It has, been known that some of the features of cancer cells resemble features of cells exposed to hormones. For example, cells in tumors grow and multiply rapidly, crowding out normal cells and robbing the rest of the body of nutrients. Cells exposed to hormones also can grow rapidly, although they don’t have the wild, uncontrolled growth of tumors.
Also, some organs that are sensitive to steroid hormones, such as the breasts, the prostate gland, and the testes, tend to become cancerous more frequently and have tumors that may require steroid hormones to grow. We know that these shared properties of cancerous and hormone induced growth are not simply coincidences.
Research over the last ten years has identified genes in the DNA that appear to cause cells to become cancerous. These genes have been given abbreviated names by molecular biologists: scr, for example, is found in sarcoma type tumors, whereas other cancer causing genes like ras, raf, erb, myc, and jun were identified in other types of cancer. These genes apparently cause the production of proteins that regulate cell growth in a variety of ways. Some of these genes are also activated by hormones to increase cell growth.
Insulin and IGFs, for example, apparently cause certain muscle cells to grow by activating the myc gene. Other cancer causing genes apparently produce hormone receptor proteins that are permanently activated even if no hormone is present, leading to uncontrolled cell growth. Still other cancer producing genes, like erb, resemble steroid hormone receptors and bind DNA to cause uncontrolled cell growth.
While an understanding of these relationships between cancerous and hormone included changes in cell function is still in the early stages, there is much reason for optimism that the molecular mechanism underlying these changes will become known reasonably soon.
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