2018
DOI: 10.1111/ejh.13037
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MLL‐rearranged acute myeloid leukemia: Influence of the genetic partner in allo‐HSCT response and prognostic factor of MLL 3′ region mRNA expression

Abstract: We show that the MLL genetic partner could have implications in allo-HSCT response, and we propose three genes whose expression could be useful for the prognosis of this leukemia in patients undergoing allo-HSCT: 3' region of MLL, EVI1, and FLT3.

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Cited by 5 publications
(2 citation statements)
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“…Nowadays, allo-HSCT remains the only therapy to cure high-risk KMT2A r AML patients [32]; however, different KMT2A genetic fusions have shown different prognostics. Data from Burillo-Sanz et al [33] showed that OS of patients undergoing allo-HSCT was longer for patients harboring KMT2A r fusions with MLLT3 and MLLT1 than the remaining KMT2A fusions. This result is in concordance with that obtained from other authors, in which rearrangements t (9;11) and t (11;19) showed a better outcome when subjected to allo-HSCT rather than t (6;11) and t (10;11), being extended to other types of KMT2A rearrangement [34].…”
Section: Discussionmentioning
confidence: 99%
“…Nowadays, allo-HSCT remains the only therapy to cure high-risk KMT2A r AML patients [32]; however, different KMT2A genetic fusions have shown different prognostics. Data from Burillo-Sanz et al [33] showed that OS of patients undergoing allo-HSCT was longer for patients harboring KMT2A r fusions with MLLT3 and MLLT1 than the remaining KMT2A fusions. This result is in concordance with that obtained from other authors, in which rearrangements t (9;11) and t (11;19) showed a better outcome when subjected to allo-HSCT rather than t (6;11) and t (10;11), being extended to other types of KMT2A rearrangement [34].…”
Section: Discussionmentioning
confidence: 99%
“…Similarly, histone methyltransferases can be dysregulated in AML. These include mutations in ASXL1 (5%), associated with relapsed AML 344 ; MLL1 (11q23) rearrangements (5-10%) with more than 80 partner genes 345 , including AF4, AF9, ENL, and ELL, which belong to and recruit the SEC complex and DOT1L to deposit H3K4me1 and H3K79me2 marks on active chromatin 346 ; and mutations in SETD2 (5%) 325 . Moreover, AML cases have shown histone acetyl-transferase CREBBP1 (CBP) and EP300 (p300) rearrangements with KAT6 (MOZ) 325,336 .…”
Section: Epigenetic Dysregulation In Acute Myeloid Leukaemiamentioning
confidence: 99%