By: Beth Walsh for Fibroids1
Scientists and researchers looking for new, better ways to fight breast cancer are examining every angle. Identifying genes involved in the creation and growth of cancer cells offers them new targets for drug therapy.
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For more information about cutting-edge cancer research, take a look at the following Web sites:
National Cancer Institute www.cancer.gov
American Association for Cancer Research www.aacr.org
Cancer Research and Prevention Foundation www.preventcancer.org
National Foundation for Cancer Research www.nfcr.org
American Cancer Society www.cancer.org |
A new breast cancer susceptibility gene, the “Rap80” gene, is required for the normal DNA-repair function of the well-known breast cancer gene BRCA1. Because mutations in the BRCA1 protein fail to bind to the Rap80 protein, BRCA1 can’t identify DNA damage sites in the genome. When BRCA1 fails to fix DNA damage, cancer-causing mutations add up and lead to the development of breast and ovarian malignancies. A related genetic mutation, BRCA2, also increases the risk of both breast and ovarian cancer, but to a lesser extent. Researchers will now study families with a history of breast cancer but no evidence of BRCA1 and BRCA2 mutations to see if they have any gene sequence changes in Rap80.
Another newly-discovered breast cancer gene, “IKBKE,” has been found in up to 40 percent of all breast cancers. The IKBKE gene makes a protein called IKK, which is part of the kinases family of proteins. In some breast cancers, the IKBKE gene mutates and in turn increases IKK production – which can spur cancer growth. Scientists are seeking a method to target this protein product, which may translate to an effective path for fighting breast cancer. IKBKE differs from other breast cancer genes in that it is not inherited; scientists don’t yet know how or why the IKBKE gene mutates in some breast cancers and not others. Researchers also hope to find similar genes that play a role in other cancers.
A team of researchers at the National Cancer Institute, which is part of the National Institutes of Health, has uncovered a set of genes that are turned on, or expressed, at high levels only in the blood vessels that feed tumors in mice and humans. These genes, and the proteins they encode, are important new targets for novel drugs that could selectively cut off a tumor’s blood supply. The key is that they would do so without affecting the blood vessels of healthy tissue, thus overcoming one of the major concerns of current anticancer therapies targeted at blood vessel growth.
Blood vessel growth is a normal process, essential for organ growth and repair. But this process becomes unbalanced in most forms of cancer, and normal blood vessel growth is redirected toward supplying nutrients and oxygen to diseased tissue. Out-of-control growth also increases the chance that tumor cells will escape and travel to other sites in the body (metastasize).
Researchers found that CD276, a gene that encodes a protein located on the cell surface, is over-expressed in tumor-associated blood vessels from colon, lung, breast, esophageal and bladder cancers. The gene also is often over-expressed in tumor cells themselves. The right development could kill two birds with one stone: the tumor and the blood vessel that feeds it.
