021-01-31T11:00:35Z-
dc.date.created2020-12-23-
dc.date.created2020-12-23-
dc.date.created2020-12-23-
dc.date.created2020-12-23-
dc.date.issued2011-03-28-
dc.identifier.citationCancer Letters, Vol.302 No.2, pp.155-165-
dc.identifier.issn0304-3835-
dc.identifier.other119682-
dc.identifier.urihttps://hdl.handle.net/10371/172959-
dc.description.abstractTrastuzumab, a HER2 directed treatment has shown clinical benefit in HER2 amplified gastric cancer. This study demonstrated the potent antitumor activity of HM781-36B, a quinazoline-based irreversible pan-HER inhibitor, in HER2 amplified gastric cancer cells (SNU216 and N87) in vitro and in vivo. HM781-36B inhibited phosphorylation of HER family and downstream signaling molecules, and induced apoptosis and G1 arrest. Furthermore, HM781-36B exerted synergistic effects with chemotherapeutic agents in both HER2 amplified and HER2 non-amplified gastric cancer cells. Therefore, HM781-36B may be useful for the treatment of HER2 amplified gastric cancer alone or in combination with chemotherapeutic agents. (C) 2011 Elsevier Ireland Ltd. All rights reserved.-
dc.language영어-
dc.publisherElsevier BV-
dc.titleAntitumor activity of HM781-36B, an irreversible Pan-HER inhibitor, alone or in combination with cytotoxic chemotherapeutic agents in gastric cancer-
dc.typeArticle-
dc.contributor.AlternativeAuthor임석아-
dc.identifier.doi10.1016/j.canlet.2011.01.010-
dc.citation.journaltitleCancer Letters-
dc.identifier.wosid000288357300010-
dc.identifier.scopusid2-s2.0-79951580512-
dc.citation.endpage165-
dc.citation.number2-
dc.citation.startpage155-
dc.citation.volume302-
dc.identifier.sci000288357300010-
dc.description.isOpenAccessN-
dc.contributor.affiliatedAuthorIm, Seock-Ah-
dc.contributor.affiliatedAuthorKim, Tae-You-
dc.contributor.affiliatedAuthorOh, Do-Youn-
dc.contributor.affiliatedAuthorBang, Yung-Jue-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusGROWTH-FACTOR RECEPTOR-
dc.subject.keywordPlusTYROSINE KINASE INHIBITOR-
dc.subject.keywordPlusCELL LUNG-CANCER-
dc.subject.keywordPlusHUMAN-BREAST-CANCER-
dc.subject.keywordPlusIN-VITRO-
dc.subject.keywordPlusRESISTANCE-
dc.subject.keywordPlusGEFITINIB-
dc.subject.keywordPlusEGFR-
dc.subject.keywordPlusAMPLIFICATION-
dc.subject.keywordPlusTRASTUZUMAB-
dc.subject.keywordAuthorHM781-36B-
dc.subject.keywordAuthorPan-HER inhibitor-
dc.subject.keywordAuthorGastric cancer-
dc.subject.keywordAuthorAntitumor activity-
dc.subject.keywordAuthorChemotherapeutic agents-
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Im, Seock Ah임석아
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  • College of Medicine
  • Department of Medicine
Research Area Clinical Medicine
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