Prostate cancer

Introduction: Prostate cancer is one of the leading causes of cancer death in men and women in Europe and America. The incidence rate increases with age. Half of the prostates over the age of 80 have cancer lesions, but the actual clinical incidence is far below this number. There are obvious regional and ethnic differences in prostate cancer incidence. According to statistics, the Chinese are the lowest, the Europeans are the highest, and Africa is the highest. In Israel, countries such as China and Japan are low-risk areas for prostate cancer, but there is no choice of males over 50 years old. The number of lesions of the prostate cancer is similar to that of Europe and the United States. Therefore, some people think that the growth of oriental cancer is slower than that of Westerners. There are fewer cases. In addition, prostate cancer is also related to the environment. Etiology: (1) The cause of the disease has not been fully ascertained, and may be related to race, genetics, sex hormones, food, and the environment. According to research from countries such as Northern Europe, Sweden, and Finland, a large extent (40%) is due to genetic variation, and recent molecular biology studies have revealed multiple chromosomal aberrations. The complex and interdependent relationship between these factors and environmental carcinogens (60%) is not well understood. (B) the pathogenesis of cancer is now known to be a few important steps in the mechanism of prostate cancer. About 9% of prostate cancers and 45% of prostate cancers under 55 years of age are due to a hereditary oncogene. It is extremely useful to understand that these genes are undoubtedly understood for the cancer-causing principle of prostate cancer. Recently, Ohio reported that they found that the allelic imbalance in the 23.2 segment of the long arm of chromosome 16 may be a tumor suppressor gene for familial hereditary prostate cancer (Paris et al., 2000). Another idea is that the intensity of the androgen receptor response to androgen in the epithelial cells is inversely proportional to the length of the CAG microsatellite in the 5promotor promoter region of the receptor gene, and the shorter the length, the response of the cells to androgens The stronger, the faster the cells grow. The length of CAG was shorter in blacks and whites with cancer than in the control group. Clearly, the length of the androgen receptor CAG microrepetition region is potentially related to the development of prostate cancer. DNA methylation changes in the early stages of solid tumor growth, and prostate cancer is no exception. High methylation of DNA can lead to the inactivation of many tumor suppressor genes. For example, the hypermethylation of the short arm of chromosome 17 is inactivated, and tumor suppressor genes in this region may lead to prostate cancer. Prostate cancer growth depends on the balance between cell proliferation and mortality. Normal prostate epithelial hyperplasia and mortality are low and balanced, with no net growth, but when epithelial cells are converted to high grade prostate In high grade prostatic intraepithelial neoplasia (HGPIN), cell proliferation has exceeded cell death. In the early stage of prostate cancer, cell proliferation is due to inhibition of apoptosis (not due to increased cell division, further leading to gene dissimilation). Increased risk. Increased expression of cdc37 gene in precancerous lesions and cancer cells may be an important step in the initiation of canceration. It has been speculated that the androgen receptor gene is catabolized to allow the androgen receptor to respond to its growth factors, such as insulin-like growth factor I or keratinocyte growth factor. These growth factors are activated by the binding of the growth factor to the androgen receptor after the cancer cells are not sensitive to androgen, resulting in cancer growth. Androgen promotes prostate cancer growth through an androgen receptor-mediated mechanism that enhances the activity of endogenous genetically altered carcinogens, such as estrogen metabolites, estrogen-induced oxides, oxides produced by prostate cancer, and Fat and other substances. In addition, methylation of the androgen receptor is associated with prostate cancer that is not sensitive to hormone therapy in the advanced stage. The interaction of growth factors with the epidermal matrix is also associated with the development of prostate cancer. Transfoming growth factor-beta, epidermal growth factor, platelet derived growth factor, and neuroendocrine peptides have been shown to be involved in proliferation, differentiation, and invasion of the prostate epithelium. These growth factors produced by the epithelium interact with the tissue matrix to cause stromal cells to produce growth factors, which in turn act on epithelial cells. For example, it has been shown that bone cells secrete growth factors that stimulate prostate epithelial growth, while prostate epithelium is also produced. A growth factor that stimulates bone formation. These explain why prostate cancer can be selectively transferred to the bone. Symptoms: Clinical manifestations in the early stages of prostate cancer, due to tumor limitations, most prostate cancer patients have no obvious symptoms, often found by chance during physical examination, can also be found in surgical specimens of benign prostatic hyperplasia. As the tumor continues to develop, prostate cancer will have a variety of different symptoms, mainly in three aspects: 1. Obstructive symptoms can have dysuria, urinary retention, pain, hematuria or urinary incontinence. 2. Local invasive symptoms The bladder rectal space is often the first to be involved. This gap includes the prostate, seminal vesicle, vas deferens, and the lower end of the ureter. Organs such as tumor invasion and compression of the vas deferens can cause low back pain and side testicular pain. Some patients Also complained that the ejaculation pain. 3. Other metastatic symptoms Prostate cancer is prone to bone metastasis. It can be disease-free at the beginning, and there are also cases of prostate cancer caused by nerve compression or pathological fracture caused by bone metastasis. 98% of prostate cancer is adenocarcinoma, and about 2% is squamous cell carcinoma. 75% originated in the peripheral zone, 20% originated in the transition zone, and 5% originated in the central zone. The staging of prostate cancer is as follows: T1: T1a is clinically negative, TUR specimen cancer accounts for less than 5% of total volume; T1b is clinically negative, TUR specimen cancer accounts for more than 5% of total volume; T1c is clinically negative, PSA>4μg/L, and biopsy confirms cancer. T2: T2a is limited to 2 leaves; T2b is limited to 2 leaves. T3: T3a breaks through the capsule; T3b invades the seminal vesicle. T4: Violation of surrounding tissues. N: N0 lymph nodes without metastasis; N1 basin lymph node metastasis; N2 distant lymph node metastasis. M: M0 has no metastasis in the distance; M1 distant organ metastasis. Prostate cancer is classified according to gland differentiation, polymorphism, and nuclear abnormality. Gleason classification is used to divide cancer cell differentiation into two major and minor grades, each of which is 1 to 5 points. The scores of the two grades are added together, and the total score is 2 to 4 points, which is a well-differentiated cancer, 5 to 7 points are moderately differentiated cancer, and 8 to 10 are moderately differentiated cancers. Prostate cancer is mostly androgen-dependent, its occurrence and development are closely related to androgen, and non-hormone-dependent type is only a minority. Prostate cancer can be spread through local, lymphatic and blood lines, and blood is transferred to the spine and pelvis. Diagnosis 1. Asymptomatic early, the prostate can be found in the physical examination, hard as a stone, the surface is not flat. 2. Late symptoms of prostatic hypertrophy, such as frequent urination, dysuria, fine urine flow, difficulty urinating, etc., may be associated with prostatic hypertrophy. However, at this time, rectal examination can be found that the gland is hard and fixed to the surrounding tissue, and the activity is poor, which is very important for clinical diagnosis. Metastatic symptoms such as low back pain, hematuria, weight loss, fatigue, loss of appetite, etc. may also occur. 3. Prostate specific antigen (PSA) serum determination of patients with serum PSA levels can be increased, the ratio of free PSA to total PSA decreased; serum acid phosphatase may increase when there is metastasis. The combined inspection and diagnosis rate of the two is higher. 4. B-ultrasound examination of hypoechoic nodules in the prostate, but must be differentiated from inflammation or stones. 5. Radionuclide bone scans often show metastatic lesions earlier than X-ray films. 6. CT or MRI examination can show prostate morphology changes, tumors and metastasis. 7. Prostate biopsy can be used as a method to diagnose prostate cancer. Failure to puncture and remove the tumor tissue cannot be denied. Read more...