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.
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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