Open AccessInterrelationship between Estradiol and Tamoxifen Responses for Clinical Breast Carcinoma Cells Cultured on Contact‐sensitive Plates
Author(s) -
Matsuoka Hideo,
Nakamura Yasuya,
Ueo Hiroaki,
Sugimachi Keizo,
Tomoda Hirotsugu,
Saito Takao,
Seo Yousuke
Publication year - 1994
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1994.tb02404.x
Subject(s) - tamoxifen , estrogen receptor , breast cancer , estrogen , medicine , in vitro , endocrinology , cancer , breast carcinoma , cancer research , cancer cell , oncology , chemistry , biochemistry
An in vitro assay system for predicting the estradiol (E 2 ) sensitivity of clinical cancer cells was applied to 54 patients with breast carcinoma to compare the responses to E 2 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 E 2 . It is suggested that ER status alone can not predict the response of cultured cells to E 2 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 E 2 . Since the cases inhibited by E 2 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 E 2 . 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 E 2 were inhibited by TAM, 10 (91%) of the 11 E 2 ‐insensitive cases were insensitive to TAM and 13 (68%) of the 19 cases inhibited by E 2 were stimulated by TAM. In short, TAM response and E 2 response tended to be inversely related (43/54=80%, P <0.01). Furthermore, the E 2 ‐response rate showed a good correlation with the TAM‐response rate (R 2 = 0.825). These results indicate the feasibility of predicting individual tumor responses to either E 2 or TAM by using CSPs.