Decreased luteinizing hormone receptor mRNA expression in human ovarian epithelial cancer

Jean J. Lu, Yu Zheng, Xin Kang, Jian Min Yuan, Stuart C. Lauchlan, Malcolm C. Pike, Wenxin Zheng

Research output: Contribution to journalArticle

42 Citations (Scopus)

Abstract

Objectives. The objective of this study was to examine the distribution and cellular localization of luteinizing hormone receptor (LHR) in ovarian epithelial tumors (OETs) and their presumed precursor lesionsovarian epithelial inclusions (OEIs). The clinicopathologic correlation of the receptor expression 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 for LHR expression by using reverse transcription polymerase chain reaction and in situ hybridization. LHR expression in tumor epithelium and tumor stroma was analyzed separately. The clinicopathologic correlation data were analyzed by standard analysis of variance and contingency table methods. Results. LHR expression was identified in the majority of OSE and OEI samples. In OETs, LHR positivity was found in the epithelial cells in 27% of cases and in the stromal compartment in 37% of cases. LHR-positive stromal cells were mainly luteinized cells. Within the tumor epithelium, LHR expression was detected in 42% of benign, 24% of borderline, and 17% of malignant OETs. LHR expression in tumor stroma showed a similar trend of reduction from benign to malignant OETs. Within the 17 carcinomas, LHR was expressed in the epithelium in 47% of grade 1, 12% of grade 2, and only 5% of grade 3 cancers. The mean age of the LHR-positive group was younger than that of the receptor-negative patients. Compared with mucinous and other types of OETs, serous OETs showed higher LHR expression in the epithelium. Compared with the OETs removed in the different menstrual phases, OETs in the secretory phase showed higher LHR in the tumor stroma than in the proliferative phase. No receptor mRNA was detected in the epithelium of five carcinomas metastatic 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 compared with precursor lesions and benign and borderline OETs. LHR expression shows a steady decline from low-grade to high-grade ovarian cancer. The presence of LHR receptor in tumor epithelium suggests that luteinizing hormone 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 development of OETs. (C) 2000 Academic Press.

Original languageEnglish (US)
Pages (from-to)158-168
Number of pages11
JournalGynecologic Oncology
Volume79
Issue number2
DOIs
StatePublished - Jan 1 2000

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LH Receptors
Messenger RNA
Neoplasms
Epithelium
Carcinoma
Ovarian epithelial cancer
Ovary
Cystadenoma

Keywords

  • Gonadotropin receptors
  • Luteinizing hormone
  • Ovarian cancer
  • Ovarian epithelial tumor

ASJC Scopus subject areas

  • Oncology
  • Obstetrics and Gynecology

Cite this

Decreased luteinizing hormone receptor mRNA expression in human ovarian epithelial cancer. / Lu, Jean J.; Zheng, Yu; Kang, Xin; Yuan, Jian Min; Lauchlan, Stuart C.; Pike, Malcolm C.; Zheng, Wenxin.

In: Gynecologic Oncology, Vol. 79, No. 2, 01.01.2000, p. 158-168.

Research output: Contribution to journalArticle

Lu, Jean J. ; Zheng, Yu ; Kang, Xin ; Yuan, Jian Min ; Lauchlan, Stuart C. ; Pike, Malcolm C. ; Zheng, Wenxin. / Decreased luteinizing hormone receptor mRNA expression in human ovarian epithelial cancer. In: Gynecologic Oncology. 2000 ; Vol. 79, No. 2. pp. 158-168.
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title = "Decreased luteinizing hormone receptor mRNA expression in human ovarian epithelial cancer",
abstract = "Objectives. The objective of this study was to examine the distribution and cellular localization of luteinizing hormone receptor (LHR) in ovarian epithelial tumors (OETs) and their presumed precursor lesionsovarian epithelial inclusions (OEIs). The clinicopathologic correlation of the receptor expression 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 for LHR expression by using reverse transcription polymerase chain reaction and in situ hybridization. LHR expression in tumor epithelium and tumor stroma was analyzed separately. The clinicopathologic correlation data were analyzed by standard analysis of variance and contingency table methods. Results. LHR expression was identified in the majority of OSE and OEI samples. In OETs, LHR positivity was found in the epithelial cells in 27{\%} of cases and in the stromal compartment in 37{\%} of cases. LHR-positive stromal cells were mainly luteinized cells. Within the tumor epithelium, LHR expression was detected in 42{\%} of benign, 24{\%} of borderline, and 17{\%} of malignant OETs. LHR expression in tumor stroma showed a similar trend of reduction from benign to malignant OETs. Within the 17 carcinomas, LHR was expressed in the epithelium in 47{\%} of grade 1, 12{\%} of grade 2, and only 5{\%} of grade 3 cancers. The mean age of the LHR-positive group was younger than that of the receptor-negative patients. Compared with mucinous and other types of OETs, serous OETs showed higher LHR expression in the epithelium. Compared with the OETs removed in the different menstrual phases, OETs in the secretory phase showed higher LHR in the tumor stroma than in the proliferative phase. No receptor mRNA was detected in the epithelium of five carcinomas metastatic 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 compared with precursor lesions and benign and borderline OETs. LHR expression shows a steady decline from low-grade to high-grade ovarian cancer. The presence of LHR receptor in tumor epithelium suggests that luteinizing hormone 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 development of OETs. (C) 2000 Academic Press.",
keywords = "Gonadotropin receptors, Luteinizing hormone, Ovarian cancer, Ovarian epithelial tumor",
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T1 - Decreased luteinizing hormone receptor mRNA expression in human ovarian epithelial cancer

AU - Lu, Jean J.

AU - Zheng, Yu

AU - Kang, Xin

AU - Yuan, Jian Min

AU - Lauchlan, Stuart C.

AU - Pike, Malcolm C.

AU - Zheng, Wenxin

PY - 2000/1/1

Y1 - 2000/1/1

N2 - Objectives. The objective of this study was to examine the distribution and cellular localization of luteinizing hormone receptor (LHR) in ovarian epithelial tumors (OETs) and their presumed precursor lesionsovarian epithelial inclusions (OEIs). The clinicopathologic correlation of the receptor expression 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 for LHR expression by using reverse transcription polymerase chain reaction and in situ hybridization. LHR expression in tumor epithelium and tumor stroma was analyzed separately. The clinicopathologic correlation data were analyzed by standard analysis of variance and contingency table methods. Results. LHR expression was identified in the majority of OSE and OEI samples. In OETs, LHR positivity was found in the epithelial cells in 27% of cases and in the stromal compartment in 37% of cases. LHR-positive stromal cells were mainly luteinized cells. Within the tumor epithelium, LHR expression was detected in 42% of benign, 24% of borderline, and 17% of malignant OETs. LHR expression in tumor stroma showed a similar trend of reduction from benign to malignant OETs. Within the 17 carcinomas, LHR was expressed in the epithelium in 47% of grade 1, 12% of grade 2, and only 5% of grade 3 cancers. The mean age of the LHR-positive group was younger than that of the receptor-negative patients. Compared with mucinous and other types of OETs, serous OETs showed higher LHR expression in the epithelium. Compared with the OETs removed in the different menstrual phases, OETs in the secretory phase showed higher LHR in the tumor stroma than in the proliferative phase. No receptor mRNA was detected in the epithelium of five carcinomas metastatic 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 compared with precursor lesions and benign and borderline OETs. LHR expression shows a steady decline from low-grade to high-grade ovarian cancer. The presence of LHR receptor in tumor epithelium suggests that luteinizing hormone 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 development of OETs. (C) 2000 Academic Press.

AB - Objectives. The objective of this study was to examine the distribution and cellular localization of luteinizing hormone receptor (LHR) in ovarian epithelial tumors (OETs) and their presumed precursor lesionsovarian epithelial inclusions (OEIs). The clinicopathologic correlation of the receptor expression 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 for LHR expression by using reverse transcription polymerase chain reaction and in situ hybridization. LHR expression in tumor epithelium and tumor stroma was analyzed separately. The clinicopathologic correlation data were analyzed by standard analysis of variance and contingency table methods. Results. LHR expression was identified in the majority of OSE and OEI samples. In OETs, LHR positivity was found in the epithelial cells in 27% of cases and in the stromal compartment in 37% of cases. LHR-positive stromal cells were mainly luteinized cells. Within the tumor epithelium, LHR expression was detected in 42% of benign, 24% of borderline, and 17% of malignant OETs. LHR expression in tumor stroma showed a similar trend of reduction from benign to malignant OETs. Within the 17 carcinomas, LHR was expressed in the epithelium in 47% of grade 1, 12% of grade 2, and only 5% of grade 3 cancers. The mean age of the LHR-positive group was younger than that of the receptor-negative patients. Compared with mucinous and other types of OETs, serous OETs showed higher LHR expression in the epithelium. Compared with the OETs removed in the different menstrual phases, OETs in the secretory phase showed higher LHR in the tumor stroma than in the proliferative phase. No receptor mRNA was detected in the epithelium of five carcinomas metastatic 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 compared with precursor lesions and benign and borderline OETs. LHR expression shows a steady decline from low-grade to high-grade ovarian cancer. The presence of LHR receptor in tumor epithelium suggests that luteinizing hormone 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 development of OETs. (C) 2000 Academic Press.

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KW - Luteinizing hormone

KW - Ovarian cancer

KW - Ovarian epithelial tumor

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