作者: J Alsner , M Yilmaz , P Guldberg , LL Hansen , J Overgaard
DOI: 10.1186/BCR109
关键词:
摘要: TP53 mutation is a strong independent marker for survival in breast cancer with some heterogeneity the clinical phenotype of various types mutations. Based on 315 patients carcinoma, we suggest new model differentiation Although general was associated aggressive tumor/patient characteristics, missense mutations outside any conserved or structural domain did not affect outcome (risk disseminated disease and death). In contrast, affecting amino acids directly involved DNA zinc binding displayed very phenotype. Null (including disrupting tetramerization domain) remaining an intermediate When primary early were divided into three groups (wild-type together structural/conserved domains, null phenotype, mutations), disease-specific rates 89%, 58%, 35% (5-year actuarial values, P < 0.0001), respectively. Cox proportional hazards analysis, separation according to these criteria eliminated prognostic importance all investigated classical factors except nodal status.