作者: John MS Bartlett , Daniella Brawley , Ken Grigor , Alison F Munro , Barbara Dunne
DOI: 10.1002/PATH.1735
关键词: Endocrinology 、 Prostate cancer 、 Androgen receptor 、 Tyrosine kinase 、 Medicine 、 Internal medicine 、 Cancer research 、 Receptor tyrosine kinase 、 Anatomical pathology 、 Fluorescence in situ hybridization 、 Immunohistochemistry 、 Hormone 、 Pathology and Forensic Medicine
摘要: Relapse during androgen withdrawal therapy is a significant cause of morbidity and mortality from prostate cancer. Androgen receptor mutations (6-10%) amplifications (20-30%) may explain relapse in some patients, but approximately 70% cases, alternative mechanisms must be invoked preliminary evidence suggests that type I tyrosine kinases play role mediating hormone escape. In this study, EGFR HER2 gene amplification expression were analysed by fluorescence situ hybridization immunohistochemistry, respectively, cohort matched tumour pairs (one taken before one after relapse) 49 cancer patients. No low-level, heterogeneous observed (6.5%). correlation between EGFR/HER2 copy protein was found. Almost quarter the cases (12/49, 24.5%) showed increased or at relapse; associated with reduction time to death (p = 0.0003). do not cancer, influence progression independence about as rise death. These findings support development targeted therapies androgen-independent demonstrate, using carefully characterized patient cohort, pathway represent number independent routes escape