TY - JOUR
T1 - Analysis of estrogen receptor α and β in endometrial carcinomas
T2 - Correlation with ERβ and clinicopathologic findings in 45 cases
AU - Utsunomiya, Hiroki
AU - Suzuki, Takashi
AU - Harada, Nobuhiro
AU - Ito, Kiyoshi
AU - Matsuzaki, Sachiko
AU - Konno, Ryo
AU - Sato, Shinji
AU - Yajima, Akira
AU - Sasano, Hironobu
PY - 2000
Y1 - 2000
N2 - Estrogens play important roles in the pathogenesis of the great majority of endometrial endometrioid adenocarcinoma. Recently, a novel estrogen receptor (ER), ERβ, has been characterized, but little is known about the status of ERβ in endometrial carcinoma. We therefore examined expression of both ERα and ERβ in 45 cases of endometrioid endometrial adenocarcinoma using mRNA in situ hybridization, reverse transcription and polymerase chain reaction (RT-PCR), and immunohistochemistry. We also correlated the findings with various clinicopathologic parameters in these cases to examine their possible biologic significance. Accumulation of mRNA hybridization signals for both ERα and ERβ was detected predominantly in the cytoplasm of carcinoma cells, and to a lesser extent in some stromal cells. ERβ mRNA was detected in 16/45 cases (35.6%), and ERα mRNA hybridization signals were detected in 36/45 cases (80.0%). Among the 16 ERβ positive cases, 15 cases also had ERα mRNA hybridization signals. In the cases that expressed both ERα and ERβ, ERα mRNA hybridization signals were more widely distributed than ERβ mRNA. In 21 cases, carcinoma cells had ERα mRNA hybridization signals but not ERβ mRNA. There was a statistically significant positive correlation between the results of mRNA in situ hybridization and semiquantitative RT-PCR or immunohistochemistry for both ERα and ERβ. There were no significant correlations between ERβ mRNA expression and PR labeling index, Ki67 LI, age, or histologic grade. The results from our study indicate that ERβ is coexpressed with ERα, and that the estrogenic effects occur predominantly through ERα in endometrial carcinomas.
AB - Estrogens play important roles in the pathogenesis of the great majority of endometrial endometrioid adenocarcinoma. Recently, a novel estrogen receptor (ER), ERβ, has been characterized, but little is known about the status of ERβ in endometrial carcinoma. We therefore examined expression of both ERα and ERβ in 45 cases of endometrioid endometrial adenocarcinoma using mRNA in situ hybridization, reverse transcription and polymerase chain reaction (RT-PCR), and immunohistochemistry. We also correlated the findings with various clinicopathologic parameters in these cases to examine their possible biologic significance. Accumulation of mRNA hybridization signals for both ERα and ERβ was detected predominantly in the cytoplasm of carcinoma cells, and to a lesser extent in some stromal cells. ERβ mRNA was detected in 16/45 cases (35.6%), and ERα mRNA hybridization signals were detected in 36/45 cases (80.0%). Among the 16 ERβ positive cases, 15 cases also had ERα mRNA hybridization signals. In the cases that expressed both ERα and ERβ, ERα mRNA hybridization signals were more widely distributed than ERβ mRNA. In 21 cases, carcinoma cells had ERα mRNA hybridization signals but not ERβ mRNA. There was a statistically significant positive correlation between the results of mRNA in situ hybridization and semiquantitative RT-PCR or immunohistochemistry for both ERα and ERβ. There were no significant correlations between ERβ mRNA expression and PR labeling index, Ki67 LI, age, or histologic grade. The results from our study indicate that ERβ is coexpressed with ERα, and that the estrogenic effects occur predominantly through ERα in endometrial carcinomas.
KW - Endometrial carcinoma
KW - Estrogen in situ hybridization
KW - Estrogen receptor α
KW - Estrogen receptor β
KW - RT-PCR
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U2 - 10.1097/00004347-200010000-00007
DO - 10.1097/00004347-200010000-00007
M3 - Article
C2 - 11109162
AN - SCOPUS:0033738376
VL - 19
SP - 335
EP - 341
JO - International Journal of Gynecological Pathology
JF - International Journal of Gynecological Pathology
SN - 0277-1691
IS - 4
ER -