Abstract
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy derived from early T-cell progenitors. The recognition of clinical, genetic, transcriptional, and biological heterogeneity in this disease has already translated into new prognostic biomarkers, improved leukemia animal models, and emerging targeted therapies. This work reviews our current understanding of the molecular mechanisms of T-ALL.
Copyright © 2020 Cold Spring Harbor Laboratory Press; all rights reserved.
MeSH terms
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Animals
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Antineoplastic Agents / therapeutic use
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Biomarkers, Tumor / genetics*
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Disease Models, Animal
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Gene Expression Regulation, Leukemic
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Humans
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Mutation
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Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
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Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics*
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Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism
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Receptor, Notch1 / antagonists & inhibitors*
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Receptor, Notch1 / genetics*
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Receptor, Notch1 / metabolism
Substances
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Antineoplastic Agents
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Biomarkers, Tumor
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NOTCH1 protein, human
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Receptor, Notch1