Allele losses and onco-suppressor genes

Article Abstract:

The loss of function of genes known as tumor suppressor or onco-suppressor genes, can result in the development of cancer. Studies have shown that tumor suppressor genes exist on various chromosomes in humans. Each gene is present in two copies, one on each of the two parts of a chromosome. The development of cancer is a multi-step process. In certain cancers, one of the steps is thought to be the inactivation of both copies of a tumor suppressor gene, whose function it is to regulate cell growth and replication. Diseases such as retinoblastoma (a cancer of the retina of the eye) and Wilms' tumor (a cancer of the kidney) are inheritable childhood cancers involving the loss of tumor suppressor gene activity. In adults, inheritable cancers thought to be the result of the loss of suppressor gene function include a form of colorectal cancer, adenomatous polyposis, and inherited breast cancer. The inactivation of the tumor suppressor genes can result from the loss of large pieces of chromosomes. These losses can be analyzed and the chromosomal regions involved in the cancer can be identified. This genetic information can then be used as a screen to detect others who may develop the cancer or to determine whether the cancer will occur in a developing embryo. (Consumer Summary produced by Reliance Medical Information, Inc.)

Tumor suppressor genes

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The Li-Fraumeni cancer family syndrome

Article Abstract:

Recently, extensive research has focused on genetic susceptibility to cancer. Certain specifically defined conditions have been identified as predisposing individuals to cancer. These include childhood onset of polyposis coli, numerous intestinal mucosal polyps which increase with age and usually lead to colon carcinoma; and neurofibromatosis, various sized tumors on the peripheral nerves. Additionally, family clustering of cancers has also been demonstrated, and suggests a possible genetic origin. In 1969, Li and Fraumeni described a cancer family syndrome (LFCFS), defined as the occurrence of soft-tissue sarcomas in children and young adults, along with early onset of breast cancer in the mothers and young female family members of these individuals. Many of these diseases develop before the age of 45 years, and other tumors occur in excess in these families. Risks increase for family members if a close relative is diagnosed at an early age with soft-tissue sarcoma. Other researchers have suggested that the retinoblastoma susceptibility gene, located at chromosome 13q14, and chromosomes 11p and 17p may be related to LFCFS because these sites have been associated with sarcomas and breast cancer. (Consumer Summary produced by Reliance Medical Information, Inc.)

Sarcoma, editorial

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Chromosome rearrangement, oncogene activation, and other clonal events in cancer: their use in molecular diagnostics

Article Abstract:

Abnormalities in chromosomes (cellular structures on which genes are located) have been found in the majority of tumors of the blood cells, such as leukemias and lymphomas, and in specific types of solid tumors, such as sarcomas and neural tumors. These abnormalities can include the rearrangement of portions of chromosomes and other mutations causing the activation of cancer-causing genes, known as oncogenes. The rearrangement of the chromosomes can cause a portion of one gene to be placed next to portion of another gene, causing an abnormal gene or abnormal activation of the gene. The genetic analysis of these chromosomal abnormalities can lead to the understanding of the structural defect, which can hopefully be used to develop methods for treating the cancers. The genetic abnormalities can also be used to monitor the spread of disease in an individual and to screen for genetic defects in others. (Consumer Summary produced by Reliance Medical Information, Inc.)

Abnormalities, Cloning, Cell interaction, Cell interactions, Oncogenes

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