This is a multi-center study to explore the molecular phenotypic changes in castration-resistant prostate cancer by histopathological,immunohistochemical and molecular analysis of cancer related genes in castration-resistant prostate cancer.After patient eligibility is determined, tumor tissue will be acquired from archival or transurethral resection or from re-biopsy specimens from patients with recurrence, visceral metastasis, bone metastases. According to the molecular phenotypic changes, personalized treatment were performed.
Participants will be screened with a full medical history and physical examination, blood and urine tests, and tumor imaging studies. The tumor specimens at diagnosis of prostate cancer should be needed for all the participants.
After assessing for the prostate specific antigen (PSA) level and the tumor molecular phenotypic features,participants will be separated into different treatment groups:
1. Participants with "AR dependent" CRPC (generally with high PSA level and/or high AR expression) and with druggable gene mutations will receive Docetaxel/prednisone+Target drugs.
2. Participants with "AR dependent" CRPC (generally with high PSA level and/or high AR expression) and without druggable gene mutations will receive Docetaxel/ Prednisone.
3. Participants with "AR independent" CRPC (generally without AR expression and/or rapid progression with low PSA level) and with druggable gene mutations will receive Cisplatin/Etoposide+Target drugs.
4. Participants with "AR independent" CRPC (generally without AR expression and/or rapid progression with low PSA level) and without druggable gene mutations will receive Cisplatin/Etoposide.
Participants with druggable gene mutations will receive the corresponding molecular targeted drugs.
Participants with epidermal growth factor receptor (EGFR) gene mutation will receive a drug called Gefitinib, which inhibits a protein called EGFR that is thought to be a key factor in the development and progression of some cancers.
Participants with B-type Raf kinase (BRAF) gene mutations will receive a drug called Vemurafenib, which inhibits a protein called mitogen-activated or extracellular signal-regulated protein kinase kinase (MEK) that is thought to be a key factor in the development and progression of some cancers.
Participants with v-akt murine thymoma viral oncogene homologue 1 (AKT1) gene mutations will receive a drug called Celecoxib, which inhibits a protein called v-akt murine thymoma viral oncogene homologue (AKT) that is thought to be a key factor in the development and progression of some cancers.
Participants who have erythroblastic leukemia viral oncogene homolog 2 (ERBB2) gene mutation will receive a drug called lapatinib, which inhibits some proteins that are thought to be key factors in the development and progression of some cancers.
Participants with PDGFRA gene mutations will receive a drug called sunitinib, which inhibits some proteins that are thought to be key factors in the development and progression of some cancers.
Participants with PIK3CA gene mutations will receive a drug called Everolimus, which inhibits a protein called AKT that is thought to be a key factor in the development and progression of some cancers.
