Micrograph of a<unk> , showing the characteristic histomorphologic features (peripheral palisading, myxoid stroma, artefactual clefting). H&E stain<unk> s are currently considered to have origin from the folliculo-sebaceous-apocrine germ, also known as trichoblast. The differential diagnosis with trichoblastic<unk> , a rare malignant form of trichoblastoma, can be challenging. Alternatively, one argument is that<unk>  is trichoblastic<unk> . 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<unk> s.<unk> s can often come in association with other lesions of the skin, such as actinic keratosis, seborrheic keratosis, squamous<unk><unk> . In a small proportion of cases,<unk>  also develops as a result of<unk> -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<unk> .
Basal-cell carcinoma
Melanoma
Lymphoepithelioma
Seborrheic keratosis
Trichoepithelioma
Psoriasis
Angiokeratoma
Milium (dermatology)