Expression of cell cycle and apoptosis regulatory proteins in keratoacanthoma and squamous cell carcinoma

Keratoacanthoma and squamous cell carcinoma are distinct from a molecular perspective

“…22 Others have shown that keratoacanthoma strongly expresses the proteins bax and bak, which are considered essential for apoptosis execution. 23 Another study examined keratoacanthomas showed lower expression of the anti-apoptotic protein Bcl-xL that is consistent with a possible role of apoptosis in keratoacanthoma regression. 24 BCL-2 is a proto-oncogene involved in protecting cells from undergoing apoptosis and has been shown to have decreased expression in regressing keratoacanthomas.…”

“…24 BCL-2 is a proto-oncogene involved in protecting cells from undergoing apoptosis and has been shown to have decreased expression in regressing keratoacanthomas. 23,25 We hypothesize that prominent enrichment of the clathrin-mediated endocytosis signaling pathway may be because of granzyme-mediated apoptosis. Cytotoxic T cells and natural killer cells utilize lytic effector proteins of perforin and granzymes to eliminate target cells.…”

High expression of Ki-67 and cyclin D1 in invasive extramammary Paget's disease

“…Several new tumor markers are under investigation to enhance our understanding of tumor biology and to delineate their potential in predicting prognosis [5][6][7]. These markers include the proto-oncogenes p53 and Her2 (c-erbB-2/neu), the cell cycle regulatory proteins cyclin D1 and Ki-67, and the apoptotic marker Bcl-2.…”

The Role of p16, p21, p27, p53 and Ki-67 Expression in the Differential Diagnosis of Cutaneous Squamous Cell Carcinomas and Keratoacanthomas: An Immunohistochemical Study

“…Some KA cases that were initially diagnosed as benign progressed to be metastatic, exhibiting aggressive behavior (3)(4)(5). The immunohistochemical markers that have been used for years to distinguish between SCC and KA in studies are: p53, proliferating cell nuclear antigen , telomerase and COX-2 , transforming growth factor-α, angiotensin-type I receptor, vascular cell adhesion molecule, intercellular adhesion molecule, Ki-67, p16 tumor suppressor antigen, matrix metalloproteinases, syndecan-1 and Bcl-2 (6)(7)(8)(9)(10)(11)(12)(13)(14)(15). However, none of these studies have been able to provide reliable and specific criteria with which to distinguish between these two tumors.…”