Melanoma is a skin cancer that develops in melanocytes, the cells that produce skin pigment. While less common than other skin cancers, melanoma is more dangerous due to its higher likelihood of spreading if not detected and treated early. The development of this cancer is tied to specific genetic changes that can disrupt a cell’s normal life cycle, leading to uncontrolled growth.
The Role of Oncogenes in Cancer
Genes are segments of DNA that hold instructions for bodily functions. Some of these are proto-oncogenes, which are healthy genes that regulate processes like cell growth and division. A proto-oncogene can be compared to a car’s accelerator, ensuring the cell divides at a controlled rate.
A mutation can convert a proto-oncogene into an oncogene, a malfunctioning version of the gene. This is like the accelerator pedal getting stuck, causing the cell to receive constant signals to grow and divide. This uncontrolled proliferation of cells is a characteristic of cancer, as the abnormal cells accumulate and form tumors.
The BRAF Gene and Melanoma
The primary oncogene implicated in melanoma is BRAF. The BRAF gene holds the instructions for creating a protein that is part of a signaling route called the MAPK pathway. This pathway is a chain of proteins that relays signals from the cell surface to the nucleus, managing cell growth and survival.
In about half of all melanoma cases, a specific mutation occurs in the BRAF gene, most commonly a change known as V600E. This error results in a constantly active BRAF protein, which keeps the MAPK pathway permanently switched on. This signaling drives melanocytes to proliferate uncontrollably, leading to melanoma. While the BRAF V600E mutation is the most frequent driver, other oncogenes like NRAS and KIT can also be mutated, though less commonly.
Genetic Factors and Melanoma in Men
The BRAF oncogene is a factor in melanomas found in both men and women. However, statistics show that men have a higher incidence of melanoma and face a worse prognosis. This disparity is not fully understood but points to a complex interplay of biological and genetic differences.
One area of investigation involves different immune responses to cancer. Hormones may play a role, with some studies suggesting estrogen could enhance immune function, offering a protective effect for women. Genetic differences on the sex chromosomes are also considered. The X chromosome contains a large number of genes that regulate tumor suppression, whereas the Y chromosome is much smaller. These biological distinctions likely contribute to the observed differences in how melanoma affects men and women.
Testing and Targeted Therapies
When a patient is diagnosed with melanoma, a biopsy sample of the tumor is often tested to determine if it carries a BRAF mutation. This molecular testing is a standard part of clinical practice because the result directly influences treatment decisions, allowing for the use of “targeted therapy.”
Drugs have been developed to block the malfunctioning proteins created by these oncogenes. BRAF inhibitors, such as vemurafenib and dabrafenib, are designed to target and shut down the overactive BRAF protein. To improve effectiveness, these are often combined with MEK inhibitors, which block another protein in the same MAPK pathway. This dual-action approach can halt or significantly slow the growth of the cancer, demonstrating how understanding a specific oncogene leads to more precise treatments.