Suppression with a difference

Article Abstract:

As the list of known tumor suppressor genes continues to grow, researchers have recently identified another of these genes. As the name implies, tumor suppressor genes normally suppress the development of tumors, which may arise if such a gene is altered by a mutation. However, the newest gene on the list, adenomatous polyposis coli (APC), has some properties that make it unusual. Patients with familial adenomatous polyposis (FAP) develop hundreds of polyps in their colon at an early age, and eventually develop colon cancer. A search for the genetic basis for this familial cancer previously uncovered mutated in colorectal cancer (MCC). Further investigation revealed that this gene was only mutated in somatic cells. That is, the cancerous body cells contained mutations in MCC, but the MCC mutation in patients with FAP was not passed from generation to generation in the germ cells. Therefore, MCC cannot be the fundamental mutation responsible for FAP. Continued research has now uncovered APC, a gene that is passed between generations in families with FAP. Mutations in this gene can be found in the cancers of patients with sporadic colorectal cancer. Both APC and MCC are located very close to one another on the long arm of chromosome 5, at 5q21. Much is still unknown about APC and colorectal cancer. The prototypical tumor suppressor gene is the gene for the retinal cancer retinoblastoma. Since there are two copies of most genes, including retinoblastoma, the tumor results in a cell in which one gene is inherited with a mutation and the other gene develops a spontaneous mutation. If the cell has only the inherited mutation, the other normal gene is sufficient to prevent tumor growth. This does not seem to be the case for APC. In patients with the APC mutation, the other corresponding gene is normal, but the cancer develops anyway. This may be a result of another mutation occurring spontaneously in another gene that has not yet been identified. (Consumer Summary produced by Reliance Medical Information, Inc.)

Polyposis, Familial, Familial polyposis

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Consider the coiled cell...

Article Abstract:

A review is presented of the structure, behavior, and functional significance of the MCC (mutated in colorectal cancer) gene, whose normal function is to suppress tumor growth. Parts of the protein product of the MCC are similar to the m3 muscarinic acetylcholine receptor, a protein that interacts with a G protein (a group of proteins that is involved in cell division). It is possible that when MCC binds to G proteins and inhibits the intracellular signalling that is normally a function of G proteins, it leads to reduced cell division. In cases where MCC is inactivated, cell division would be enhanced. Such a case is familial adenomatous polyposis (FAP), a hereditary condition in which large numbers of polyps develop in the colon, many of which become malignant. Research has indicated that MCC is a coiled coil protein, a structure shared with other proteins such as keratins, vimentin, intermediate-filament proteins, and myosins. Its structure is explained and diagrammed. The functional significance of the coiled coil is that distances between protein binding sites act at ''spacers'' that can organize the cell cytoplasm to a considerable extent. Since cell division can be regulated by cell shape and certain physical effects of neighboring cells, it is plausible that genetic alteration of a coiled coil shape may inhibit cell division. The possible consequences of different kinds of MCC mutations are discussed. Tumor progression could be the result of a particular group of mutations that act together to cause abnormal cell proliferation. Research is ongoing to determine the true structure of MCC. (Consumer Summary produced by Reliance Medical Information, Inc.)

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Team blue sees red

Article Abstract:

Shc, an adaptor protein in the tyrosine kinase/Ras family, appears to be responsible for mediating relay messages from blue signalling proteins to green signalling proteins as revealed by the study of signal transduction, showing unexpected interaction between the two proteins. Protein tyrosine kinase PKY2 has also been discovered that activates Ras-mediated regulation by relaying messages. However, the tyrosine kinase that phosphorylates Shc is still unknown though it is unlikely to coexist or coactivate with PKY2 since the stimuli are antagonists.

Cellular signal transduction, Physiological regulation, Biological control systems, Protein kinases

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