Final answer:
Xeroderma Pigmentosum patients have a defect in the nucleotide excision repair mechanism, leading to the formation of thymine dimers that distort DNA structure and increase skin cancer risk after UV exposure.
Step-by-step explanation:
Xeroderma Pigmentosum patients cannot repair damage caused by UVB light, leading to a high risk of contracting skin cancer. This is because these patients lack the ability to employ the nucleotide excision repair mechanism. As a result, when exposed to UV light, thymine dimers are formed within the DNA, and these patients are not equipped to repair this defect. The formation of thymine dimers distorts the structure of DNA, hampering normal DNA replication processes and significantly increasing the likelihood of skin cancer development. This condition is marked by a high sensitivity of the skin to UV rays and the presence of skin lesions following sun exposure.