Objective: To evaluate the levels of bone morphogenetic protein-15 (BMP-15) in human follicular fluid (FF) and its association with response to ovarian stimulation.
Methods: Western blotting was performed to determine the levels of BMP-15 in FF obtained from follicle aspirates in 70 patients undergoing IVF treatment. According to the response to ovarian stimulation the patients were divided into poor responder group and normal responder group.
Result: BMP-15 levels in FF of poor responders were significantly higher than those in normal responders (1.01 +/- 0.34 vs 0.77 +/- 0.24, P<0.01).
Conclusion: Increased levels of BMP-15 in FF may be associated with poor response to ovarian stimulation.
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http://dx.doi.org/10.3785/j.issn.1008-9292.2007.05.005 | DOI Listing |
Front Immunol
January 2025
Sahlgrenska Center for Cancer Research, University of Gothenburg, Gothenburg, Sweden.
Introduction: Ovarian cancer is a lethal disease with low survival rates for women diagnosed in advanced stages. Current cancer immunotherapies are not efficient in ovarian cancer, and there is therefore a significant need for novel treatment options. The β-galactoside-binding lectin, Galectin-3, is involved in different immune processes and has been associated with poor outcome in various cancer diagnoses.
View Article and Find Full Text PDFFront Oncol
December 2024
Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
fusion is one of the classes of emerging therapeutic targets of precision oncology and is observed in many solid tumor types. Our understanding of oncogenic mechanisms and therapy effects of molecular targets tends to reflect those occurring in overrepresented tumor types, posing a challenge in therapy planning of the same targets occurring in unusual tumor types. We present a case of a primary high-grade serous tubo-ovarian carcinoma with a novel fusion, an exceedingly rare combination of tumor type and fusion class, with an unusually short-lived response to futibatinib.
View Article and Find Full Text PDFiScience
December 2024
Department Gynecological Oncology, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, Affiliated Cancer Hospital of University of Electronic Science and Technology of China, Chengdu 610041, China.
Reprogramming tryptophan metabolism (TRP) may be able to overcome immunosuppression and restore the immune checkpoint blockade (ICB) response in patients with epithelial ovarian cancer (EOC) resistant to ICB therapy because TRP metabolism is involved in the kynurenine/indole and serotonin pathways of tryptophan metabolism. Herein, employing amitriptyline (AMI), an antagonist of TLR4 and serotonin transporter (SERT), we revealed that AMI remodels the immunological landscape of EOC. In particular, AMI lowered the expression of IDO1, IL-4I1, and PD-L1, the quantity of KYN and indoles, and the level of immunosuppressive immune cells MDSC, Tregs, and CD8CD39+/PD-1+ T cell.
View Article and Find Full Text PDFJ Control Release
January 2025
Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, People's Republic of China. Electronic address:
Ovarian cancer (OC) is a highly malignant gynecological tumor, and its effective treatment is frequently impeded by drug resistance and recurrent tumor growth. The reprogramming of glutamine metabolism in ovarian cancer is closely associated with tumor progression and the immunosuppressive tumor microenvironment. Recently, targeting metabolic reprogramming has emerged as a promising approach for cancer therapy.
View Article and Find Full Text PDFNPJ Precis Oncol
January 2025
Zentalis Pharmaceuticals, Inc., San Diego, CA, USA.
Upregulation of Cyclin E1 and subsequent activation of CDK2 accelerates cell cycle progression from G1 to S phase and is a common oncogenic driver in gynecological malignancies. WEE1 kinase counteracts the effects of Cyclin E1/CDK2 activation by regulating multiple cell cycle checkpoints. Here we characterized the relationship between Cyclin E1/CDK2 activation and sensitivity to the selective WEE1 inhibitor azenosertib.
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