title: Effects of short-term tamoxifen administration in patients with invasive cervical carcinoma.
abstract: Cervical cancer is not considered a hormone-responsive tumor in spite of the presence of estrogen receptors (ER) and progesterone receptors (PgR) in some of them. Endocrine treatments have not achieved clinical responses, however, tamoxifen has been reported to induce PgR and to inhibit cell growth of many cervical carcinoma cell lines. In this study we investigated whether tamoxifen administration affects the histopathological characteristics of cervical cancer and the expression of ER, PgR, HER-2/neu and p53 protein. Nineteen patients with invasive cervical cancer free of previous treatments were studied. The triphenylethylene antiestrogen tamoxifen was given orally during 10 days (20 or 40 mg/day). Pre- and post-tamoxifen biopsies were evaluated using slides stained with hematoxylin and eosin and immunostained (ER, PgR, HER-2/neu, p53, PCNA, keratin, heat shock protein 27,000 daltons). Estrogen receptors were present in 37% and PgR in 16% of the biopsies from untreated patients. Only one case that was PgR-negative before tamoxifen administration showed weak PgR-positivity following antiestrogen administration. No obvious changes were observed in ER, HER-2/neu and p53 proteins. A statistically significant decrease in the number of mitotic figures was obtained in 16% (3/19) of the post-tamoxifen biopsies and two of them showed higher differentiation. The results showed that tamoxifen did not induce changes in estrogen-regulated proteins in cervical cancer. However, the data showed that certain cervical carcinomas had changes in their proliferation and differentiation levels following tamoxifen administration. These findings suggest that tamoxifen may affect some cervical cancer tissues by a hormone-independent mechanism(s).
authors.affiliation: Laboratorio de Reproducción y Lactancia, LARLAC, Mendoza, Argentina.
authors.forename: L M
authors.initials: LM
authors.lastname: Vargas Roig
authors.forename: H
authors.initials: H
authors.lastname: Lotfi
authors.forename: J E
authors.initials: JE
authors.lastname: Olcese
authors.forename: G
authors.initials: G
authors.lastname: Lo Castro
authors.forename: D R
authors.initials: DR
authors.lastname: Ciocca
mesh_terms: D000284:Administration, Oral; D000328:Adult; D000368:Aged; D002455:Cell Division; D004334:Drug Administration Schedule; D005260:Female; D006360:Heat-Shock Proteins / Q000032:analysis; D006801:Humans; D008875:Middle Aged; D009687:Nuclear Proteins / Q000032:analysis; D009856:Oncogene Proteins, Viral / Q000032:analysis; D018809:Proliferating Cell Nuclear Antigen; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen / Q000032:analysis; D011980:Receptors, Progesterone / Q000032:analysis; D013629:Tamoxifen / Q000008:administration & dosage*; D016159:Tumor Suppressor Protein p53 / Q000032:analysis; D002583:Uterine Cervical Neoplasms / Q000737:chemistry / Q000188:drug therapy* / Q000473:pathology
chemical_list: D006360:Heat-Shock Proteins; D009687:Nuclear Proteins; D009856:Oncogene Proteins, Viral; D018809:Proliferating Cell Nuclear Antigen; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D013629:Tamoxifen; D016159:Tumor Suppressor Protein p53