| Literature DB >> 30466748 |
Abstract
Progress in our understanding of the central genes, pathways, and mechanisms in the pathobiology of T-cell acute lymphoblastic leukemia (T-ALL) has identified key drivers of the disease, opening new opportunities for therapy. Drugs targeting highly prevalent genetic alterations in NOTCH1 and CDKN2A are being explored, and multiple other targets with readily available therapeutic agents, and immunotherapies are being investigated. The molecular basis of T-ALL is reviewed here and potential targets and therapeutic targets discussed.Entities:
Keywords: CDKN2A; Chimeric antigen receptor; GSI; Gamma secretase inhibitor; JAK/STAT; Mutations; NOTCH1; NT5C2CAR; NUP214-ABL1; PTEN; T-ALL; T-cell acute lymphoblastic leukemia
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Year: 2018 PMID: 30466748 PMCID: PMC6294319 DOI: 10.1016/j.beha.2018.10.001
Source DB: PubMed Journal: Best Pract Res Clin Haematol ISSN: 1521-6926 Impact factor: 3.020