Zeroing in on individual cancer risk

Article Abstract:

With recent advances in biomedical research, the risk of an individual for developing certain types of cancer may soon be evaluated. For example, with the identification of the gene responsible for Li-Fraumeni syndrome (a cancer in which multiple tumors develop), those who have the gene can be identified. The same is likely to be true for hereditary colon cancer. However, most cancers are not caused by inherited abnormalities in one gene, but by exposure to environmental carcinogens. Although there is no cure for cancer, there may be ways to prevent the development of cancer in persons who are at high risk, such as by minimizing exposure to the risk. In the future, there may be ways to prevent cancer with drugs or diet. Researchers are looking for genetic effects of cancer-causing agents by examining the genes of patients with cancer. One such carcinogen is aflatoxin, which is thought to be involved in liver cancer. Aflatoxin causes mutation (genetic change) in a tumor suppressor gene, which suppresses the development of tumors. However, the mutation is only present in cancerous cells and, thus, can not be used to predict the development of cancer. Scientists are looking for other indications that aflatoxin is causing cancer, such as the presence of adducts, or compounds that bind the carcinogen. This is being done with aflatoxin and other powerful carcinogens, such as polycyclic aromatic hydrocarbons (found in iron and coke) and 4-aminobiphenyl (found in cigarette smoke). Because these compounds only last a short while in the body, they have limited use. Therefore, researchers are also looking for genetic changes caused by these carcinogens in other genes besides those involved in cancer development as a way to predict the risk of cancer development. (Consumer Summary produced by Reliance Medical Information, Inc.)

Risk factors, Carcinogens

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Oncogenes evoke new cancer therapies

Article Abstract:

Cancer therapy that targets oncogenes (genes that cause cancer) is about to begin; it will be the outgrowth of years of research on these abnormal genes and the growth factors and other proteins whose manufacture they direct. A symposium at Cold Spring Harbor Laboratory concerning the origins of human cancer included presentations from laboratories planning clinical trials of experimental therapies. Growth factors (proteins made by the oncogenes), such as bombesin, are a good treatment target, since they are located in the cell membrane. In addition, many cancers produce high levels of growth factors, so control of these could reduce the spread of cancer. One oncogene is erbB2 (also called HER2 or neu), extra copies of which were identified in the breast cancer tumors of women who were found likely to relapse and die; erbB2 is also implicated in ovarian cancer. The growth of tumor cells in mice has been stopped when the receptor protein for the erbB2 product is blocked, and clinical studies of women with advanced breast cancer, using an antibody against that protein, may begin in 1991. While some growth factors made by oncogenes act on the cells that make them, others, such as fibroblast growth factors (FGFs) stimulate other cell types. Examples include the cells that build blood vessels, which proliferate to supply growing tumors with blood. Pentosan polysulfate, which binds to FGFs, appears able to block tumor growth in animals; it is already used in Europe as an anticoagulant (to prevent clotting) and will begin clinical trials soon. (Consumer Summary produced by Reliance Medical Information, Inc.)

Care and treatment, Research, Cancer treatment, Growth factors, Oncogenes

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Genetic defect identified in rare cancer syndrome

Article Abstract:

There are approximately 100 families in the world known to have Li-Fraumeni syndrome, a rare genetic disorder, in which individuals have a high risk of developing several types of malignant tumor, especially breast cancer, at an unusually early age and with a consequent high death rate. The Li-Fraumeni syndrome is evidence that cancer can be inherited. The genetic defect of Li-Fraumeni syndrome has been identified by Stephen Friend and colleagues at Massachusetts General Hospital Cancer Center in Boston. The defect is in a gene which encodes a protein known as p53. The gene is a tumor suppressor gene, in which a mutation, or genetic change, that inactivates the gene prevents production of the p53 protein, causing uncontrolled cell growth, or cancer. The understanding of the genetic defect will allow identification of members of families with Li-Fraumeni syndrome who carry the defect gene and are at high risk of developing cancer. These individuals can be monitored so that any cancer can be detected early, when it is most easily treated. It is hoped that the study of the p53 gene will allow understanding of genetic susceptibility to cancer in general. Mutations which cause inactivation of tumor suppressor genes have also been shown to cause two other types of hereditary cancer, retinoblastoma (an eye cancer) and Wilms tumor (a kidney cancer). (Consumer Summary produced by Reliance Medical Information, Inc.)

Breast cancer, Identification and classification, Tumors, Tumor suppressor genes, Li-Fraumeni syndrome

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