Basal cell carcinoma pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
Basal cell carcinomas develop in the basal cell layer of the skin. Sun light exposure leads to the formation of thymine dimers, a form of DNA damage.
While DNA repair removes most UV-induced damage, not all crosslinks are excised. There is, therefore, cumulative DNA damage leading to mutations. Apart from the mutagenesis, sunlight depresses the local immune system, possibly decreasing immune surveillance for new tumor cells.
Basal-cell carcinoma also develops as a result of basal-cell nevus syndrome, or Gorlin's syndrome, which is also characterized by odontogenic keratocysts of the jaw, palmar or plantar (sole of the foot) pits, calcification of the falx cerebri (in the center line of the brain) and rib abnormalities.
The cause of the syndrome is a mutation in the PTCH1 tumor-suppressor gene at chromosome 9q22.3, which inhibits the hedgehog signaling pathway. A mutation in the SMO gene, which is also on the hedgehog pathway, also causes basal-cell carcinoma.[1]
References
- ↑ Epstein EH, Shepard JA, Flotte TJ (2008). "Case records of the Massachusetts General Hospital. Case 3-2008. An 80-year-old woman with cutaneous basal-cell carcinomas and cysts of the jaws". N Engl J Med. 358 (4): 393–401. doi:10.1056/NEJMcpc0707893. PMID 18216361. Unknown parameter
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