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Many pathological characteristics have utility for predicting prognosis in colorectal carcinoma (CRC). Some of the most important include tumor stage (TS), lymph node status (LNS) and tumor budding (TB). Tumor budding is a phenomenon originally described in 1949 as sprouting. TB assessment is not always reliable however, as it is subject to high inter-observer variation. This finding persists despite the current trends for sub-specialty training in surgical pathology. In light of this, new and reproducible histological prognostic markers could change the way we diagnose and manage patients with colorectal carcinoma. Studies have shown that desmoplastic reaction (DR) categorization can actually outperform other conventional prognostic factors, including tumor budding and tumor stage in predicting disease-free survival (DFS). Our study aimed to evaluate and assess the prognostic value of desmoplastic reaction in an American cohort with colorectal cancer using 3 different stromal classification scoring systems. In all three stromal grading systems, immature stroma was the most significant independent prognostic factor in CRC. Currently, none of the reporting protocols for the College of American Pathologists, the Royal College of Pathologists of the United Kingdom, and the Japanese Society for Cancer report on the presence of immature stroma. Importantly, regarding the ability to predict survival outcomes, our novel classification system has the potential to outperform other scoring methodologies.Human Herpesvirus 8 (HHV8) has been associated with a wide spectrum of B-cell lymphoproliferative disorders, including Primary Effusion Lymphoma, Multicentric Castleman Disease, HHV8-positive Diffuse Large B-cell Lymphoma, not otherwise specified and germinotropic lymphoproliferative disorder. The association of different HHV8-related lymphoproliferative disorders is described in immunodeficient patients. We report a case of Primary Effusion Lymphoma metachronous to Multicentric Castleman Disease in an immunocompetent patient.Objective Integrin αvβ6 is associated with an extremely aggressive cancer phenotype. However, little is known about the clinicopathological significance and prognostic value of integrin αvβ6 in human hilar cholangiocarcinoma. Methods In the present study, bioinformatics analysis demonstrated a significant increase of integrin β6 gene expression in cholangiocarcinoma tissues compared to non-tumorous tissues, which was further validated in clinical samples through RT-qPCR and western blotting analyses. Integrin αvβ6 was observed to be expressed in 48.6% of tumors, and its expression was related to a poor tumor differentiation (p = 0.002), lymph node metastasis (p less then 0.001) and advanced TNM stage (p=0.001). Furthermore, patients who were αvβ6-positive showed a significantly shorter overall survival period than those who were αvβ6-negative (p=0.004). Multivariate analysis confirmed that integrin αvβ6 was an independent prognostic factor (p=0.002). In addition, loss- and gain-of-function assays showed integrin αvβ6 not only played an important role in colony formation, but also protected cholangiocarcinoma cells from cisplatin-induced growth inhibition and apoptosis. ERK/MAPK signaling pathway was involved in integrin αvβ6-mediated resistance of cholangiocarcinoma cells to cisplatin. Conclusions Taken together, the present findings revealed that integrin αvβ6 could serve as a potential prognostic predictor and contribute to cisplatin resistance, which might prove to be a promising target candidate for the clinical intervention of human hilar cholangiocarcinoma.Aims The expression of glucose-related protein 94 (GRP94), a member of the heat shock protein 90 family, was correlated with a variety of clinicopathological factors and patient survival in a large colorectal cancer (CRC) cohort. We aimed to elucidate the role of GRP94 in the prognosis of CRC patients. Methods Tissue microarray blocks were generated from 709 CRC samples and immunohistochemically stained for GRP94. Results Of the 709 tumours, 164 (23.1%) and 545 (76.9%) were classified in the low and high expression groups, respectively. GRP94 expression was high in CRC cases with larger tumours (p = 0.005) and advanced pT stage (p = 0.021). GRP94 expression was higher in females than males (p = 0.024). In univariate and multivariate survival analyses, high GRP94 expression was unexpectedly associated with better overall survival in CRC patients younger than 65 years of age (p = 0.001) CONCLUSION Our conflicting results indicate that GRP94 has the ability to switch between oncogenic and tumour-suppressive roles depending on the conditions and microenvironment of the tumour cells. Furthermore, GRP94 could be a candidate biomarker to predict better prognosis in CRC patients.Background Cervical cancer is among the most aggressive gynecological tumors and is a consequence of interactions between genetic and epigenetic factors. Several genetic polymorphisms related to cervical cancer have been reported in previous clinical studies. In this study, we aimed to explore the possible relationship between polymorphisms of the ANGPTL4 gene locus and susceptibility to cervical cancer. Methods We investigated the relationship between a single nucleotide polymorphism (SNP) in the ANPGTL4 gene (rs116843064) and risk of cervical cancer in a total of 378 individuals with (n = 151), or without (n = 227) cancer. DNA was extracted, and genotyped using a Taq-Man based real time PCR. Results The ANPGTL4 polymorphism was found to be associated with an increased risk of developing cervical neoplasia using dominant model (OR = 12.48, CI = 4.9-31.82, p less then 0.0001) and additive model (OR = 30.54, CI = 7.35-126.89, p less then 0.0001). this website Conclusion Our results indicate that there is a strong association between ANPGTL4 and the susceptibility for cervical cancer suggesting that it is a potential risk factor for cervical neoplasia.Metastasis is a complex process which contributes to the dissemination of cancer cells to other organs and forms new tumor sites. The proliferation of tumor cells is a necessary step for the initiation and progression of cancers and is associated with the formation of new vessels. In the latter stages of metastasis, cancer cells may spread into the extracellular matrix and may form metastatic nodules. Despite efforts to prevent this, effective therapies are limited in the treatment of some malignancies. Among the different tumor properties which could be usefully employed as a cancer target, metastasis may be one suitable target. The renin- angiotensin system is a physiological pathway that contributes to the proliferation of tumor cells, angiogenesis and the inflammatory response in tumor tissue. Angiotensin II (ANGII), a key peptide of this pathway, induces cell proliferation through the activation of two cellular pathways (mitogen-activated protein kinase (MAPK)-STAT3 and phosphoinositide 3-kinase (PI3K) -AKT pathway).