To test the latter possibility, we evaluated 10 ER (+)/PR (-) resected human breast cancers for small deletions and point mutations in the DNA binding domain of the ER gene.
These data demonstrate that methylation of the ER and PR gene CpG islands is associated with the lack of ER and PR gene expression in a significant fraction of human breast cancers.
Prior to BRCA1 analysis, 79 breast and 19 ovarian tumours from 57 breast and breast-ovarian cancer families, and 170 tumours from a comparison group of stage II breast cancers were studied with regard to histopathological features; immunohistochemistry [c-erbB-2, p53, oestrogen receptor (ER) and progesterone receptor (PR)], DNA flow cytometry and S-phase fraction.
Estrogen receptor-negative/progesterone receptor-positive Evsa-T mammary tumor cells: a model for assessing the biological property of this peculiar phenotype of breast cancers.
Caucasian patients with the m1 Val/Val genotype have a significantly higher percentage of estrogen receptor-positive (P = 0.02) and progesterone receptor-positive breast cancers (P = 0.003).
If this smaller PR species exhibits similar differences in function as have been evidenced in vitro for PR A relative to PR B, it is possible that this PR species may be an important component in determination of progesterone response in breast cancer.
The relative level of expression of some estrogen receptor variant mRNAs and possibly progesterone receptor variant mRNAs is altered during breast tumorigenesis and breast cancer progression.
Patients with BRCA1-associated breast cancer had twice as many progesterone-receptor-negative tumours (p<0.005) and development of contralateral breast cancer was four to five times as frequent as in the sporadic group (p<0.001).
However, few data about the mRNA expression of ER, PR, pS2, and PAI-1 in breast cancer are available, which is mostly due to the limitations of conventional techniques for mRNA analysis.
Thus, loss of PR expression in breast cancercannot be explained only by loss of chromosome 11; other genetic or non-genetic mechanisms should be advanced.
Induction of progesterone receptor by E2 is suppressed by 1,25(OH)2D3, and the E2-mediated increase in breast cancer susceptibility gene (BRCA1) protein is reduced by 1,25(OH)2D3 treatment.
Our study is an immunohistochemical analysis of p53 in 82 cases of breast cancer in young (< or = 30 years old) Kuwaiti women, correlating it with histopathological grade, lymph node status, estrogen (ER) and progesterone receptor (PgR) content, tumor cell proliferation (immunostaining for Ki-67) and expression of c-erbB-2 oncoprotein. p53 immunostaining was found in 47 (57.32%) of the carcinomas.
To clarify this hypothesis, the effects of hypoxia on the growth responses to hormonal agents and the expression levels of estrogen receptor (ER)-alpha and progesterone receptor (PgR) were investigated in two human breast cancer cell lines, ML-20 and KPL-1.