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|Variant||KMT2A - MLLT10|
|Protein Effect||gain of function|
|Gene Variant Descriptions||KMT2A-MLLT10 results from the fusion of KMT2A (MLL) and MLLT10 (AF10), resulting in the transformation of primitive myeloid progenitor cells in mouse models, which eventually leads to leukemogenesis (PMID: 11986236). KMT2A-MLLT10 has been identified in acute myeloid leukemia (PMID: 34551411, PMID: 33020282)|
|Associated Drug Resistance|
|Molecular Profile||Indication/Tumor Type||Response Type||Therapy Name||Approval Status||Evidence Type||Efficacy Evidence||References|
|KMT2A - MLLT10||leukemia||sensitive||EPZ004777||Preclinical||Actionable||In a preclinical study, transformed cells expressing the fusion, KMT2A-MLLT10, demonstrated sensitivity to EPZ004777 in culture and in mouse models, resulting in cell cycle arrest, increased apoptotic activity, and inhibition of cell proliferation (PMID: 23138183).||23138183|
|KMT2A - MLLT10||acute myeloid leukemia||sensitive||I-BET151 + SGC0946||Preclinical - Patient cell culture||Actionable||In a preclinical study, I-BET151 and SGC0946 synergistically inhibited proliferation of patient-derived acute myeloid leukemia cells harboring KMT2A-MLLT10 in culture (PMID: 27294782).||27294782|