Abstract
Acute lymphoblastic leukemia (ALL) is the most common type of cancer in children. In recent Total Therapy studies conducted at St. Jude Children’s Research Hospital, children with ALL had a 5-year overall survival of around 94%. This is the result of a combination of risk stratification based on the biological features of the leukemic cells and the response to treatment (as assessed by the detection of minimal residual disease), treatment modification based on pharmacodynamic and pharmacogenomic data, and improved supportive care. However, innovative approaches are required to further improve survival to as close to 100% as possible and to reduce the adverse effects of treatment. Next-generation sequencing of leukemic cell DNA and RNA, as well as of germline DNA, can identify submicroscopic genetic structural changes and sequence alterations that contribute to leukemogenesis. Next-generation sequencing data can be used to define new ALL subtypes, to help improve treatment response and reduce adverse effects, and to identify novel prognostic markers and therapeutic targets to facilitate personalized precision medicine. In this article, we describe our approach to detecting targetable lesions in patients with ALL by next-generation sequencing and explain how we integrate the sequencing data into the treatment of these patients.
Highlights
PDGFRA DasatinibJAK2 inhibitor JAK2 inhibitor Unknown JAK1/JAK3 inhibitor TRK inhibitor FAK inhibitor TYK2 inhibitor FLT3 inhibitor Sorafenib/ dasatinib aCited from Ref. [7,11]
United States Yana Pikman, Dana–Farber Cancer Institute, United States Jose Andres Yunes, Centro Infantil Boldrini, Brazil
We describe our approach to detecting targetable lesions in patients with Acute lymphoblastic leukemia (ALL) by next-generation sequencing and explain how we integrate the sequencing data into the treatment of these patients
Summary
JAK2 inhibitor JAK2 inhibitor Unknown JAK1/JAK3 inhibitor TRK inhibitor FAK inhibitor TYK2 inhibitor FLT3 inhibitor Sorafenib/ dasatinib aCited from Ref. [7,11]. JAK2 inhibitor JAK2 inhibitor Unknown JAK1/JAK3 inhibitor TRK inhibitor FAK inhibitor TYK2 inhibitor FLT3 inhibitor Sorafenib/ dasatinib aCited from Ref. CENPC, ETV6, FOXP1, LSM14, NUP153, NUP214, RCSD1, RANBP2, SNX2, SFPQ, SPTAN1, ZMIZ1. ATF7IP, BCR, EBF1, ETV6, PAX5, PCM1, PPFIBP1, RFX3, SSBP2, STRN3, TERF2, TPR, USP25, ZNF274, GOLGA5, SMU1, HMBOX1, SNX29, ZNF340. These mutations include those in genes encoding cytokine receptors (IL7R or IL2RB); activating mutations in the Janus kinase genes themselves (JAK1 or JAK3); and mutations that impair the function of negative regulators of JAK–STAT signaling (SH2B3) [7, 11]
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