Oncoproteins: GAPs in understanding Ras

Article Abstract:

The identification of oncogenes, or cancer-causing genes, in some viruses led quickly to the observation that oncogenes are closely related to certain normal genes in healthy cells. These normal proto-oncogenes seem to be involved in the regulation of cell replication. Although it is presumed that the transformation of a normal cell to a tumor cell can result from the corruption of the normal function of a proto-oncogene, there is little real knowledge about the mechanisms by which these genes operate. However, in the August 23, 1990 issue of Nature, two groups of researchers reveal new insights into the function of c-ras, an important proto-oncogene. The c-ras gene is of special interest since it seems to be highly conserved through evolution, and an analogous gene has been found in every species yet studied. Ras, the protein product of this gene, slowly hydrolyzes GTP, an intracellular messenger molecule. However, the function of Ras seems to be closely related to the function of another protein called GAP, for GTPase-activating protein. In one of the Nature articles, investigators showed that the transformation of fibroblasts by c-ras could be inhibited by GAP. That is, the change of test cells to a cancerous appearance, induced by the transfection of the cells with c-ras, could be inhibited by transfection with the gene for GAP. This result suggests that GAP may help regulate the function of Ras. This view is strengthened by the finding that transformation by v-ras, or the cancer causing viral analogue of c-ras, is not inhibited by GAP. The other group reporting in Nature showed how T-cell activation, which involves the replication of T-cells after stimulation with specific antigen, results in increased activity of the Ras protein. Perhaps ironically, the most interesting aspect of the story may come from researchers in another field. The newly identified gene for neurofibromatosis bears some similarity to GAP, and may turn out to be a tumor inhibitor, similar to that found to be defective in retinoblastoma. The neurofibromatosis gene is even more similar to IRA-1, another gene found in creatures ranging from yeasts to humans, and similar in function to GAP. Some researchers suspect that IRA-1 and GAP may be members an important family of molecules which play a critical role in the proper regulation of cell replication. (Consumer Summary produced by Reliance Medical Information, Inc.)

Ras genes, Oncogenic viruses, editorial

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Negative regulation of human c-fos expression by the retinoblastoma gene product

Article Abstract:

In recent years, research has identified numerous proto-oncogenes, normal genes which control cell reproduction which may, under pathological conditions, active the unregulated cell replication resulting in cancer. The gene which is affected in the inherited cancer retinoblastoma has been found to have the opposite function; it is a tumor repressor gene. Retinoblastoma is thought to result when a mutation obliterates the normal function of RB-1, or the retinoblastoma gene. However, it is not clear what function the Rb protein, the product of the RB-1 gene, might have in the regulation of cell reproduction. Since RB-1 is involved in human osteosarcoma (a bone cancer), and v-fos, a cancer virus gene, can cause osteosarcomas in mice, the normal cellular proto-oncogene called c-fos might be a target for repression by Rb. Using techniques of molecular biology, researchers have confirmed that this is what occurs. The human c-fos gene was cloned into bacteria. Pieces of DNA from these bacteria, called plasmids, can be used to transfect mouse cells. The growth of the mouse cells then indicates whether the c-fos gene is active or repressed. It was found that the transfection of human RB-1 DNA into the mouse cells repressed the expression of c-fos. The study has not yet determined whether the Rb product is a true negative regulator of the c-fos gene, or whether it simply interferes with the action of some positive regulator acting in the test system. However, the results do demonstrate one specific function of the Rb product, and provide a method for the investigation of the inhibitors of cancer genes. (Consumer Summary produced by Reliance Medical Information, Inc.)

Suppression, Genetic, Suppressor mutation (Molecular genetics), Carcinogenesis, Retinoblastoma

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Specific protection against breast cancers by cyclin D1 ablation

Article Abstract:

Research is presented concerning the resistance of mice bred to be cyclin D1 deficient to breast cancer which has been induced by ras and neu oncogenes. The full sensitivity of the mice to other oncogenic pathways is discussed.

Prevention, Physiological aspects, Breast cancer, Cells (Biology), Cells

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