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由BCR-ABL诱导的急性淋巴细胞白血病中CDKN2A/B（INK4A/B-ARF）介导的肿瘤抑制失败及对靶向治疗的耐药性。

Failure of CDKN2A/B (INK4A/B-ARF)-mediated tumor suppression and resistance to targeted therapy in acute lymphoblastic leukemia induced by BCR-ABL.

作者信息

Mullighan Charles G, Williams Richard T, Downing James R, Sherr Charles J

机构信息

Department of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.

出版信息

Genes Dev. 2008 Jun 1;22(11):1411-5. doi: 10.1101/gad.1673908.

DOI:10.1101/gad.1673908
PMID:18519632
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2732413/
Abstract

Deletions of the CDKN2A/B tumor suppressor locus and of the IKAROS and PAX5 genes that promote B-lineage development occur frequently in lymphoid, but not myeloid leukemias initiated by the BCR-ABL tyrosine kinase. Why is this the case, and how do these genetic lesions contribute to an aggressive disease that fails to durably respond to targeted kinase inhibitors?

摘要

CDKN2A/B肿瘤抑制基因座以及促进B细胞谱系发育的IKAROS和PAX5基因的缺失，在由BCR-ABL酪氨酸激酶引发的淋巴系白血病中频繁发生，但在髓系白血病中却不常见。为何会出现这种情况，以及这些基因损伤如何导致一种对靶向激酶抑制剂无法产生持久反应的侵袭性疾病？

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本文引用的文献

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