SKIN+CANCER-EMMA

delicious tag=emmaskincancer 1. sun--> damage DNA 2. pigment
 * Ultraviolet light can damage all layers of your skin: the epidermis, dermis and subcutaneous tissue (fat). To protect itself from damage, your skin increases the production of melanocytes, which produce the dark brown pigment, melanin. The extra melanin makes your skin look darker or suntanned.**

Two Genes: Their research indicates that early life sun exposure, from birth to 20 years old, may specifically increase the risk of melanomas with BRAF gene mutations. A different mutation, on the NRAS gene, was found in patients who had sun exposure later in life (between ages 50 to 60 years old). The results indicate that different subtypes of melanoma are associated with different risk factors Skin Cancer Presentation:
 * Mutations can be acquired in two ways: either when DNA is damaged by such toxins as radiation, chemicals or viruses, or when mistakes are made before cell division.**

The researchers found that the code letters in the B-RAF gene were shuffled in 70 percent of melanoma cases, making it the most frequently messed up gene in melanoma. Most of the //BRAF// mutations involve a change in a single letter of DNA, which prevents the gene from switching on and off normally. Malignant melanoma accounts for only about ten percent of skin cancers, but almost all of the deaths.

inherited: A. There are some rare, inherited skin diseases that make people highly sensitive to sunlight and much more likely to get any type of skin cancer. People inherit their normal skin type and skin cancer is more common in paler, freckly skin. In addition, there is good evidence that, if you have a close relative (brother, sister parent or child) with skin cancer, you have about twice the normal risk of getting that type of skin cancer.** SLIDE 3

Current News: "Once the skin is exposed to UVB it leads to mutations in the p53 gene, and it becomes nonfunctional, and then you see induction of skin cancer" explained study lead author Mohammad Athar, a professor of dermatology at the University of Alabama, Birmingham. "But this compound we used interacts with the p53 mutant genes and converts them back into functional genes," he said. "And that led to less incidence of skin cancer tumors, fewer numbers of tumors, and slower tumor growth in the UVB-exposed mice populations we tested."

sources: http://www.cbsnews.com/stories/2002/06/10/health/main511698.shtml http://www.genomenewsnetwork.org/articles/06_02/cgp_skin.shtml http://www.aicr.org.uk/skincancerfaqs.stm?source=Adwords http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/dermatology/nonmelanoma/nonmelanoma.htm