p53 as an Effector or Inhibitor of Therapy Response

被引：8

作者：

Ablain, Julien ^{[1
,2
,3
]}

Poirot, Brigitte ^{[1
,2
,3
,4
]}

Esnault, Cecile ^{[1
,2
,3
]}

Lehmann-Che, Jacqueline ^{[1
,2
,3
,4
]}

de The, Hugues ^{[1
,2
,3
,4
,5
]}

机构：

[1] Univ Paris Diderot, Sorbonne Paris Cite, Inst Univ Hematol, Hop St Louis, F-75475 Paris, France

[2] Hop St Louis, INSERM, Equipe Labellise Ligue Natl Canc, UMR 944, F-75475 Paris, France

[3] Hop St Louis, CNRS, UMR 7212, F-75475 Paris, France

[4] Hop St Louis, AP HP, Oncol Mol, F-75475 Paris, France

[5] Coll France, F-75005 Paris, France

来源：

COLD SPRING HARBOR PERSPECTIVES IN MEDICINE | 2016年 / 6卷 / 01期

基金：

欧洲研究理事会;

关键词：

ACUTE PROMYELOCYTIC LEUKEMIA; PML NUCLEAR-BODIES; ALPHA RAR-ALPHA; RETINOIC ACID; ARSENIC TRIOXIDE; BREAST CANCERS; DOSE INTENSIFICATION; INTERFERON-ALPHA; GENE-MUTATIONS; ACHILLES-HEEL;

D O I：

10.1101/cshperspect.a026260

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

100103 [病原生物学]; 100218 [急诊医学];

摘要：

Although integrity of the p53 signaling pathway in a given tumor was expected to be a critical determinant of response to therapies, most clinical studies failed to link p53 status and treatment outcome. Here, we present two opposite situations: one in which p53 is an essential effector of cure by targeted leukemia therapies and another one in advanced breast cancers in which p53 inactivation is required for the clinical efficacy of dose-dense chemotherapy. If p53 promotes or blocks therapy response, therapies must be tailored on its status in individual tumors.

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收藏

页数：10

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