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The genetics and mechanisms of T cell acute lymphoblastic leukaemia
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Journal Article
The genetics and mechanisms of T cell acute lymphoblastic leukaemia
2016
Overview
Key Points
T cell acute lymphoblastic leukaemia (T-ALL) is an aggressive haematological tumour resulting from the malignant transformation of T cell progenitors.
T-ALL is biologically and genetically heterogeneous with gene expression signatures that identify different clinico-biological groups associated with T cell arrest at different stages of thymocyte development.
Oncogenic NOTCH signalling resulting from activating mutations in
NOTCH1
is a major driver of T-ALL transformation.
Aberrant expression of transcription factor oncogenes as a result of chromosomal translocations and other chromosomal rearrangements is common in T-ALL.
Recurrent mutations and deletions in T-ALL frequently involve cell cycle regulators, but also transcription factors, tumour suppressors, epigenetic factors and negative regulators of NOTCH1, Janus kinase (JAK)–signal transducer and activator of transcription (STAT), PI3K and MAPK signalling.
Relapsed T-ALL is associated with a poor prognosis, and relapse-associated activating mutations in the cytosolic 5′-nucleotidase II gene,
NT5C2
, induce resistance to 6-mercaptopurine chemotherapy.
This Review discusses the increased understanding of the biology of T cell acute lymphoblastic leukaemia (T-ALL) and how this has translated into new prognostic biomarkers, improved animal models and the emergence of targeted therapies to combat this disease.
T cell acute lymphoblastic leukaemia (T-ALL) is an aggressive haematological malignancy derived from early T cell progenitors. In recent years genomic and transcriptomic studies have uncovered major oncogenic and tumour suppressor pathways involved in T-ALL transformation and identified distinct biological groups associated with prognosis. An increased understanding of T-ALL biology has already translated into new prognostic biomarkers and improved animal models of leukaemia and has opened opportunities for the development of targeted therapies for the treatment of this disease. In this Review we examine our current understanding of the molecular mechanisms of T-ALL and recent developments in the translation of these results to the clinic.
Publisher
Nature Publishing Group UK,Nature Publishing Group
