Emerging treatment options for patients with p53-pathway-deficient CLL

被引:14
作者
Aitken, Marisa J. L. [1 ,3 ]
Lee, Hun J. [2 ]
Post, Sean M. [1 ]
机构
[1] Univ Texas MD Anderson Canc Ctr, Dept Leukemia, 1515 Holcombe, Houston, TX 77030 USA
[2] Univ Texas MD Anderson Canc Ctr, Dept Lymphoma & Multiple Myeloma, Houston, TX 77030 USA
[3] Univ Texas MD Anderson Canc Ctr, UT Hlth Grad Sch Biomed Sci, Houston, TX 77030 USA
关键词
17p deletion; CLL; ibrutinib; idelalisib; TP53; mutation; venetoclax; CHRONIC LYMPHOCYTIC-LEUKEMIA; B-CELL RECEPTOR; ATM-DEPENDENT PHOSPHORYLATION; TUMOR-SUPPRESSOR P53; OPEN-LABEL; PHASE-III; CLONAL EVOLUTION; TP53; MUTATIONS; DOUBLE-BLIND; MOUSE MODEL;
D O I
10.1177/2040620719891356
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Over the past 40 years, p53 has been the most widely studied protein in cancer biology. Originally thought to be an oncogene due to its stabilization in many cancers, it is now considered to be one of the most critical tumor suppressors in a cell's ability to combat neoplastic transformation. Due to its critical roles in apoptosis, cell-cycle arrest, and senescence, TP53 deletions and mutations are commonly observed and are often a portent of treatment failures and poor clinical outcomes. This is particularly true in chronic lymphocytic leukemia (CLL), as patients with p53 alterations have historically had dismal outcomes. As such, the tremendous efforts made to better understand the functions of p53 in CLL have contributed substantially to recent advances in treating patients with p53-pathway-deficient CLL.
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页数:18
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