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Apoptosis, Proliferation, and Expression of p53 and bcl-2 in Endocervical Glandular Intraepithelial Lesions and Invasive Endocervical Adenocarcinoma

Ali-Fehmi, Rouba M.D.; Qureshi, Faisal M.D.; Lawrence, W. Dwayne M.D.; Jacques, Suzanne M. M.D.

International Journal of Gynecological Pathology: January 2004 - Volume 23 - Issue 1 - p 1-6
doi: 10.1097/01.pgp.0000102453.84429.85
Original Contributions
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We evaluated apoptosis, proliferation, and p53 and bcl-2 expression in a spectrum of intraepithelial and invasive endocervical glandular lesions currently recognized by the World Health Organization as adenocarcinoma in situ, lesions with atypia “less than adenocarcinoma in situ ” (endocervical glandular dysplasia and endocervical glandular atypia), and invasive adenocarcinoma. Aside from nuclear atypia, increased mitotic activity and apoptosis are consistent and closely correlated morphologic features of endocervical adenocarcinoma in situ. Apoptotic bodies and mitotic figures were counted in 32 examples of normal endocervical glands, 35 of endocervical glandular atypia, 30 of endocervical glandular dysplasia, 34 of adenocarcinoma in situ, and 30 of invasive adenocarcinoma. These results were correlated with immunohistochemical staining for MIB1, bcl-2, and p53 performed on 20 examples of each. Mitotic counts, p53 expression, and bcl-2 expression all increased significantly and in proportion to the degree of atypia in the spectrum of endocervical lesions. Apoptotic body counts and MIB1 expression also increased significantly with increasing atypia, but showed higher levels in adenocarcinoma in situ than in invasive adenocarcinoma. Apoptosis correlates with proliferation as measured by mitotic counts and MIB1, and also with p53 and bcl-2 expression. Apoptosis appears to be an important mechanism in the pathogenesis of endocervical glandular lesions and may be useful as an aid in their evaluation and diagnosis.

From the Department of Pathology (R.A-F., F.Q., S.M.J), Hutzel Hospital, Wayne State University School of Medicine, Detroit, Michigan; and the Women and Infants Hospital of Rhode Island and Brown Medical School (D.L.), Providence, Rhode Island.

Address correspondence and reprint requests to Rouba Ali-Fehmi, M.D., Wayne State University School of Medicine, Harper University Hospital, 3990 John R, Detroit, MI 48201. E-mail: rali@dmc.org.

©2004International Society of Gynecological Pathologists