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Expression of ras, c‐myc, and p53 proteins in cervical intraepithelial neoplasia

We read with interest the article by Slagle et al. who investigated potential prognostic markers in cervical intraepithelial neoplasia (CIN). The altered expression of these genes is known to be a likely contributor to the development of cervical carcinoma; 4 the stated goal of the authors was to investigate the possible relation between the altered expression of these genes and precursor forms of invasive carcinoma (Grades 1, 2, and 3 CIN). It would be interesting to determine significant correlating alterations in the expression of such genes in preinvasive forms of cervical carcinoma that will enable them to be used in clinical practice as prognostic indicators of the progression of CIN. If we examine the histologic study results of the normal group (comprised of 142 patients who were referred to the authors’ colposcopy clinic with abnormal cytology) squamous metaplasia was detected in 54%, squamous metaplasia with inflammation was detected in 33%, and chronic inflammation was detected in 4%; no data were available regarding 9% of the normal tissues that most likely were relatively closer to normal in spite of abnormal cytology. Perhaps no dysplastic changes were observed in this normal group, and with these histologic findings this group can be included in the noninvasive disease group. Nevertheless one cannot rule out that these normal findings were not accompanied by alterations in the gene expression level. It is likely that the reason no correlation could be found between the normal accepted group and the CIN group with regard to p21ras and p62myc was that there was no rational selection of the patients for the normal group. When one considers the localization of immunohistochemical (IHC) positive staining cells to the upper layers of the epithelium in 50% of specimens whereas 34% were accepted as normal, it could be suggested that these findings may be attributable to metaplastic changes present in the cervical epithelia of these patients. With regard to the results related to mutant ras expression, the authors found mutant ras IHC positivity in 17% of 144 patients. However, it is not clear whether each of those 144 patients was positive for pan-ras IHC. There were approximately 65 patients in whom pan-ras IHC findings were negative. More important, the authors provided no explanation regarding the mutant-ras IHC findings, which could have taken place within the discussion section. Because the percentage of positive staining reactions did not vary significantly with the increasing severity of dysplasia, it may be concluded that although alterations in the expression of these genes are known to be present in patients with invasive cervical carcinoma, they do not appear to play a significant role in the precursor lesions of this disease, which may lead to the concurrent explanation of why cervical intraepithelial cells do not invade beyond the basement membrane. We believe it would have been better, when trying to 2668