A Case of Acantholytic Squamous Cell Carcinoma: DISCUSSION

Posted by James

SCC is an uncommon variant of SCC that was first described by Lever in 1947 as adenoacanthoma of the sweat glands. It was also known as adenoid , lobular SCC, or pseudoglandular SCC. As can be guessed by the name, it was previously thought to be a tumor of a sweat gland origin because of gland-like and solid epithelial prolifera¬tions extending into the dermis. However, A-SCC is now accepted as a distinct variant of SCC rather than a sweat gland tumor.

Clinically, A-SCC is usually found on the sun- exposed areas of elderly patients with notable male predominance. It presents most often on the head and neck, but other sites of origin have been reported, including the vulva, penis, oral mucosa, nasopharynx, and breast. It appears as flesh-colored, pink, red, or brown nodules in most cases, and it is frequently accompanied by scaling, crusting, and ulceration like the other SCC variants. Therefore, histological examination is necessary for making the accurate diagnosis.

Histologically, the tumor is composed of a epidermal-derived cystic proliferation extending into the dermis, and this forms lobules or nests, columns and island-like structures. Many of the tumor strands exhibit tubular and gland-like structures due to the loss of intercellular cohesion, which is referred to as a “pseudoglandular” appearance. Within the central spaces, there are many floating individual acantholytic cells that show atypical dyskera- tosis. These acantholytic cells appear extremely bizarre, large, and multinucleated. Slightly baso- philic amorphous material can sometimes be seen within the central spaces, and this material has a suspected glandular origin. But the tumor is negative on both dPAS and mucicarmine staining, and this is unlike other eccrine neoplasms. The overlying epidermis may show hyperkeratosis and parakeratosis, and the connection to the underlying tumor can be seen in most cases.
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Although classic type SCC may also show some clefts with dyskeratosis and acantholysis, it does not have a definite wall or a cohesive layer of cells surrounding the acantholytic cells, as is seen in A-SCC. Some authors have suggested the hypo¬thesis that A-SCC originates from premalignant acantholytic actinic keratosis. However, clinically it can occur on sun-protected areas and histologically there may be no sign of solar damage. In addition, Nappi et al did not find the exact association between A-SCC and acantholytic actinic keratosis in their 55 cases. According to these reasons, it is now thought that acantholytic actinic keratosis is not the precursor lesion of A-SCC. Although there are no specific risk factors for A-SCC, it is supposed that other predisposing factors for SCC, including immunosuppression, scars, burns and human papillomavirus infection as well as ultraviolet radiation, may be involved in the development of this tumor. It has been documented to arise in areas of pre-existing scarring and in patients with chronic lymphocytic leukemia.