Afficher la notice abrégée

dc.contributor.authorWynford-Thomas, D.fr_FR
dc.date.accessioned2013-02-15T12:00:58Z
dc.date.available2013-02-15T12:00:58Z
dc.date.issued1994fr_FR
dc.identifier.citationWynford-Thomas, D., Mutation de la p53 dans les cancers humains : existe-t-elle pour faire sauter l'obstacle de la sénescence cellulaire ?, Med Sci (Paris), 1994, Vol. 10, N° 8-9; p.912fr_FR
dc.identifier.issn1958-5381fr_FR
dc.identifier.urihttp://hdl.handle.net/10608/2735
dc.description.abstractMore than 90 % of cancers in man are of epithelial origin. Recent technological advances, notably the advent of PCR, have led to a rapid expansion in our knowledge of the somatic genetic abnormalities in such tumours, including some of the most clinically important examples (breast, lung and colon). However, a list of genetic lesions does not by itself provide an explanation of tumour behaviour at the biochemical and cellular levels. This review illustrates the need to address the interface between molecular genetics and classical tumour pathology, by comparing and contrasting the molecular and cellular biology of tumorigenesis in two model epithelia - thyroid and colon. The influence of normal cell kinetics on the predicted sequence of molecular events provides a good example of the importance of tissue context in molecular oncology.fr
dc.language.isofrfr_FR
dc.publisherJohn Libbey Eurotext, Montrougefr_FR
dc.rightsArticle en libre accèsfr
dc.rightsMédecine/Sciences - Inserm - SRMSfr
dc.sourceM/S. Médecine sciences [revue papier, ISSN : 0767-0974], 1994, Vol. 10, N° 8-9; p.912fr_FR
dc.titleMutation de la p53 dans les cancers humains : existe-t-elle pour faire sauter l'obstacle de la sénescence cellulaire ?fr
dc.typeArticlefr_FR
dc.identifier.doi10.4267/10608/2735


Fichier(s) constituant ce document

Thumbnail

Ce document figure dans la(les) collection(s) suivante(s)

Afficher la notice abrégée