Researchers are one step closer to understanding the growth process of melanoma skin cancer. This also brings them closer to solving a complex problem commonly associated with treating the deadliest form of skin cancer: drug resistance.
Melanoma is an aggressive form of skin cancer that starts in melanocytes which are skin cells that make the pigment melanin. They are the cells responsible for a person’s skin color, their ability to tan or freckle, and the color of their hair and eyes.
Research shows that about 40 percent of advanced melanoma tumor growth is fueled by BRAF gene mutations. The BRAF gene belongs to a class of genes known as oncogenes. When mutated — prolonged UV sun exposure and tanning beds are primary triggers — oncogenes have the potential to cause normal cells to become cancerous.
Today, more people are diagnosed with this dangerous form of skin than ever before. From 1975 to 2010, new melanoma cancer cases have steadily climbed each year from 8 cases per 100,000 men and women per year, to nearly 21.1 cases per 100,000. In 2013, an estimated 76,690 new melanomas cases were diagnosed, some in people as early as their 20s.
The 5-year survival rate for melanoma is improving, even as the number of new cases increase. This higher survival rate is largely due to new drugs called BRAF inhibitors. These treatments have shown unprecedented responses in rapidly shrinking melanoma tumors.
However, these BRAF-mutated tumors frequently show early resistance to treatment and respond only partially to BRAF inhibitors, leaving behind cancer cells that eventually lead to tumor regrowth.
Dr. Roger Lo, an associate professor and director of the melanoma clinic in dermatology at UCLA’s Jonsson Comprehensive Cancer Center (JCCC) led an international collaboration of translational research-physicians in two back-to-back studies that provide critical insights into key areas of how tumors resist BRAF inhibitor drugs.