Final answer:
Xeroderma Pigmentosa patients have a deficit in the nucleotide excision repair mechanism, cannot repair thymine dimers caused by UV exposure, leading to DNA distortion and a significant increase in skin cancer risk.
Step-by-step explanation:
Cells from patients with Xeroderma Pigmentosa (XP) do exhibit deficits in excision repair, specifically in the nucleotide excision repair mechanism. When exposed to UV light, these cells fail to recognize and repair pyrimidine dimers, such as thymine dimers, that can form between adjacent thymines. This incapability to repair the damage is due to a defect in the nucleotide excision repair enzymes. As a result, these thymine dimers can distort the structure of DNA, leading to issues with DNA replication. This defect greatly increases the risk of contracting skin cancer for those with the condition.