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The expression of progesterone receptors coincides with an arrest of DNA synthesis in human breast cancer
Author(s) -
Ballare C.,
Bravo A. I.,
Sorin I.,
Guman N.,
Schiaffi J. A.,
Yomha R.,
Bagnati A.,
Lema B.,
Mordoh J.
Publication year - 1991
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(19910301)67:5<1352::aid-cncr2820670514>3.0.co;2-s
Subject(s) - estrogen receptor , progesterone receptor , breast cancer , receptor , estrogen , immunohistochemistry , cell growth , medicine , thymidine , cancer , cancer research , estrogen receptor alpha , endocrinology , biology , dna , genetics
Two main models to account for the heterogeneous expression of estrogen receptors (ER) and progesterone receptors (PR) in human breast cancer have been proposed: the clonal model and the stem cell model. The authors previously provided evidence supporting the stem cell model since it was found that most of the proliferating cells in ER‐positive (ER + ) human breast cancer lack ER and that the ER‐negative (ER − ) and ER + subpopulations are interrelated. The authors have analyzed in eighteen ER + /PR + primary breast tumors the simultaneous expression of ER or PR (by immunohistochemistry) and DNA synthesis (by autoradiography) after 30 minutes of 3 H‐thymidine incorporation. The authors demonstrated that: (1) the average numbers of ER + and PR + cells were similar (36.8 ± 10.7% and 39.3 ± 17.6%, respectively); (2) The thymidine‐labeling indexes of the ER + , ER − , PR + , and PR − subpopulations were 0.53 ± 0.69%, 0.74 ± 0.49%, 0.21 ± 0.21 and 0.94 ± 0.54%, respectively; and (3) 75.2% of the DNA‐synthesizing cells were ER − , and 88.8% of them were PR − . The authors conclude that the cellular subpopulations expressing ER and PR were not identical, and the expression of PR was associated with a lower rate of cellular proliferation than was ER expression.