GPR30: a novel indicator of poor survival for endometrial carcinoma

Smith, Harriet O.; Leslie, Kimberly K.; Singh, Meenakshi; Qualls, Clifford; Revankar, Chetana M.; Joste, Nancy E.; Prossnitz, Eric R.

doi:10.1016/j.ajog.2007.01.004

Cited by 188 publications

(198 citation statements)

References 23 publications

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“…In this study, GPR30 expression was found in both Ishikawa and KLE cell lines, and ER-negative KLE cells showed a stonger expression of GRP30 than ER-positive Ishikawa cells. This is consistent with the finding that GRP30 expession is inversely correlated with the ER status (25,26).…”

Section: Gpr30-pi3k/akt Signaling In Regulation Of Proliferation In Nsupporting

confidence: 82%

“…Therefore, research has focused on GPR30 signaling. In a previous study, it was confirmed that overexpression of GPR30 more frequently occurred in endometrial tumors with deep myometrial invasion, high-grade, biologically aggressive histological subtypes, and advanced stage, and elevated GRP30 protein in tumors strongly associated with poor survival (25). In this study, GPR30 expression was found in both Ishikawa and KLE cell lines, and ER-negative KLE cells showed a stonger expression of GRP30 than ER-positive Ishikawa cells.…”

Section: Gpr30-pi3k/akt Signaling In Regulation Of Proliferation In Nsupporting

confidence: 58%

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Nuclear estrogen receptor-mediated Notch signaling and GPR30-mediated PI3K/AKT signaling in the regulation of endometrial cancer cell proliferation

Zhang

Liao³

et al. 2011

Oncol Rep

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Section: Gpr30-pi3k/akt Signaling In Regulation Of Proliferation In Nsupporting

confidence: 82%

Section: Gpr30-pi3k/akt Signaling In Regulation Of Proliferation In Nsupporting

confidence: 58%

Nuclear estrogen receptor-mediated Notch signaling and GPR30-mediated PI3K/AKT signaling in the regulation of endometrial cancer cell proliferation

Zhang

Liao³

et al. 2011

Oncol Rep

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“…Surprisingly, a member of the GPCR family, GPR30/GPER, was recently shown to mediate the multifaceted actions of estrogens in different tissues including cancer cells [135] . Importantly, GPER overexpression was associated with lower survival rates in endometrial and ovarian cancer patients and with an elevated risk of developing metastases in patients with breast cancer [136][137][138] . GPER by transactivating EGFR triggers numerous transduction pathways including the intracellular cAMP, calcium mobilization, MAPK, PI3-K and phospholipase C activation in a variety of cell types [139] .…”

Section: Gpcrs Activated By Hormonesmentioning

confidence: 99%

GPCRs and cancer

Lappano

2012

Acta Pharmacol Sin

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G-protein-coupled receptors (GPCRs), which represent the largest gene family in the human genome, play a crucial role in multiple physiological functions as well as in tumor growth and metastasis. For instance, various molecules like hormones, lipids, peptides and neurotransmitters exert their biological effects by binding to these seven-transmembrane receptors coupled to heterotrimeric G-proteins, which are highly specialized transducers able to modulate diverse signaling pathways. Furthermore, numerous responses mediated by GPCRs are not dependent on a single biochemical route, but result from the integration of an intricate network of transduction cascades involved in many physiological activities and tumor development. This review highlights the emerging information on the various responses mediated by a selected choice of GPCRs and the molecular mechanisms by which these receptors exert a primary action in cancer progression. These findings provide a broad overview on the biological activity elicited by GPCRs in tumor cells and contribute to the identification of novel pharmacological approaches for cancer patients.

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“…[20][21][22] Recent advances in molecular biology have led to the identification of biomarkers that can be used to allow accurate identification of high risk endometrial carcinomas preoperatively. 23,24 Biomarkers that can assist pathologists in distinguishing between endometrial cancer, atypical endometrial hyperplasia, and benign forms of hyperplasia (simple hyperplasia and complex hyperplasia without atypia) have also been found. One example is GLUT-1, a facilitative glucose transporter found in a wide variety of cells including endometrial.…”

Section: Discussionmentioning

confidence: 99%

Significance of Concurrent Endometrial Cancer in Women With a Preoperative Diagnosis of Atypical Endometrial Hyperplasia

Giede

Yen

Chibbar

et al. 2008

Journal of Obstetrics and Gynaecology Canada

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Objectives-Our objectives were (1) to review the rate of concurrent endometrial cancer in patients with a preoperative diagnosis of atypical endometrial hyperplasia (AEH); (2) to determine the proportion of patients with concurrent endometrial cancer who have high-risk disease; and (3) to re-evaluate our surgical management of AEH.Methods-We performed a retrospective chart review of all patients who had surgery on the basis of a preoperative diagnosis of atypical endometrial hyperplasia between January 2001 and December 2006. Demographic data, the method of preoperative diagnosis, postoperative grade of tumour, and other postoperative findings were recorded. When applicable, this included cancer stage, lymph node status, and presence of lymphovascular space invasion. In postoperative review, patients were considered to be high risk if they had disease beyond the uterus or a combination of other risk factors.Results-Of 70 patients, 25 (35.7%) were found to have concurrent endometrial cancer. This was higher than the commonly accepted rate of 25% (P = 0.03). Of the 25 patients upgraded, 4 (16%) had high-risk cancer on final pathologic evaluation.Conclusion-Simple hysterectomy in women with AEH may result in inadequate surgical management. Simple methods are required to identify patients with a preoperative diagnosis of AEH who may harbour significant cancers.

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GPR30: a novel indicator of poor survival for endometrial carcinoma

Cited by 188 publications

References 23 publications

Nuclear estrogen receptor-mediated Notch signaling and GPR30-mediated PI3K/AKT signaling in the regulation of endometrial cancer cell proliferation

Nuclear estrogen receptor-mediated Notch signaling and GPR30-mediated PI3K/AKT signaling in the regulation of endometrial cancer cell proliferation

GPCRs and cancer

Significance of Concurrent Endometrial Cancer in Women With a Preoperative Diagnosis of Atypical Endometrial Hyperplasia

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