What causes prostate cancer

With the change of eating habits, the incidence rate is getting higher and higher. So we all need to know about the causes of prostate cancer. So what exactly causes prostate cancer? Let's learn about the causes of prostate cancer.

1. Causes of disease

The cause of the disease has not been fully identified, but it may be related to race, genetics, sex hormones, food, and environment. According to research, a large part (40%) is due to genetic gene mutations, and recent molecular biology research has also revealed a variety of chromosomal aberrations. The complex and interdependent relationship between these factors and environmental carcinogens (accounting for 60%) is not yet clear.

2. Pathogenesis

Several important steps in the carcinogenesis of prostate cancer are now known. About 9% of prostate cancers and 45% of prostate cancers under the age of 55 are due to a hereditary oncogene. Understanding these genes is undoubtedly extremely useful for understanding the carcinogenesis of prostate cancer. Recent reports have found that allele 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 assumption is that the intensity of the response of epithelial cell androgen receptor to androgen is inversely proportional to the length of the CAG microsatellite in the 5 promoter cocatalyst region of the receptor gene. The shorter the length, the stronger the cell's response to androgen and the faster the cell grows. The length of CAG is shorter in both blacks and whites with cancer than in the control group. Obviously, the length of the CAG microsatellite of the androgen receptor has a potential relationship with the development of prostate cancer.

There are changes in DNA methylation in the early stages of solid tumor growth, and prostate cancer is no exception. Hypermethylation of DNA can lead to the inactivation of many tumor suppressor genes. For example, hypermethylation of the short arm of chromosome 17 is inactivated, and tumor suppressor genes in this region may lead to the occurrence of prostate cancer. The growth of prostate cancer depends on the balance between the proliferation rate and mortality rate of cells. The proliferation rate and mortality rate of normal prostate epithelium are both very low and balanced, with no net growth. However, when epithelial cells are transformed into high-grade prostatic intraepithelial neoplasia (HGPIN), cell proliferation exceeds cell death. In the early stages of prostate cancer, cell proliferation is due to the inhibition of apoptosis rather than increased cell division, which further leads to an increased risk of genetic alienation. Increased expression of the cdc37 gene in prostate precancerous lesions and cancer cells may be an important step in the onset of carcinogenesis.

Some people speculate that the androgen receptor gene is mutated, which can make the androgen receptor respond to its growth factors, such as insulin-like growth factor I or keratinocyte growth factor. These growth factors bind to androgen receptors after cancer cells become insensitive to androgens and activate them, leading to cancer growth. Androgens promote the growth of prostate cancer through an androgen receptor-mediated mechanism that enhances the activity of endogenous gene mutation carcinogens, such as estrogen metabolites, estrogen-induced oxides, oxides produced by prostate cancer, and fats. In addition, methylation of androgen receptors is associated with advanced prostate cancer that is insensitive to hormone therapy.

The interaction between growth factors and epidermal matrix is ​​also related to the occurrence of prostate cancer. Transforming growth factor-beta, epidermal growth factor, platelet-derived growth factor, and neuroendocrine peptides have all been shown to be related to the proliferation, differentiation, and infiltration of prostate epithelium. These growth factors produced by the epithelium interact with the tissue matrix, causing the matrix cells to produce growth factors, which then act on the epithelial cells. For example, it has been shown that bone cells secrete growth factors that can stimulate the growth of prostate epithelium, and prostate epithelium also produces growth factors that can stimulate bone formation. These explain why prostate cancer can selectively metastasize to bones.

The above is an introduction to the causes of prostate cancer. I hope it helps. If you find any abnormal symptoms, please go to the hospital in time. If you still have questions, please consult our online doctor and we will give you a detailed answer. Feihua Health Network wishes you good health!

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