Background: Endocervical adenocarcinomas (ECAs) and endometrial adenocarcinomas (EMAs) are malignancies that affect uterus; however, their biological behaviors are quite different. This distinction has clinical significance, because the appropriate therapy may depend on the site of tumor origin. The purpose of this study is to evaluate 3 different scoring mechanisms of p16 INK4a immunohistochemical (IHC) staining in distinguishing between primary ECAs and EMAs.

This month we revisit the problem of distinguishing endocervical from endometrial adenocarcinomas, a topic that was previously addressed in the January 2002 issue of "Focus on Immunohistochemistry". Most surgical pathologists know very well that there is substantial morphologic overlap between these entities, but differences in therapeutic approaches necessitate attempts to distinguish these 2 tumors.In the January 2002 issue of the International Journal of Gynecological Pathology, two papers addressed this problem. Castrillon et al (1) studied 30 endometrial adenocarcinomas and 29 endocervical adenocarcinomas, and included tumors with overlapping morphologic features. CEA was more common in endocervical adenocarcinomas (62%), than in endometrial adenocarcinomas (27%). The authors also noted that CEA appeared to be particularly useful for tumors that had endometrioid morphology, since only 14% of the endometrial endometrioid adenocarcinomas were CEA positive, in contrast to 67% of the endocervical adenocarcinomas with endometrioid morphology. 97% of the endometrial adenocarcinomas were vimentin positive, in contrast to only 7% of the endocervical adenocarcinomas. McCluggage et al (2) evaluated 30 endometrial adenocarcinomas and 26 endocervical adenocarcinomas. In their study, 93% of endometrial adenocarcinomas were strongly estrogen receptor (ER) positive, whereas focal weak ER positivity was noted in 38% of endocervical adenocarcinomas. Vimentin was diffusely positive in 97% of the endometrial adenocarcinomas, but in only 8% of the endocervical adenocarcinomas. Prior studies have reported ER in 70% of endometrial adenocarcinomas, in contrast to 10-20% of endocervical adenocarcinomas, vimentin reactivity in 50-81% of endometrial adenocarcinomas vs. <13% of endocervical adenocarcinomas, and CEA in 65-95% of endocervical adenocarcinomas. Staebler et al (4) studied 24 endometrial and 24 endocervical carcinomas, and found that only 1 of 24 (4.2%) endocervical carcinomas expressed both ER and PR. In contrast, 18 of 24 (75%) of endometrial carcinomas expressed ER, and 23 of 24 (95.8%) expressed PR. HPV in situ hybridization on formalinfixed paraffin-embedded sections was also performed, which found HPV DNA in 16 of the 24 (66.7%) endocervical carcinomas, but in none of the 24 endometrial carcinomas. In light of the association of immunostaining of p16 (INK4a) with high-risk HPV infection, one might surmise that immunostains for p16 (INK4a) might also be of use in the differential diagnosis of endometrial adenocarcinoma vs. endocervical adenocarcinoma. Although immunohistochemical expression of p16 (INK4a) has been described in both of these tumors, in a study of 24 unequivocal endometrial adenocarcinomas and 18 unequivocal endocervical adenocarcinomas, reported at the recent 2003 USCAP meeting that the pattern of p16 (INK4a) expression allowed distinction of the two tumors. All endocervical adenocarcinomas showed strong and diffuse p16 (INK4a) immunostaining, with a mean of 94% of tumor cells reacting (range 90-100%...

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