The NCI study in July 2003 (N Eng J Med) found that 18,800 cases were treated with oral finasteride 5mg/d in the prophylactic group and that the cancer rate was 18.4% (803/4368) in the prophylactic group and 24.4% (1147/4692) in the control group. The NCI study found that most of the Caps in the prevention group had higher Gleason scores: 7, 8, 9, and 10, suggesting that finasteride should not be used for prostate cancer prevention. In 2003, Marberger et al. also found that people with testosterone less than 3ng/ml were more likely to develop tumors of high malignancy. Prens used androgens to prevent prostate cancer and found that low concentrations stimulated prostate cell proliferation and cancer; high concentrations inhibited prostate cell growth. Intermittent estrogen therapy and anti-androgen withdrawal therapy are recommended. The current PSA has a poor specificity of only 25%, resulting in “PSA panic”. pPSA (precursor PSA ): also known as ProPSA, is secreted by prostate cancer cells and can detect 75% of tumors and reduce unnecessary biopsies by 59%. ProPSA/fPSA reduces unnecessary biopsies by only 33%. Catalona found that the PSA criterion for biopsy in patients younger than 60 years of age, when reduced from 4.0 ng/ml to 2.6 ng/ml, increased the detection rate from 18% to 36%, with a significant increase in postoperative 10-year survival. The question is whether the “overtreatment” resulting from a lower PSA threshold is appropriate for Chinese men? Other specific tests include: genetic proteomic tests, Liotta et al. studied 167 cases of prostate cancer, 77 cases of BPH, and 82 controls. The sensitivity of the genetic proteomic test was 83% and the specificity was 97%. The sensitivity and specificity of DD3 mRNA were higher than 90%. Glutathione-S-transferase Pi, urine DNA Hespin fragment sequence and gene expression also have good application prospects. The first orchiectomy performed by Huggins in 1941 was the earliest debulking treatment for prostate cancer. 30 years later Schally proposed pharmacological debulking, but it is prone to the following complications: anemia, loss of libido, decreased muscle strength, decreased bone density, and susceptibility to fracture, and also prone to androgen reduction and conversion of androgen-dependent cells to non-dependent cells. Umekita et al. cultured LNCaP cells in androgen-deficient medium and found that after 2 years and 100 generations, the cell surface AR increased more than 10-fold and was not proliferated by androgen stimulation, but was inhibited by the concentration of 0.1 nmol/L androgen. A mouse tumor model was made, and extensive tumor necrosis and hemorrhage occurred after one week of testosterone use. Zhong’s in vitro culture of a highly malignant prostate cancer cell line was inhibited by androgens to produce the androgen-suppressed prostate cancer cell line ARCaP, and demonstrated that androgen-dependent cancer cells could be transformed into androgen-non-dependent cancer cells under androgen-deficient conditions, and finally be inhibited by androgens again. Androgen non-dependent cancer cells may be associated with stimulation of the androgen receptor (AR) by certain cytokines. In 1999, researchers reported that intramuscular estrogen injection reduced the chance of combined deep vein thrombosis and myocardial infarction (Prostate 1999 ), and 900 cases were followed up for 2 years without the occurrence of vascular embolism. The efficacy was similar to that of bilateral orchiectomy, LHRH-A, and CAB, with no difference in overall mortality. Prostate cancer is also treated with Zoledronic acid, which can inhibit osteoclast activity and reduce bone resorption; it can also inhibit tumor VEGF and PDGF, which may slow down the growth of cancer tumors. COX-II inhibitors: Celecoxib (Celebrex) has been FDA has been approved for the treatment of prostate cancer. fap (familial adenomatous polyposis) 200-400mg Bid po, can make cell apoptosis by inhibiting PGE2, inhibiting Akt , Bcl-2. The growth of prostate cancer cells transplanted subcutaneously in nude mice after treatment was significantly slower than that of the control group. Rapamycin is an immunosuppressant that inhibits the rejection of renal transplantation. It inhibits the PTEN-P13K-Akt-mTOR pathway, whose target protein is mTOR, and has an inhibitory effect on solid tumors. In Pienta, a 3-week treatment with Etopside resulted in a 69% decrease in PSA and a rapid decrease in T, LH, and FSH, with some patients surviving up to 23 months with a 70% decrease in PSA. Dexamethasone may be associated with blocking IL-6, using doses of 1.5-2.25 mg/d. In 2003 Kyprianou treated prostate cancer with doxazosin. The mechanism may induce apoptosis in prostate cancer cells through the Quinazoline pathway. varambelly (Nature 2002) found that EZH2 in prostate cancer tissues was closely associated with metastasis, with an 80% inhibition of cancer cell growth within 24-120h after transfer of EZH2 SiRNA.