| Literature DB >> 27766616 |
Fiona C Brown1, Paolo Cifani1, Esther Drill2, Jie He3, Eric Still1, Shan Zhong3, Sohail Balasubramanian3, Dean Pavlick3, Bahar Yilmazel3, Kristina M Knapp4, Todd A Alonzo5,6, Soheil Meshinchi5,7, Richard M Stone8, Steven M Kornblau9, Guido Marcucci10, Alan S Gamis5,11, John C Byrd12, Mithat Gonen2, Ross L Levine13, Alex Kentsis1,14.
Abstract
Cure rates of children and adults with acute myeloid leukaemia (AML) remain unsatisfactory partly due to chemotherapy resistance. We investigated the genetic basis of AML in 107 primary cases by sequencing 670 genes mutated in haematological malignancies. SETBP1, ASXL1 and RELN mutations were significantly associated with primary chemoresistance. We identified genomic alterations not previously described in AML, together with distinct genes that were significantly overexpressed in therapy-resistant AML. Defined gene mutations were sufficient to explain primary induction failure in only a minority of cases. Thus, additional genetic or molecular mechanisms must cause primary chemoresistance in paediatric and adult AML.Entities:
Keywords: cytogenetically normal acute myeloid leukaemia; induction failure; paediatric leukaemia; primary chemoresistance; targeted deep sequencing genomics
Mesh：
Substances：
Year: 2016 PMID： 27766616 PMCID： PMC5177472 DOI： 10.1111/bjh.14413
Source DB: PubMed Journal: Br J Haematol ISSN： 0007-1048 Impact factor: 6.998