title: Interrelationship between estradiol and tamoxifen responses for clinical breast carcinoma cells cultured on contact-sensitive plates.
abstract: An in vitro assay system for predicting the estradiol (E2) sensitivity of clinical cancer cells was applied to 54 patients with breast carcinoma to compare the responses to E2 and tamoxifen (TAM) with the estrogen receptor (ER) status. We found that 18 of the 35 cases in the ER-positive group and 6 of the 19 cases in the ER-negative group were stimulated by E2. It is suggested that ER status alone can not predict the response of cultured cells to E2 in clinical breast cancer. Cell growth of 11/35 (31%) of the ER-positive cases and that of 8/19 (42%) of the ER-negative cases was inhibited by E2. Since the cases inhibited by E2 could not be distinguished by ER status alone, an assay system based on a quantitative proliferative response was considered necessary. There were 20 (83%) cases of inhibition by TAM among the 24 stimulated by E2. Only 18/35 (51%) of the ER-positive group exhibited growth inhibition by TAM. In our (CSP) assay, 20 (83%) of the 24 cases stimulated by E2 were inhibited by TAM, 10 (91%) of the 11 E2-insensitive cases were insensitive to TAM and 13 (68%) of the 19 cases inhibited by E2 were stimulated by TAM. In short, TAM response and E2 response tended to be inversely related (43/54 = 80%, P < 0.01). Furthermore, the E2-response rate showed a good correlation with the TAM-response rate (R2 = 0.825). These results indicate the feasibility of predicting individual tumor responses to either E2 or TAM by using CSPs.
authors.affiliation: Clinical Research Institute, National Kyushu Cancer Center, Fukuoka.
authors.forename: H
authors.initials: H
authors.lastname: Matsuoka
authors.forename: Y
authors.initials: Y
authors.lastname: Nakamura
authors.forename: H
authors.initials: H
authors.lastname: Ueo
authors.forename: K
authors.initials: K
authors.lastname: Sugimachi
authors.forename: H
authors.initials: H
authors.lastname: Tomoda
authors.forename: T
authors.initials: T
authors.lastname: Saito
authors.forename: Y
authors.initials: Y
authors.lastname: Seo
mesh_terms: D016475:3T3 Cells; D000818:Animals; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000473:pathology / Q000648:ultrastructure; D002450:Cell Communication / Q000502:physiology; D002455:Cell Division / Q000187:drug effects; D004354:Drug Screening Assays, Antitumor; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D006801:Humans; D051379:Mice; D008807:Mice, Inbred BALB C; D009376:Neoplasms, Hormone-Dependent / Q000188:drug therapy* / Q000473:pathology / Q000648:ultrastructure; D011960:Receptors, Estrogen / Q000502:physiology; D013268:Stimulation, Chemical; D013629:Tamoxifen / Q000494:pharmacology*; D014407:Tumor Cells, Cultured / Q000187:drug effects
chemical_list: D011960:Receptors, Estrogen; D013629:Tamoxifen; D004958:Estradiol