关键词: CDKN2A Chimeric antigen receptor GSI Gamma secretase inhibitor JAK/STAT Mutations NOTCH1 NT5C2CAR NUP214-ABL1 PTEN T-ALL T-cell acute lymphoblastic leukemia

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

来  源:   DOI:10.1016/j.beha.2018.10.001   PDF(Sci-hub)   PDF(Pubmed)

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.
摘要:
我们对中心基因的理解有了进展,通路,T细胞急性淋巴细胞白血病(T-ALL)的病理生物学机制已经确定了该疾病的关键驱动因素,为治疗开辟了新的机会。正在探索针对NOTCH1和CDKN2A中高度流行的遗传改变的药物,和多个其他目标与现成的治疗剂,和免疫疗法正在研究中。本文综述了T-ALL的分子基础,并讨论了潜在的靶点和治疗靶点。
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