PSA (prostate-specific antigen) is a single-chain polypeptide containing 237 amino acids and belongs to a family of serine proteases with tissue-specific chymotrypsin-like effects that break down the major colloidal proteins in semen and have a diluting effect on semen. Initially secreted into the prostatic ducts is an inactive zymogen (proPSA), which cleaves off seven amino acids at the amino terminus to form an active prostate-specific antigen. Most of the prostate-specific antigen that enters the blood circulation rapidly binds to protein hydrolase inhibitors, mainly alpha-1 anti-chymotrypsin (ACT) and alpha-2 macroglobulin binding (MG), while some is also inactivated by protein hydrolases and exists in the free state. PSA is tissue specific and is only present in the cytoplasm of human prostate alveoli and ductal epithelial cells and is not expressed in other cells. However, it is not tumor specific. PSA is elevated in most clinically significant prostate cancers and is its most important early detection indicator. Although PSA is the most commonly used means of detecting prostate cancer, benign prostatic hyperplasia and prostatitis can also present with positive PSA results, and one way to address this issue is to test for free prostate-specific antigen. Studies have shown that in patients with prostate cancer, the vast majority of PSA is in the bound state and their free PSA/total PSA ratio is lower than that of normal individuals or patients with BPH. Therefore, in men with abnormally elevated total PSA, testing for free PSA and calculating the free PSA to total PSA ratio can improve the specificity of screening and diagnosis of prostate cancer. The normal value of serum prostate-specific antigen (PSA) is usually <4ng/mL, and when prostate cancer occurs PSA >10ng/mL, it is significant for the diagnosis of early asymptomatic prostate cancer. Normally, PSA is a serine protease produced by prostate epithelial cells that secrete a glycoprotein directly into the prostatic ductal system. There is a blood-epithelial barrier around the normal prostatic duct system that prevents PSA produced by the prostatic epithelium from entering the bloodstream directly, thus maintaining a low concentration of PSA in the blood. It is generally accepted that a serum PSA of less than 4.0 ng/ml is normal, and a PSA of more than 10 ng/ml increases the risk of developing precancerous cancer. The higher the malignancy of the cancer, the greater the damage to the normal prostate tissue and the higher the PSA in the serum. The gold standard for a tumor-free state after radical surgery for prostate cancer is a zero PSA. Since almost all PSA in the serum is produced by prostate epithelial cells, radical prostate cancer surgery removes all prostate tissue, and if the tumor is eradicated, the serum PSA will drop to zero within 1 month. The half-life of PSA in the serum of patients with prostate cancer after surgery is 33 hours. According to this calculation, if PSA is 20ng/ml in 1 patient before surgery, PSA should not be detected in 12 days after surgery; if it is 10ng/ml before surgery, it will take 10 days; if it is 4ng/ml before surgery, it will take 8 days. Elevated serum PSA in non-malignant lesions of the prostate: inflammation of the prostate, prostatic hyperplasia, acute urinary retention, and prostate massage can increase PSA, but when the causative factors are eliminated, it can normalize in about a month. Serum PSA can be increased 1-fold after rectal examination, 4-fold after cystoscopy, and 53-57-fold after prostate puncture biopsy or transurethral electrodesection of the prostate. The PSA can also be increased by ejaculation in the normal state. Therefore, PSA testing should not be performed until one week after the anal examination and at least 6 weeks after prostate biopsy and puncture. The elevated PSA caused by cancer is persistent and continues to rise as the tumor progresses. How to distinguish between benign and malignant PSA elevation: 1. Application of free state PSA (fPSA): PSA levels in prostate hyperplasia and prostate cancer overlap in a larger portion at 4 to 10 ng/ml, and it is difficult to distinguish between prostate hyperplasia and prostate cancer based on PSA levels in this so-called gray area. PSA can exist in serum in both free and bound forms, and free PSA is the The free PSA is the part of PSA that is not bound in the plasma and is denoted as fPSA; total serum PSA is denoted as tPSA. fPSA concentrations are lower in patients with cancer than in patients with benign hyperplasia. It is this difference that is applied clinically to screen out early prostate cancer from patients with benign prostatic hyperplasia. The application of the fPSA/tPSA ratio to assist in the identification of prostate cancer from BPH is currently gaining widespread use. The reference value is 0.16, i.e., a ratio <0.16 is associated with a high likelihood of prostate cancer. a low percentage of fPSA suggests a higher likelihood of prostate cancer. 2. PSA rate: From the present study, people with age increase PSA less than 0.75 ng/ml per year, generally do not suffer from prostate cancer. If it is greater than 0.75 ng/ml, the risk of prostate cancer increases. It has been studied that in patients with prostate cancer whose preoperative PSA increases at a rate greater than 2 ng/ml within 1 year, and in patients whose PSA doubling time ≤ 3 months after prostate cancer resection or radiation therapy suggests recurrence, is associated with an increased risk of death. A recent study concluded that a PSA rate threshold of 0.75 ng/ml?yr is indeed too high for men under 60 years of age and will result in a significant number of missed prostate cancers. men with PSA rates above 0.5 ng/ml.yr are at higher risk of prostate cancer and should be followed closely.