The positivity of G-protein-coupled receptor-30 (GPR 30), an alternative estrogen receptor is not different between type 1 and type 2 endometrial cancer
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Jiayi Wan1,*, Yongxiang Yin2,*, Min Zhao2, Fang Shen3, Miaoxin Chen4 and Qi Chen3,5
1Department of Pathology, Wuxi No2 People’s Hospital, Nanjing Medical University, Wuxi, China
2Department of Pathology, Wuxi Maternity and Children Hospital, Nanjing Medical University, Wuxi, China
3The Hospital of Obstetrics and Gynaecology, Fudan University, Shanghai, China
4Centre for Reproductive Medicine, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, China
5Department of Obstetrics and Gynaecology, The University of Auckland, Auckland, New Zealand
*These authors contributed equally to this work
Qi Chen, email: [email protected]
Keywords: endometrial cancer, GPR30, estrogen receptor, menopause, type 1 and type 2
Received: February 13, 2017 Accepted: June 04, 2017 Published: June 17, 2017
It is well-known that the clinical outcomes are different between type 1 (estrogen dependent) and type 2 (estrogen independent) endometrial cancer. Studies have suggested that the estrogen receptor (ER) is positively correlated with endometrial cancer survival, however we previously reported that there is no difference in the positivity of ER as well as sex hormone levels between subtypes of cancer. G-protein-coupled receptor-30 (GPR 30), an alternative estrogen receptor has been suggested to be negatively correlated with clinical outcomes of endometrial cancer. In this study we investigated whether the positivity of GPR30 is different between subtypes of cancer. The immunostaining of GPR30 and ER was examined and analysed in 128 cases taking into account menopausal status. Overall, 105 (82%) cases were GPR30 positive and 118 (92%) cases were ER positive. The positivity of GPR30 in type 1 endometrial cancer (83%) was not statistically different to type 2 endometrial cancer (78%). In addition, intensity of immunostaining of GPR30 in type 1 endometrial cancer was also not different to type 2 endometrial cancer quantified by semi-quantitative analysis (p = 0.268). Menopausal status was not associated with the positivity of GPR30 in both type 1 and type 2 endometrial cancer. Furthermore, the positivity and intensity of immunostaining of GPR30 were not correlated with the positivity and intensity of immunostaining of ER in endometrial cancer (p = 0.689). Our data further confirm that type 2 endometrial cancer may not be completely estrogen independent, and suggest that type 1 and type 2 endometrial cancer may have similar pathogenesis.
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