Microscopic histopathological analyses of KTs commonly reveal a lesion with epidermal acanthosis (i.e. thickening of the skin), hyperkeratosis (i.e. thickening of the outermost layer of the epidermis), and skin features typical of angiofibroma viz., spindle-shaped or star-shaped fibroblasts and ectatic blood vessels in a dense collagen fiber connective tissue background. Etiology== In cases associated with tuberous sclerosis, KTs appear to be a result of this disease's associated genetic abnormalies, i.e. loss-of-function mutations in one of the two normally paired TSC1 or one of the two normally paired TSC2<unk>  suppressor genes. As a part of their functions, the TSC1 and TSC2<unk>  suppressor genes act to suppress the abnormal growth of cells by contributing to the suppression of the mammalian target of rapamycin (i.e. mTOR) protein that promotes cell growth and proliferation. Inactivation of one of the TSC1 or TSC2 genes appears responsible for unleashing mTor and thereby promoting the growth of the many strictly benign lesions, including KTs, that develop in individuals with tuberous sclerosis. mTOR is inhibited by rapamycin, a drug which has been used as a topical application to successfully treat a few cases of<unk> s. A small number of cases in individuals including those that do not have tuberous sclerosis may develop KTs as reactions to local traumas.
Koenen's tumor
Askin's tumor
Baker's cyst
Tarlov cyst
Krukenberg tumor
Bartholin's cyst
Tornwaldt cyst
Klatskin tumor