Immunohistochemical Evaluation of Ki-67 Antigen, p27 and MCM3 Proteins in Ameloblastoma

Statement of Problem: Ameloblastomas are locally aggressive tumors with which the researchers have been mostly concerned to understand their biological behavior. Overexpression of minichromosome maintenance 3 (MCM3, a recently introduced marker) has been reported in different cancers. There is no study about MCM3 expression in ameloblastoma. This study aims at the evaluation of MCM3, Ki-67 and p27 in ameloblastoma.Methods and Material: In this analytical study, 18 ameloblastomas were selected. Clinicohistopathological data were recorded and immuohistochemical staining was done on the newly cut sections for Ki-67 antigen, p27 kip1 and MCM3. The immunostained cells were counted on 10 HPF (Labeling Index) and then classified into negative (LI5), low (550) levels. Statistical analysis was done performed in SPSS, version 13, using ordinal regression and Freidman tests. P value less than 0.05 was considered significant.

Results

Among the lesions, 5 (27.8%) and 13 (72.2%) were negative and weak for Ki-67, respectively. Also, 5 (27.8%), 11(61.1%) and 2 (11.1%) lesions were negative, weak and moderate, respectively for p27. Ki-67 and p27 staining were seen more frequently in the ameloblast layer and stellate reticulum, respectively. None of the samples was stained by MCM3. There were significant differences among Ki-67, p27 and MCM3 expression in ameloblastomas but no differences were found between sex, age and tumor size and expression of these markers.

Conclusion

Most of the ameloblastomas expressed low levels of Ki-67 and p27 (72.2% and 61.1%, respectively). It could not be concluded exactly how these tumors will behave in the future, because low expression of p27 is in favor of cell proliferation (in contrast to low expression of Ki-67). To find out how biological behavior of these tumors will be in the future, other markers should be evaluated and all the patients should be followed up. Regarding the negative expression of MCM3 in all lesions, it seems that MCM3 is not involved in the pathogenesis of ameloblastoma.