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Integration of ruxolitinib into dose‐intensified therapy targeted against a novel JAK2 F694L mutation in B‐precursor acute lymphoblastic leukemia
Author(s) -
Mayfield Jodi R.,
Czuchlewski David R.,
Gale James M.,
MatlawskaWasowska Ksenia,
Vasef Mohammad A.,
Nickl Christian,
Pickett Gavin,
Ness Scott A.,
Winter Stuart S.
Publication year - 2017
Publication title -
pediatric blood and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.116
H-Index - 105
eISSN - 1545-5017
pISSN - 1545-5009
DOI - 10.1002/pbc.26328
Subject(s) - medicine , minimal residual disease , ruxolitinib , mutation , complete remission , stem cell , chemotherapy , oncology , lymphoblastic leukemia , acute lymphocytic leukemia , cancer research , hematopoietic stem cell transplantation , leukemia , disease , gene , bone marrow , genetics , biology , myelofibrosis
A 17‐year‐old girl with B‐cell precursor acute lymphoblastic leukemia (BCP‐ALL) with persistent minimal residual disease (MRD) who underwent standard chemotherapy was found to have a BCR‐ABL1 ‐like gene expression pattern. Genome sequencing revealed a JAK2 mutation not previously described in BCP‐ALL and a potential therapeutic target. Due to concern for an on‐therapy relapse, the JAK2 inhibitor ruxolitinib was incorporated into a modified chemotherapy backbone to achieve complete remission prior to stem cell transplant. Treatment was well tolerated and she had undetectable MRD prior to a matched allogeneic stem cell transplant and remained in remission at day +100.
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