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|Ref Type||Journal Article|
|Authors||Yoon JH, Kim HJ, Kim JW, Jeon YW, Shin SH, Lee SE, Cho BS, Eom KS, Kim YJ, Lee S, Min CK, Cho SG, Lee JW, Min WS, Park CW|
|Title||Identification of molecular and cytogenetic risk factors for unfavorable core-binding factor-positive adult AML with post-remission treatment outcome analysis including transplantation.|
|Journal||Bone marrow transplantation|
|Abstract Text||Emerging molecular studies have identified a subgroup of patients with unfavorable core-binding factor-positive (CBF)-AML who should be treated by intensified post-remission treatments. We analyzed 264 adults with CBF-AML from 2002 to 2011, and focused on 206 patients who achieved CR after standard '3+7' induction chemotherapy. Patients who achieved CR with an available donor were treated with allogeneic hematopoietic SCT (allo-HSCT, n=115) and the rest were treated with autologous (auto) HSCT (n=72) or chemotherapy alone (n=19). OS was not significantly different between CBFβ/MYH11 (n=62) and RUNX1/RUNX1T1 (n=144), and auto-HSCT showed favorable OS compared with allo-HSCT or chemotherapy alone. Cytogenetic analysis identified that inv(16) without trisomy had a favorable OS and t(8;21) with additional chromosomes had an unfavorable OS, but multivariate analysis revealed those were NS. Patients with c-kit mutation showed inferior OS. For transplanted patients, residual post-transplant CBF-minimal residual disease quantitative PCR with higher WT1 expression at D+60 showed the worst OS with a higher incidence of relapse. Conclusively, we found that unfavorable CBF-AML can be defined with risk stratification using cytogenetic and molecular studies, and a careful risk-adapted treatment approach using frontline transplantation with novel therapies should be evaluated for this particular risk subgroup.|
|Molecular Profile||Treatment Approach|
|Gene Name||Source||Synonyms||Protein Domains||Gene Description||Gene Role|
|Therapy Name||Drugs||Efficacy Evidence||Clinical Trials|
|Drug Name||Trade Name||Synonyms||Drug Classes||Drug Description|
|Gene||Variant||Impact||Protein Effect||Variant Description||Associated with drug Resistance|
|Molecular Profile||Indication/Tumor Type||Response Type||Therapy Name||Approval Status||Evidence Type||Efficacy Evidence||References|
|RUNX1 - RUNX1T1||acute myeloid leukemia||not applicable||N/A||Clinical Study||Prognostic||In clinical analyses, the t(8;21) cytogenetic abnormality, which leads to the RUNX1-RUNX1T1 fusion, is associated with core-binding factor acute myeloid leukemia and favorable prognosis (PMID: 22180162, PMID: 9746770, PMID: 25111512).||9746770 25111512 22180162|
|RUNX1 - RUNX1T1 KIT mut||acute myeloid leukemia||not applicable||N/A||Clinical Study||Prognostic||In clinical analyses, coincident KIT mutations were associated with higher relapse rate and decreased overall survival in acute myeloid leukemia patients with RUNX1-RUNX1T1 fusions (PMID: 18648004, PMID: 16384925, PMID: 25111512).||25111512 16384925 18648004|