In this study, we evaluated the expression of SHP-1 (PTPN6) in endometrioid (Ec) and serous (Sc) subtypes of endometrial carcinoma by immunohistochemical analysis. In total, 114 patients with Ec carcinoma and 48 patients with Sc carcinoma were enrolled in this study. The correlation between the type of histology, the grade of tumor, the stage of development, and immunoreactivity to SHP-1 was evaluated. Kaplan-Meier and multivariate survival analyses, using a Cox regression model, were performed to establish whether this marker has prognostic value in these malignancies, on the basis of follow-up and stratification of the patients according to their SHP-1 immunoreactivity. A significantly higher SHP-1 expression was observed in the Ec group compared with the Sc group (P=0.0005, Fisher exact test). In the Ec group, SHP-1 immunoreactivity was correlated with grading, demonstrating that more differentiated lesions expressed SHP-1 more frequently than less differentiated neoplasms (G1 vs. G2, P=0.0243, statistically significant value, Fisher exact test; G1 vs. G3, P=0.0088, extremely significant value, Fisher exact test). Instead, in the Sc group, SHP-1 expression was not correlated with grading, as Sc is now defined as a high-grade carcinoma. SHP-1 expression did not change with neoplastic progression in Ec and Sc groups. From both univariate and multivariate analysis in the Ec group, expression of SHP-1 remained a positive prognostic factor (P=0.004, log-rank test) [HR=0.32 (0.11 to 0.94), P=0.039]. In contrast, in the Sc group, no correlation between SHP-1 expression and survival was noted (P=0.77, log-rank test). In this study, we observed that the absence of SHP-1 in immunohistochemical analysis might serve as a marker of poor prognosis for a subset of high-grade endometrial cancer.
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http://dx.doi.org/10.1097/PAI.0000000000000456 | DOI Listing |
Chemosphere
January 2025
Department of Pharmacology/Toxicology, School of Medicine, Daegu Catholic University, Daegu, Republic of Korea. Electronic address:
Perfluorooctane sulfonate (PFOS), a widely distributed and persistent organic pollutant, is known to cause immune dysfunction. In a previous study, we reported that PFOS modestly increases mast cell activation. However, its effects on FcεRI (a high-affinity IgE receptor)-mediated mast cell activation, a pivotal process in inflammatory allergic reactions and innate immunity, have not been clearly demonstrated.
View Article and Find Full Text PDFCancer Cell
January 2025
Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. Electronic address:
Disseminated cancer cells in the peritoneal fluid often colonize omental fat-associated lymphoid clusters but the mechanisms are unclear. Here, we identify that innate-like B cells accumulate in the omentum of mice and women with early-stage ovarian cancer concomitantly with the extrusion of chromatin fibers by neutrophils called neutrophil extracellular traps (NETs). Studies using genetically modified NET-deficient mice, pharmacologic inhibition of NETs, and adoptive B cell transfer show that NETs induce expression of the chemoattractant CXCL13 in the pre-metastatic omentum, stimulating recruitment of peritoneal innate-like B cells that in turn promote expansion of regulatory T cells and omental metastasis through producing interleukin (IL)-10.
View Article and Find Full Text PDFInt J Biol Sci
December 2024
Liver Research Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan.
Pseudogene-derived long non-coding RNAs (lncRNAs) have become crucial regulators in cancer progression. Extensive research highlights the pivotal role of signal transducer and activator of transcription 3 (STAT3) in promoting hepatocellular carcinoma (HCC) progression. As a result, targeting aberrant STAT3 activation presents a promising therapeutic strategy for HCC.
View Article and Find Full Text PDFCurr Diabetes Rev
December 2024
Department of Medical Physiology, School of Medicine, Neyshabur University of Medical Sciences, Neyshabur, Iran.
Chrysin, a flavone nutraceutical, possesses several beneficial pharmacological properties, which has gained much emphasis in recent years. The biological effects of chrysin are exerted due to impeding or activating multifarious cellular and molecular pathways. Our findings indicated that chrysin inhibited tumor progression in various cancer cell lines by repressing the formation of a sphere and upregulated protein expression of Src homology region 2 domain-containing phosphatase-1 (SHP-1), alleviating phosphorylated-signal transducer and activator of transcription 3 (p-STAT3) and transaction workflow innovation standards team1 (Twist1), sustaining phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and endorsing mitogen-activated protein kinase kinase1 (MEK1) overexpression, increasing the cytochrome c release, mitochondrial reactive oxygen species (ROS) formation, matrix metalloproteinases (MMP) collapse, and caspase-3 activity, modulating p53/ B-cell lymphoma-2 (Bcl-2)/caspase-9 cascade, cyclooxygenase- 2 (COX-2), nuclear factor kappa B proposition 65 (NF-kB p65) expression and also decreasing the expression of nuclear factor erythroid 2-related factor 2 (Nrf2).
View Article and Find Full Text PDFShock
December 2024
Institute of Clinical and Experimental Trauma-Immunology, University Medical Center Ulm, Ulm, Germany.
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