p53 polymorphism influences response in cancer chemotherapy via modulation of p73-dependent apoptosis

被引：387

作者：

Bergamaschi, D

Gasco, M

Hiller, L

Sullivan, A

Syed, N

Trigiante, G

Yulug, I

Merlano, M

Numico, G

Comino, A

Attard, M

Reelfs, O

Gusterson, B

Bell, AK

Heath, V

Tavassoli, M

Farrell, PJ

Smith, P

Lu, X

Crook, T

机构：

[1] Univ London Imperial Coll Sci Technol & Med, Fac Med, Ludwig Inst Canc Res, London W2 1PG, England

[2] Dept Med Oncol, I-12100 Cuneo, Italy

[3] Univ Birmingham, Inst Canc Studies, Canc Res UK Clin Trials Unit, Birmingham, W Midlands, England

[4] Bilkent Univ, Dept Mol Biol & Genet, Ankara, Turkey

[5] Azienda Osped S Croce & Carle, Dept Pathol, I-12100 Cuneo, Italy

[6] Univ Glasgow, Western Infirm, Dept Pathol, Glasgow G11 6NT, Lanark, Scotland

[7] Kings Coll London, Sch Med & Dent, London SE5, England

[8] Brunel Univ, Dept Biol, Uxbridge UB8 3PH, Middx, England

来源：

CANCER CELL | 2003年 / 3卷 / 04期

关键词：

D O I：

10.1016/S1535-6108(03)00079-5

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Intact p73 function is shown to be an important determinant of cellular sensitivity to anticancer agents. Inhibition of p73 function by dominant-negative proteins or by mutant p53 abrogates apoptosis and cytotoxicity induced by these agents. A polymorphism encoding either arginine (72R) or proline (72P) at codon 72 of p53 influences inhibition of p73 by a range of p53 mutants identified in squamous cancers. Clinical response following cisplatin-based chemo-radiotherapy for advanced head and neck cancer is influenced by this polymorphism, cancers expressing 72R mutants having lower response rates than those expressing 72P mutants. Polymorphism in p53 may influence individual responsiveness to cancer therapy.

引用

页码：387 / 402

页数：16

共 47 条

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