Immunohistochemical analysis of the functional status of estrogen receptor cascade in breast cancer.
Hormone receptor expression in human breast cancer cells does not always reflect tumor response to therapy. Thus, relations between hormone receptor status and other parameters need further examination. The aim of this study was to test the ability of estrogen receptors (ER) to induce progesterone receptor (PR) synthesis as well as to test their role in the regulation of cell proliferation. Measurement of the relation between expressions of ER and the estrogen receptor related protein p29 (ERRP) was a further goal. The results show that some hormone receptor phenotypes are closely related to tumor proliferative activity: in the ER-group, especially ER-PR-phenotype, proliferative activity shows no obvious relationship to phenotype status, suggesting that proliferation in this group probably is not under estrogen control, while in the ER+ group, PR expression was related to reduced proliferation. There was no clear association between ERRP and nuclear ER but the highest ERRP expression was most closely related to ER negative (ER-) or slightly positive (ER +/-) hormone receptor statuses. Tumors with these phenotypes are known to have a poorer prognosis. The conclusion drawn is that simultaneous estimation of proliferative activity, ERRP p29 expression and a comparison with ER/PR hormone receptor phenotype, could provide pathologist with a valuable tool for predicting hormone response and prognosis in breast cancer patients.
Institute of Pathology, Faculty of Medicine, Palacký University, Olomouc, Czech Republic.
Z
Z
Kolár
J
J
Ehrmann
M
M
Dusková
D000328:Adult; D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D014408:Biomarkers, Tumor / Q000096:biosynthesis; D001943:Breast Neoplasms / Q000473:pathology / Q000648:ultrastructure*; D005260:Female; D006360:Heat-Shock Proteins / Q000096:biosynthesis; D006801:Humans; D007150:Immunohistochemistry; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000096:biosynthesis; D010641:Phenotype; D011960:Receptors, Estrogen / Q000096:biosynthesis / Q000502:physiology*; D011980:Receptors, Progesterone / Q000096:biosynthesis
D014408:Biomarkers, Tumor; D006360:Heat-Shock Proteins; D009363:Neoplasm Proteins; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone