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Clinical Efficacies of FLT3 Inhibitors in Patients with Acute Myeloid Leukemia

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dc.contributor.authorSong, Moo-Kon-
dc.contributor.authorPark, Byeong-Bae-
dc.contributor.authorUhm, Ji-Eun-
dc.date.accessioned2022-12-20T06:11:18Z-
dc.date.available2022-12-20T06:11:18Z-
dc.date.created2022-12-07-
dc.date.issued2022-10-
dc.identifier.issn1661-6596-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/172959-
dc.description.abstractFLT3 mutations are the most common genomic alteration detected in acute myeloid leukemia (AML) with a worse clinical prognosis. The highly frequent FLT3 mutations, together with the side effects associated with clinical prognosis, make FLT3 promising treatment targets and have provoked the advancement of FLT3 inhibitors. Recently, numerous FLT3 inhibitors were actively developed, and thus the outcomes of this aggressive subtype of AML were significantly improved. Recently, midostaurin and gilteritinib were approved as frontline treatment of AML and as therapeutic agents in the recurred disease by the United States Food and Drug Administration. Recently, numerous promising clinical trials attempted to seek appropriate management in frontline settings, in relapsed/refractory disease, or after stem cell transplantation in AML. This review follows numerous clinical trials about the usefulness of FLT3 inhibitors as frontline therapy, as relapsed/refractory conditioning, and as maintenance therapy of stem cell transplantation. The cumulative data of FLT3 inhibitors would be important clinical evidence for further management with FLT3 inhibitors in AML patients with FLT3 mutations.-
dc.language영어-
dc.language.isoen-
dc.publisherMDPI-
dc.titleClinical Efficacies of FLT3 Inhibitors in Patients with Acute Myeloid Leukemia-
dc.typeArticle-
dc.contributor.affiliatedAuthorSong, Moo-Kon-
dc.contributor.affiliatedAuthorPark, Byeong-Bae-
dc.contributor.affiliatedAuthorUhm, Ji-Eun-
dc.identifier.doi10.3390/ijms232012708-
dc.identifier.scopusid2-s2.0-85140723658-
dc.identifier.wosid000872814700001-
dc.identifier.bibliographicCitationINTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.23, no.20, pp.1 - 19-
dc.relation.isPartOfINTERNATIONAL JOURNAL OF MOLECULAR SCIENCES-
dc.citation.titleINTERNATIONAL JOURNAL OF MOLECULAR SCIENCES-
dc.citation.volume23-
dc.citation.number20-
dc.citation.startPage1-
dc.citation.endPage19-
dc.type.rimsART-
dc.type.docTypeReview-
dc.description.journalClass1-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaChemistry-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryChemistry, Multidisciplinary-
dc.subject.keywordPlusINTERNAL TANDEM DUPLICATION-
dc.subject.keywordPlusTYROSINE KINASE INHIBITOR-
dc.subject.keywordPlusPROGNOSTIC-SIGNIFICANCE-
dc.subject.keywordPlusPHASE-I-
dc.subject.keywordPlusINTENSIVE CHEMOTHERAPY-
dc.subject.keywordPlusMIDOSTAURIN PKC412-
dc.subject.keywordPlusANTITUMOR-ACTIVITY-
dc.subject.keywordPlusACTIVATION LOOP-
dc.subject.keywordPlusADULT PATIENTS-
dc.subject.keywordPlusMUTATIONS-
dc.subject.keywordAuthorFMS-like tyrosine kinase 3-
dc.subject.keywordAuthoracute myeloid leukemia-
dc.subject.keywordAuthormidostaurin-
dc.subject.keywordAuthorgilteritinib-
dc.identifier.urlhttps://www.mdpi.com/1422-0067/23/20/12708-
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서울 의과대학 > 서울 내과학교실 > 1. Journal Articles
서울 의과대학 > 서울 교육협력지원교실 > 1. Journal Articles

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