Prostate cancer is a common malignant tumor in elderly men, and its incidence is increasing year by year in China. Early stage limited prostate cancer is usually treated with surgery or local radiotherapy. For advanced prostate cancer, endocrine therapy has been recognized as an effective treatment for many years. At the beginning of endocrine therapy, most patients can achieve tumor shrinkage, decrease in serum prostate specific antigen (PSA), reduction in bone pain, relief of urinary tract obstruction and bleeding symptoms, and improvement in physical condition. However, a significant number of patients have progressed from hormone-dependent to hormone-insensitive prostate cancer (HRPC) after 2 to 5 years of endocrine therapy, and once HRPC appears, treatment is more difficult and seriously threatens patients’ lives. With the continuous development of molecular biology and genetic engineering technology, the etiology and treatment of HRPC have been further understood. Most of the endocrine treatments for prostate cancer are aimed at inhibiting the growth of hormone-dependent tumor cells by blocking the binding of androgens and androgen-receptor (AR), so the abnormal expression of AR is the main reason for the emergence of HRPC. the only gene that is consistently upregulated, mainly by increased or mutated AR expression and abnormal cytokines, growth factors or co-stimulatory factors involved in AR activation. In addition, the autocrine and paracrine effects of prostate cancer cells, inactivation of the oncogene PTEN (for phophatase and tensin homologue) and overexpression of the anti-apoptotic gene Bcl-2 were also included. The European Research and Treatment Center for Cancer (EORTC), the National Prostate Cancer Research Program (NPCP) and the Eastern Cooperative Cancer Study Group (ECOG) have proposed a series of evaluation criteria, mainly including the increase of prostate volume, the appearance of new metastatic foci on bone scan, and the appearance of new lymphatic foci. The main criteria include increased prostate volume, new metastases on bone scan, new lymph node metastases, increased subjective symptoms, etc. Some also consider the re-elevation of serum PSA after a period of androgen blockade therapy as an important sign of hormone resistance in prostate cancer. The recognized and relatively easy criteria for judging HRPC are: 1. the blood PSA measured for 3 consecutive times (interval at least 2 weeks) is greater than the reference value (0.2ng/dl); 2. the blood testosterone concentration is the depressed level; 3. the blood PSA value still does not decrease or even increases after stopping anti-androgen therapy and second-line anti-androgen drug therapy. Based on the above indicators, it can be initially estimated that prostate cancer patients were converted from hormone dependence to hormone resistance. 3. Predictors of HRPC: Studies have shown that not all HRPC change from the initial hormone-dependent to hormone-resistant type, and about 15% of prostate cancer cells do not depend on hormone growth at the beginning and thus are not sensitive to endocrine therapy. Thus, if HRPC can be detected in the early stage of the disease, comprehensive treatment can be started as early as possible to improve the treatment outcome. Hasumi et al. used gene microarray technology to detect the expression level of Neuroserpin, a neuroserine protein hydrolase inhibitor, in prostate cancer samples and analyzed the relationship between its expression level and clinical background and pathological grade in 57 prostate cancer patients. The results showed that Neuroserpin could be detected in 102 prostate tissues, including 45 normal prostate tissue specimens. Prostate cancer tissues expressed higher levels than normal prostate tissues, positively correlated with Gleason score and negatively correlated with overall survival and period of disease progression, and Neuroserpin was found to be expressed at the highest level in hormone-non-dependent prostate cancer (HRPC). Prostate cancer stem cells differentiate along two main pathways: the exocrine pathway and the neuroendocrine pathway. In HRPC, the neuroendocrine pathway is the main pathway. Chromogranin A (CgA) is a specific protein secreted by neuroendocrine cells and therefore can be used as a test for prostate cancer.Berruti et al. studied 108 patients with newly diagnosed HRPC and combined CgA in plasma with other biochemical markers such as serum PSA, AKP, acid phosphatase, serum albumin and hemoglobin concentrations. Patients were compared for physical status, Gleason score and presence of distant metastases. It is believed that plasma CgA is often elevated in patients with HRPC and suggests a poor prognosis, and its concentration is not affected by whether or not they receive treatment and is time-dependent, with the longer the time, the higher the concentration. In the past, HRPC was considered to be hypersensitive to chemotherapy, and the FDA approved mitoxantrone and estramustine for the treatment of prostate cancer, which could improve clinical symptoms and reduce serum PSA values in combination with hormones, but neither of them prolonged the survival time of patients. TAX327 and SWOG9916, two phase III clinical studies of paclitaxel-based treatment of HRPC, were reported at the 2004 Annual National Conference of Clinical Oncology (ASCO), and the results showed that they could significantly improve survival time. The TAX327 trial: 1006 patients with HRPC were selected and randomized into three groups, and the results suggested that the overall survival of the doxorubicin 3-week group, doxorubicin weekly group and mitoxantrone treatment group were 18.9 months, 17.3 months and 16.4 months, respectively. The percentage of pain reduction was: 35%, 31% and 22%, respectively. It suggested that doxorubicin combined with prednisone 3-week regimen could significantly improve symptoms and prolong survival compared with mitoxantrone combined with prednisone chemotherapy.SWOG9916 trial: comparison of doxorubicin combined with estramustine (group D/E) and mitoxantrone combined with prednisone (M/P) for 674 HRPC cases. The results suggested that the median survival time of 17.5 months in the D/E group was longer than that of 15.6 months in the M/P group (p=0.01), and the median progression-free survival time of 6.3 months in the D/E group was longer than that of 3.2 months in the M/P group, i.e., the overall survival rate was improved by 20% with the D/E combination.