Micrograph of a basal-cell carcinoma, showing the characteristic histomorphologic features (peripheral palisading, myxoid stroma, artefactual clefting). H&E stain Basal-cell carcinomas are currently considered to have origin from the folliculo-sebaceous-apocrine germ, also known as trichoblast. The differential diagnosis with trichoblastic carcinoma, a rare malignant form of trichoblastoma, can be challenging. Alternatively, one argument is that basal-cell carcinoma is trichoblastic carcinoma. Overexposure to sun 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, overexposure to sunlight depresses the local immune system, possibly decreasing immune surveillance for new tumor cells. Basal-cell carcinomas can often come in association with other lesions of the skin, such as actinic keratosis, seborrheic keratosis, squamous cell carcinoma. In a small proportion of cases, basal-cell carcinoma also develops as a result of basal-cell nevus syndrome, or Gorlin Syndrome, which is also characterized by keratocystic odontogenic tumors 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 this syndrome is a mutation in the PTCH1 tumor suppressor gene located in 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.
types of Skin cancer
symptom of Skin cancer
symptom of Melanoma
Clyde cancer cluster
medical cause of Mucosal melanoma
types of Mucosal melanoma
symptom of Psoriasis
causes of Mucosal melanoma