Can one target T-cell ALL?

Best Pract Res Clin Haematol. 2018 Dec;31(4):361-366. doi: 10.1016/j.beha.2018.10.001. Epub 2018 Oct 17.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Antineoplastic Agents / therapeutic use*
  • Cyclin-Dependent Kinase Inhibitor p16* / antagonists & inhibitors
  • Cyclin-Dependent Kinase Inhibitor p16* / immunology
  • Drug Delivery Systems / methods*
  • Humans
  • Immunotherapy*
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma* / immunology
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma* / therapy
  • Receptor, Notch1* / antagonists & inhibitors
  • Receptor, Notch1* / immunology


  • Antineoplastic Agents
  • CDKN2A protein, human
  • Cyclin-Dependent Kinase Inhibitor p16
  • NOTCH1 protein, human
  • Receptor, Notch1