It is proposed that the blockade of NF-κBs actions prolongs cell survival, stimulates high rates of cell growth, and perhaps has other effects which contribute to the formation and/or progression of SA and SAC tumors. Diagnosis
SA and SAC tumors have been confused with leiomyoma, angiolipoma, granular cell tumor, basal cell carcinoma, squamous cell carcinoma, metastatic adenocarcinoma, and adenoid cystic carcinoma tumors; the giant vascular SA form of these tumors has been mistaken for a hemangioma, angiolipoma, calcifying epithelioma, neuroma, malignant melanoma, angiosarcoma, vascular malformation, and venous thrombosis. CT scans, FDG-positron emission tomography, and magnetic resonance imaging to detect 1) the shape and local invasiveness of these tumors and 2) the presence of metastases and 2) the clinical presentation of individuals of these tumors often suggest the correct diagnosis. However, definitive separation of SA, SAC, and giant vascular SA from the just cited lesions requires histopathological examinations. The diagnosis of SA versus SAC tumors is often suggested by their clinical presentations, e.g. rapid enlargement or onset of pain in a long-standing SA tumor strongly suggests that it has become a SAC. Findings that a known SA or undiagnosed tumor has areas of SA histology transitioning to SAC histology (see above Pathology section) is virtually diagnostic for SAC.The sporadic SA and SAC tumors reviewed here must also be distinguished from the very similar appearing SA-like and SAC-like tumors in individuals afflicted with the CYLD cutaneous syndrome. CCS is a familial disease uniformly associated with the inheritance of inactivating mutations in the CYLD gene.
While death is rare among MAC patients, it can occasionally metastasize to local lymph nodes. The 10 year overall survival rate is 86.4%, however this is exceedingly close to many 10 year survival rates of populations without MACs present. Causes
Little is known about the causes of MACs, although some evidence has shown that ultraviolet light, radiation, and genes may be causation factors. A genetic role might also be plausible, according to some studies. In several cases, patients developed a MAC after immunosuppression. Treatment
Due to the invasive nature of MACs, most cases are treated with wide local excision in order to decrease the rate of reoccurrence. Increasingly however, Mohs micrographic surgery is being employed as it allows more specific margins to be removed, along with decreasing the size of postoperative scars and disfigurement. In rare cases, tumors can be deemed inoperable due to their size and location under vital structures of the face. Chemotherapy and radiation treatment have been used when metastasis has occurred or when an excision cannot be performed, but results have been inconclusive about their effectiveness. In some cases, radiation therapy has been shown to increase tumor size. While in other cases, it implies that it will decrease the success of the tumor regrowing. Long term follow-up is necessary, as some cases of local recurrence have been documented 30 years after the original diagnosis. See also
Syringofibroadenoma
Skin lesion
List of cutaneous conditions


== References ==