CD73 is a glycosylphosphatidylinositol (GPI) anchored cell surface protein that is encoded by NT5E gene, plays multiple roles in tumor processes. Previous studies have presented a potential value of CD73 served as a detectable biomarker for prognosis of several solid tumors, but the results were more controversially. A comprehensive meta-analysis was conducted to precisely evaluate the prognostic role of CD73 in solid tumors. The included studies were searched in PubMed, Web of Science and EBSCO from Jan 1990 to Jan 2016. Pooled hazard ratios (HR) and corresponding 95% confidence intervals (CI) for overall survival (OS), disease free survival (DFS) were carried out using a fixed or random effects model. Totally, 13 studies about 12,533 patients were included. CD73-high expression was correlating with poor OS (pooled HR = 1.28, 95% CI = 1.19-1.37). In addition, CD73 expression had borderline association with worse DFS (pooled HR = 1.28, 95% CI = 1.01-1.62). Egger's tests indicated that there was no evidence of significant publication bias. CD73 is an efficient prognostic biomarker in solid tumors, and over-expression of CD73 is associated with inverse OS or DFS. But this predictive value and target therapy for clinical practice yet needs advanced research.
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http://dx.doi.org/10.18632/oncotarget.16905 | DOI Listing |
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Cancer Gene Therapy Group, Translational Immunology Research Program, University of Helsinki, Helsinki, Finland
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Department of chemistry-College of Science- Mustansiriyah University, Baghdad. Electronic address:
Polycystic ovarian syndrome (PCOS) is a low-grade and chronic inflammation defined by irregular hormonal status that primarily triggers females in their reproductive age. Multi cysts are a primary manifestation of PCOS; a high level of androgen production characterizes the condition via ovaries. Rheumatoid arthritis (RA) is a chronic, systemic, and symmetrical inflammatory autoimmune disease that affects 1-2% of adults.
View Article and Find Full Text PDFPharmacol Res
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Cancer Institute, Xuzhou Medical University, 209 Tongshan Road, Xuzhou, Jiangsu, 221004, China; Center of Clinical Oncology, the Affiliated Hospital of Xuzhou Medical University, 99 West Huaihai Road, Xuzhou, Jiangsu 221002, China; Jiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Cancer Institute, Xuzhou Medical University, 209 Tongshan Road, Xuzhou, Jiangsu, 221004, China. Electronic address:
JCO Precis Oncol
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McGill University Faculty of Medicine, Montréal, QC, Canada.
Purpose: MAP2K1/MEK1 mutations are potentially actionable drivers in cancer. MAP2K1 mutations have been functionally classified into three groups according to their dependency on upstream RAS/RAF signaling. However, the clinical efficacy of mitogen-activated protein kinase (MAPK) pathway inhibitors (MAPKi) for MAP2K1-mutant tumors is not well defined.
View Article and Find Full Text PDFJAMA
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CRIMM, Center Research and Innovation of Myeloproliferative Neoplasms, University of Florence, AOU Careggi, Florence, Italy.
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