Objectives. The objective of this study was to examine the distribution and
cellular localization of luteinizing hormone receptor (LHR) in ovarian epi
thelial tumors (OETs) and their presumed precursor lesions-ovarian epitheli
al inclusions (OEIs). The clinicopathologic correlation of the receptor exp
ression in OET was also examined.
Methods. Fifteen microdissected samples of ovarian surface epithelium (OSE)
, 20 OEIs from benign ovaries, and 141 OETs, including 48 cystadenomas, 33
borderline tumors, 60 carcinomas, and 5 metastatic cancers, were examined f
or LHR expression by using reverse transcription polymerase chain reaction
and in situ hybridization. LHR expression in tumor epithelium and tumor str
oma was analyzed separately. The clinicopathologic correlation data were an
alyzed by standard analysis of variance and contingency table methods.
Results. LHR expression was identified in the majority of OSE and OEI sampl
es. In OETs, LHR positivity was found in the epithelial cells in 27% of cas
es and in the stromal compartment in 37% of cases. LHR-positive stromal cel
ls were mainly luteinized cells. Within the tumor epithelium, LHR expressio
n was detected in 42% of benign, 24% of borderline, and 17% of malignant OE
Ts. LHR expression in tumor stroma showed a similar trend of reduction from
benign to malignant OETs. Within the 17 carcinomas, LHR was expressed in t
he epithelium in 47% of grade 1, 12% of grade 2, and only 5% of grade 3 can
cers. The mean age of the LHR-positive group was younger than that of the r
eceptor-negative patients. Compared with mucinous and other types of OETs,
serous OETs showed higher LHR expression in the epithelium. Compared with t
he OETs removed in the different menstrual phases, OETs in the secretory ph
ase showed higher LHR in the tumor stroma than in the proliferative phase.
No receptor mRNA was detected in the epithelium of five carcinomas metastat
ic to the ovary. LHR transcription splicing variants from a single previous
report were confirmed in this study.
Conclusions. Malignant OETs have significant reduction of LHR expression co
mpared with precursor lesions and benign and borderline OETs. LHR expressio
n shows a steady decline from low-grade to high-grade ovarian cancer, The p
resence of LHR receptor in tumor epithelium suggests that luteinizing hormo
ne in serum may have direct influence on tumor growth, whereas the receptor
in tumor stroma may be indicative of a paracrine function of LH in the dev
elopment of OETs, (C) 2000 Academic Press.