Targeted Therapeutic Approach Based on Understanding of Aberrant Molecular Pathways Leading to Leukemic Proliferation in Patients with Acute Myeloid Leukemia
DC Field | Value | Language |
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dc.contributor.author | Song, Moo-Kon | - |
dc.contributor.author | Park, Byeong-Bae | - |
dc.contributor.author | Uhm, Ji-Eun | - |
dc.date.accessioned | 2021-07-30T04:43:38Z | - |
dc.date.available | 2021-07-30T04:43:38Z | - |
dc.date.created | 2021-07-14 | - |
dc.date.issued | 2021-06 | - |
dc.identifier.issn | 1661-6596 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/1099 | - |
dc.description.abstract | Acute myeloid leukemia (AML) is a heterogenous hematopoietic neoplasm with various genetic abnormalities in myeloid stem cells leading to differentiation arrest and accumulation of leukemic cells in bone marrow (BM). The multiple genetic alterations identified in leukemic cells at diagnosis are the mainstay of World Health Organization classification for AML and have important prognostic implications. Recently, understanding of heterogeneous and complicated molecular abnormalities of the disease could lead to the development of novel targeted therapeutic agents. In the past years, gemtuzumab ozogamicin, BCL-2 inhibitors (venetovlax), IDH 1/2 inhibitors (ivosidenib and enasidenib) FLT3 inhibitors (midostaurin, gilteritinib, and enasidenib), and hedgehog signaling pathway inhibitors (gladegib) have received US Food and Drug Administration (FDA) approval for the treatment of AML. Especially, AML patients with elderly age and/or significant comorbidities are not currently suitable for intensive chemotherapy. Thus, novel therapeutic planning including the abovementioned target therapies could lead to improve clinical outcomes in the patients. In the review, we will present various important and frequent molecular abnormalities of AML and introduce the targeted agents of AML that received FDA approval based on the previous studies. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | MDPI | - |
dc.title | Targeted Therapeutic Approach Based on Understanding of Aberrant Molecular Pathways Leading to Leukemic Proliferation in Patients with Acute Myeloid Leukemia | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Park, Byeong-Bae | - |
dc.contributor.affiliatedAuthor | Uhm, Ji-Eun | - |
dc.identifier.doi | 10.3390/ijms22115789 | - |
dc.identifier.scopusid | 2-s2.0-85106658835 | - |
dc.identifier.wosid | 000660169900001 | - |
dc.identifier.bibliographicCitation | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.22, no.11, pp.1 - 20 | - |
dc.relation.isPartOf | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | - |
dc.citation.title | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | - |
dc.citation.volume | 22 | - |
dc.citation.number | 11 | - |
dc.citation.startPage | 1 | - |
dc.citation.endPage | 20 | - |
dc.type.rims | ART | - |
dc.type.docType | Review | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | Y | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Chemistry | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Multidisciplinary | - |
dc.subject.keywordPlus | INTERNAL TANDEM DUPLICATION | - |
dc.subject.keywordPlus | ISOCITRATE-DEHYDROGENASE 1 | - |
dc.subject.keywordPlus | GEMTUZUMAB OZOGAMICIN | - |
dc.subject.keywordPlus | HEDGEHOG PATHWAY | - |
dc.subject.keywordPlus | OLDER PATIENTS | - |
dc.subject.keywordPlus | ADULT PATIENTS | - |
dc.subject.keywordPlus | OPEN-LABEL | - |
dc.subject.keywordPlus | INDUCTION CHEMOTHERAPY | - |
dc.subject.keywordPlus | YOUNGER PATIENTS | - |
dc.subject.keywordPlus | SUPPORTIVE CARE | - |
dc.subject.keywordAuthor | acute myeloid leukemia | - |
dc.subject.keywordAuthor | gemtuzumab ozogamicin | - |
dc.subject.keywordAuthor | BCL-2 | - |
dc.identifier.url | https://www.mdpi.com/1422-0067/22/11/5789 | - |
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