The majority of cancers in adults are attributable to a combination of lifestyle factors and environmental exposure. Lifestyle issues will be addressed at the primary level.
Cancer was the second-leading cause of death in the United States, accounting for nearly 25 percent of deaths in 1990. In the United States, there are 1.2 million new cancers and 500,000 deaths each year. In addition, 700,000 non-melanoma skin cancer and 100,000 local oncological carcinomas were diagnosed annually.
Although the cause of most cancers remains unclear, recent research has made significant progress in understanding the molecular basis of cell proliferation. Mutations in DNA sequences that result in the amplification or stimulation of "cancer genes" or loss of "tumor suppressor gene" or both are involved in abnormal and variable proliferation. malignant. Cancer genes are normal genes that encode for cell growth receptors, growth factors, or elements of the proliferative mechanism, cancer cells. The tumor suppressor gene codes for the regulation of the protein that normally inhibits the proliferation of cells. The consequences of this and other mutations may be due to environmental exposure, genetic susceptibility, Contraindications and other unknown causes are the development of cancer. Most tumors have one or more chromosomal abnormalities such as: loss of segment, inversion, segmentation, or segmentation. Although many of these abnormalities are non-specific, some of these lesions are closely related to specific malignancy. Identification of chromosomal abnormalities may help to diagnose as well as evaluate disease prognosis. For example, there is a specific lymphoblastic segmentation, Burkitt, in which the C - myc gene is activated. Because of the transition from chromosome 8 to chromosome 14. A large number of genetic changes (alleles loss) in colorectal cancer have poor prognosis. segment or segment. Although many of these abnormalities are non-specific, some of these lesions are closely related to specific malignancy. Identification of chromosomal abnormalities may help to diagnose as well as evaluate disease prognosis. For example, there is a specific lymphoblastic segmentation, Burkitt, in which the C - myc gene is activated. Because of the transition from chromosome 8 to chromosome 14. A large number of genetic changes (alleles loss) in colorectal cancer have poor prognosis. segment or segment. Although many of these abnormalities are non-specific, some of these lesions are closely related to specific malignancy. Identification of chromosomal abnormalities may help to diagnose as well as evaluate disease prognosis. For example, there is a specific lymphoblastic segmentation, Burkitt, in which the C - myc gene is activated. Because of the transition from chromosome 8 to chromosome 14. A large number of genetic changes (alleles loss) in colorectal cancer have poor prognosis.
The majority of cancers in adults are attributable to a combination of lifestyle factors and environmental exposure. Lifestyle issues will be addressed at the primary level. Exposure to carcinogens can cause a higher incidence of cancer. It is difficult to identify individual carcinogens because of the long latency and magnitude of the substance, the nature of the contact is unclear and has not been fully investigated. The general classification of carcinogens from the environment includes chemical elements such as benzene, asbestos, carcinogenic viruses such as human papillomavirus and Epstein-Barr virus, physical factors such as ion-exposure radiation and ultraviolet light. There is a genetic inheritance of the cancer that is associated with specific molecular changes in a gene (such as retinoblastoma and familial polyps). An abnormal gene (polyp adenoma, APC) that causes familial polyps along with the development of modern genetic analysis techniques will help the doctor diagnose accurately and give advice to patients and families. top them. Although familial polyps are a rare syndrome, mutations in the pathogenic gene can also be found in more than 60% of colon cancer patients as well as in some polyp patients. The pathogenesis of the APC gene associated with epidemiological studies may help identify environmental or lifestyle factors that increase the risk of cancer. Molecular epidemiological studies have been used to identify chemicals that may be causative agents of the Ras mutant gene associated with acute myelogenous leukemia. These studies will help determine the objective of preventive measures.
Other "carcinogenic genes" are currently being identified in families with multiple cancer. Mutations in the BRCA gene on chromosome 17 increase the risk of breast and ovarian cancer significantly. By using gene markers, it is now possible to identify people who carry the disease at home and have appropriate genetic testing as well as appropriate genetic counseling. HIV infection is associated with increased risk of cancer, particularly non-Hodgkin's lymphoma, Hodgkin's disease, Kaposi's sarcoma, cervical cancer and anal cancer. Papilovirus in humans is also associated with cervical cancer. Some types of this virus are associated with high or low risk.
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