Apoptosis(programmed cell death) plays a major role in developmental biology and homeostasis. Apoptotic cells show characteristic morphological changes, especially, DNA fragmentation. It is regarded as biochemical hallmark of apoptosis.
Neoplastic
cell
expansion is the result of cellular proliferation and inhibition of apoptosis. The bcl-2 oncogene protects cells from apoptosis. We analyzed bcl-2 expression and in situ detection of fragmented DNA in carcinoma in situ, squamous cell
carcinoma(SCC), and
kertoacanthoma(KA) to investigate the role of apoptosis in tumorigenesis. Formalin-fixed, paraffin embedded tissues from carcinoma in situ, SCC, and KA were immunostained with anti-bcl-2-monoclonal oncoprotein and ApopTagTM in situ Apoptosis
Detection
Kit(Oncor, Gaithersburg, MD). Six carcinoma in situ were examined and all expressed the bcl-2 oncoprotein. Two of twenty-seven SCCs showed bcl-2 expression. These two were well-differentiated SCCs. None of the five KAs expressed bcl-2. The
pattern
of
ApopTagTM kit staining in all tumor cells appears to be opposite to that of bcl-2 expression. Our results indicate that neoplastic growth mechanism in carcinoma in situ may be related to enhanced cellular survival by protection from apoptosis,
while
those in SCC and KA may be due to increased cellular proliferation Tumor growth factors or oncogenes other than bcl-2 may be involved in the pathogenesis of epidermal tumors such as SCC and KA, since they show difference in prognosis although
both
demonstrate similar degree of apoptosis.
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