Researchers have finally solved the mystery of how melanoma forms. Specific biochemical process that can render normal and healthy skin cells into cancerous melanoma cells has been pinpointed. This new found research will play an instrumental role in ascertaining melanoma vulnerability in patients and pave the path to future therapies. According to statistics more than 70 thousand cases of melanoma are registered each year in the United States alone but thanks to the researchers at Oregon State University and their work published in PLoS Genetics supported by national institutes of health the figure can be cut down significantly in the future.
"We believe this is a breakthrough in understanding exactly what leads to cancer formation in melanoma," said Arup Indra, an associate professor in the OSU College of Pharmacy. "We've found that some of the mechanisms which ordinarily prevent cancer are being switched around and actually help promote it. In melanoma, the immune system is getting thrown into reverse," he said. "Immune cells that previously were attracted to help deal with a problem are instead repulsed." He further added.
A protein called retinoid-X-receptor, or RXR is the key to this entire process. The adequate amount of RXR ensures and aids proper operation of the immune response in the skin. The primary protectors of the skin are called melanocytes which are responsible for the production of protective pigments or melanin when the skin is exposed to ultraviolet radiation of sunlight. The process is called suntan in layman’s term. But even with this intricate protection system in place the melanocytes and keratinocytes are prone to genetic damage. In some instances the damage can be repaired and in other cases the immune response kicks in. With adequate levels of RXR in the melanocytes, the immune response will obliterate the defective skin cells before they exhibit symptoms of malignancy.
But with RXR levels depleting in melanocytes this protective process fizzles out. The chemical agents that regulate and keep mutated cells under control are suppressed paving way for cancer. Mutated melanocytes begin to multiply whilst other skin cells die leaving more room for mutated melanocytes to thrive. This results in melanoma taking root which has the tendency to spread throughout the body from the skin.
"When there isn't enough RXR, the melanocytes that exist to help shield against cancer ultimately become part of the problem," Indra said. "It's routine to have genetic damage from sunlight, because normally those cells can be repaired or killed if necessary. It's the breakdown of these control processes that result in cancer, and that happens when RXR levels get too low." "It's quite possible that a new and effective therapy can now be developed, based on increasing levels of RXR," Indra said.
A protein called retinoid-X-receptor, or RXR is the key to this entire process. The adequate amount of RXR ensures and aids proper operation of the immune response in the skin. The primary protectors of the skin are called melanocytes which are responsible for the production of protective pigments or melanin when the skin is exposed to ultraviolet radiation of sunlight. The process is called suntan in layman’s term. But even with this intricate protection system in place the melanocytes and keratinocytes are prone to genetic damage. In some instances the damage can be repaired and in other cases the immune response kicks in. With adequate levels of RXR in the melanocytes, the immune response will obliterate the defective skin cells before they exhibit symptoms of malignancy.
But with RXR levels depleting in melanocytes this protective process fizzles out. The chemical agents that regulate and keep mutated cells under control are suppressed paving way for cancer. Mutated melanocytes begin to multiply whilst other skin cells die leaving more room for mutated melanocytes to thrive. This results in melanoma taking root which has the tendency to spread throughout the body from the skin.
"When there isn't enough RXR, the melanocytes that exist to help shield against cancer ultimately become part of the problem," Indra said. "It's routine to have genetic damage from sunlight, because normally those cells can be repaired or killed if necessary. It's the breakdown of these control processes that result in cancer, and that happens when RXR levels get too low." "It's quite possible that a new and effective therapy can now be developed, based on increasing levels of RXR," Indra said.