What is the primary mechanism by which UVB rays contribute to melanoma?

UVB rays primarily contribute to melanoma through the formation of DNA pyrimidine dimers. When skin is exposed to UVB radiation, the energy from the rays can cause chemical changes to the DNA, particularly affecting the pyrimidine bases uracil and thymine. This leads to the creation of covalent bonds between adjacent thymine bases, resulting in what is known as thymine dimers. These dimers create distortions in the DNA structure, making it more difficult for the cellular machinery to replicate the DNA accurately during cell division.

If these distortions are not correctly repaired through the DNA repair mechanisms of the cell, it can result in mutations. When mutations occur in oncogenes or tumor suppressor genes, they can lead to uncontrolled cell growth and the development of cancers, including melanoma. Therefore, the formation of DNA pyrimidine dimers is fundamental to the carcinogenic process induced by UVB exposure.

In contrast, while oxidative stress, inflammatory responses, and cellular apoptosis can also play roles in the broader context of skin damage and cancer progression, the direct primary mechanism through which UVB exposure leads to melanoma specifically involves the formation of these DNA dimers.