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

D Bergamaschi; M Gasco; Louise Hiller; AL Sullivan; N Syed; G Trigante; I Yulug; M Merlano; G Numico; M Attard; B Gusterton; AK Bell; V Heath; C Travassoli; PJ Farrell; Xiaomei Lu; T Crook

doi:10.1016/S1535-6108(03)00079-5

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

D Bergamaschi, M Gasco, Louise Hiller, AL Sullivan, N Syed, G Trigante, I Yulug, M Merlano, G Numico, M Attard, B Gusterton, AK Bell, V Heath, C Travassoli, PJ Farrell, Xiaomei Lu, T Crook

Cancer and Genomic Sciences

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367 Citations (Scopus)

Abstract

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.

Original language	English
Pages (from-to)	387-402
Number of pages	16
Journal	Cancer Cell
Volume	3
Issue number	4
DOIs	https://doi.org/10.1016/S1535-6108(03)00079-5
Publication status	Published - 1 Apr 2003

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Bergamaschi, D., Gasco, M., Hiller, L., Sullivan, AL., Syed, N., Trigante, G., Yulug, I., Merlano, M., Numico, G., Attard, M., Gusterton, B., Bell, AK., Heath, V., Travassoli, C., Farrell, PJ., Lu, X., & Crook, T. (2003). p53 polymorphism influences response in cancer chemotherapy via modulation of p73-dependent apoptosis. Cancer Cell, 3(4), 387-402. https://doi.org/10.1016/S1535-6108(03)00079-5

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abstract = "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.",

author = "D Bergamaschi and M Gasco and Louise Hiller and AL Sullivan and N Syed and G Trigante and I Yulug and M Merlano and G Numico and M Attard and B Gusterton and AK Bell and V Heath and C Travassoli and PJ Farrell and Xiaomei Lu and T Crook",

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doi = "10.1016/S1535-6108(03)00079-5",

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Bergamaschi, D, Gasco, M, Hiller, L, Sullivan, AL, Syed, N, Trigante, G, Yulug, I, Merlano, M, Numico, G, Attard, M, Gusterton, B, Bell, AK, Heath, V, Travassoli, C, Farrell, PJ, Lu, X & Crook, T 2003, 'p53 polymorphism influences response in cancer chemotherapy via modulation of p73-dependent apoptosis', Cancer Cell, vol. 3, no. 4, pp. 387-402. https://doi.org/10.1016/S1535-6108(03)00079-5

TY - JOUR

T1 - p53 polymorphism influences response in cancer chemotherapy via modulation of p73-dependent apoptosis

AU - Bergamaschi, D

AU - Gasco, M

AU - Hiller, Louise

AU - Sullivan, AL

AU - Syed, N

AU - Trigante, G

AU - Yulug, I

AU - Merlano, M

AU - Numico, G

AU - Attard, M

AU - Gusterton, B

AU - Bell, AK

AU - Heath, V

AU - Travassoli, C

AU - Farrell, PJ

AU - Lu, Xiaomei

AU - Crook, T

PY - 2003/4/1

Y1 - 2003/4/1

N2 - 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.

AB - 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.

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U2 - 10.1016/S1535-6108(03)00079-5

DO - 10.1016/S1535-6108(03)00079-5

M3 - Article

C2 - 12726864

VL - 3

SP - 387

EP - 402

JO - Cancer Cell

JF - Cancer Cell

IS - 4

ER -

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

Abstract

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