Suppression of tumorigenicity of human prostate carcinoma cells by replacing a mutated RB gene

Article Abstract:

The retinoblastoma gene (RB) codes for a protein found in normal cells and most cells grown in controlled conditions in the laboratory. Tumor cells known as retinoblastoma cells have mutations at the RB site, and when the protein manufactured by the RB gene (the RB protein) is replaced in these cells, they lose their power to induce tumors in susceptible mouse strains. The RB gene is therefore called a tumor suppressor gene. Mutations in it are found in several types of human cancer, including breast carcinoma and small-cell carcinoma of the lung. Its role in the most common cancer in men, prostatic carcinoma, has yet to be determined. The RB gene was investigated in three prostatic cancer cell lines. One of these lines contained abnormal mRNA, part of the material necessary for making the RB gene, and when RB expression was made normal in these cells by gene transfer, the transformed cells were apparently incapable of causing tumors when implanted into mice. It is suggested that inactivation of the RB gene in cells may be a way to suppress the ability of such cells to induce tumor formation (their tumorigenicity). The mechanism of action of tumor suppression by this gene may have wide applicability. (Consumer Summary produced by Reliance Medical Information, Inc.)

Prostate cancer, Growth, Tumors

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Genetic mechanisms of tumor suppression by the human p53 gene

Article Abstract:

Tumor-suppressor genes inhibit the development of cancer. If they do not function, cancer develops. The p53 gene, which encodes a large (53-kilodalton) cellular protein, is often found to be mutated in human tumor cells, suggesting that the gene is involved in cancer development. Cells obtained from a human osteosarcoma (bone cancer) that do not normally express p53 were given the p53 gene by attaching the gene to a virus. Various forms of p53 genes were then identified that were either normal or mutated. The normal p53 gene prevented the cells from becoming cancerous. The mutated p53 gene allowed the cells to grow faster than the cells that were cancerous that did not contain the p53 gene at all. Genes have two alleles, or forms, one on each chromosome. Single copies of the normal p53 gene were enough to suppress the cancerous state in human osteosarcoma cells. This indicates that the mutation is recessive, that both alleles must be mutated for p53 to be involved in cancer development. Other experiments have shown that p53 can suppress cancerous activity in many types of tumor cells. This is similar to another tumor suppressor gene, RB, found in retinoblastomas (tumor of the retina). (Consumer Summary produced by Reliance Medical Information, Inc.)

Suppression, Genetic, Suppressor mutation (Molecular genetics), Tumor suppressor genes

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Location of BCRA 1 in human breast and ovarian cancer cells

Article Abstract:

Two independent research teams found BRCA 1 gene product in the nuclei of human cells, including ovarian and breast cancer cells. In one study, the immunogen used was the BRCA1 carboxyl-terminal peptide (CQELDTYLIPQIPHSHY). The results of the two studies are compared.

Breast cancer, Ovarian cancer, Immunospecificity

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