Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
ABSENCE OF P53 PERMITS PROPAGATION OF MUTANT-CELLS FOLLOWING GENOTOXIC DAMAGE
Autore:
GRIFFITHS SD; CLARKE AR; HEALY LE; ROSS G; FORD AM; HOOPER ML; WYLLIE AH; GREAVES M;
Indirizzi:
UNIV LIVERPOOL,ROYAL LIVERPOOL HOSP,DEPT HAEMATOL,3RD FLOOR DUNCAN BLDG,PRESCOT ST LIVERPOOL L69 MERSEYSIDE ENGLAND INST CANC RES,LEUKAEMIA RES FUND CTR LONDON SW3 6JB ENGLAND ROYAL MARSDEN HOSP LONDON SW3 6JB ENGLAND INST CANC RES,CHESTER BEATTY LABS,SECT RADIOTHERAPY LONDON SW3 6JB ENGLAND UNIV EDINBURGH,SCH MED,DEPT PATHOL EDINBURGH EH8 9AG MIDLOTHIAN SCOTLAND
Titolo Testata:
Oncogene
fascicolo: 5, volume: 14, anno: 1997,
pagine: 523 - 531
SICI:
0950-9232(1997)14:5<523:AOPPPO>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
WILD-TYPE P53; RADIATION-INDUCED APOPTOSIS; TUMOR-SUPPRESSOR GENE; IONIZING-RADIATION; P53-DEFICIENT MICE; HEMATOPOIETIC-CELLS; ANTICANCER AGENTS; GAMMA-IRRADIATION; HUMAN-LYMPHOCYTES; MAMMALIAN-CELLS;
Keywords:
IONIZING RADIATION; MUTATION; P53; APOPTOSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
58
Recensione:
Indirizzi per estratti:
Citazione:
S.D. Griffiths et al., "ABSENCE OF P53 PERMITS PROPAGATION OF MUTANT-CELLS FOLLOWING GENOTOXIC DAMAGE", Oncogene, 14(5), 1997, pp. 523-531

Abstract

Much evidence has been gathered in support of a critical role for p53in the cellular response to DNA damage. p53 dysfunction is associatedwith progression and poor prognosis of many human cancers and with a high incidence of tumours in p53 knockout mice. The absence of a p53-dependent G(1) arrest that facilitates DNA repair or apoptosis might impact critically on clinical cancer in two ways. First, by abrogating the impact on therapy that operates via genotoxic damage and apoptosis;and second, by encouraging progression either by inducing genomic instability and DNA mis-repair or by permitting survival of mutants. However, experiments examining the relationship between p53 deficiency andmutation frequency have so far failed to confirm these predictions. The precise role played by p53 is therefore unclear. We now report use of a short term in vitro approach to assess the influence of p53 on radiation-induced mutations at the hprt locus in murine B cell precursors that are normally radiation ultrasensitive, We find a high number ofhprt mutants among X-irradiated p53 null cells, which results from preferential survival as clonogenic mutants rather than from a p53-dependent increase in mutation rate. This result has important implicationsfor genotoxic cancer therapy.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 15/07/20 alle ore 20:32:41