Introduction: The significance of tumor budding and programmed death ligand 1 (PD-L1) has not been established in gastric adenocarcinoma (GAC). Objectives: This study evaluated tumor budding and PD-L1 expression with regard to tumor microenvironment, clinicopathologic parameters, and overall survival in GAC. Patients and Methods: Totally, 102 GAC cases were assessed immunohistochemically. The associations of tumor budding and PD-L1 with clinicopathologic features, tumor-infiltrating lymphocytes (TILs), tumor stroma percentage (TSP), and overall survival were analyzed. Results: High tumor budding (42.2% of cases) was correlated with distal tumor location, large tumor size, Helicobacter pylori infection, poor differentiation (P = 0.0008, 0.033, 0.011, and 0.005, respectively), lymphovascular invasion, high tumor and nodal stages, and TSP (all P < 0.0001). Tumor budding was highest in the low TILs/high TSP group. PD-L1 expression (43.1% of cases) was correlated with proximal location (p = 0.00021), poor differentiation (P = 0.036), N stage (P = 0.049), high TILs (P < 0.0001), and low tumor budding (P = 0.002). PD-L1 expression was highest in the low tumor budding / high TILs category (P < 0.0001). Cox regression showed that high tumor budding (hazard ratio [HR]: 15.282, P = 0.024, 95% confidence interval [CI]: 1.441–162.069) and positive PD-L1 (HR: 7.502, P = 0.015, 95% CI: 1.469–38.31) were independent prognostic factors for overall survival. Conclusion: Tumor budding is correlated with poor prognostic parameters, whereas PD-L1 expression is inversely correlated with tumor budding. Both are independent predictors of short overall survival. Anti-PD-L1 immunotherapy could be effective in GAC with nodal metastasis, especially cases with high TILs and low tumor budding.
Background Meningiomas are the most common intracranial neoplasm together with gliomas; but unlike gliomas they are still graded according to their histopathological picture. Many growth factors and tyrosine kinase receptors have been studied in meningiomas in an attempt for prognostic stratification of patients, also to find a suitable targeted therapy for meningiomas. Aim of the study To correlate the immunohistochemical expression of HGF and cMET with the different WHO grades of meningioma in addition to brain invasion. Materials and methods This study included 60 cases of meningiomas (WHO grade I, n = 30 and WHO grade II & III, n = 30), brain invasion was present in 14 cases. Results HGF, cMET & HGF/cMET co-expression were positive in 60.0%, 65.0% and 58.3% respectively of the cases; WHO grade I meningioma showed positivity in 30.0%, 33.3% and 30.0% of the cases respectively in contrast with 90.0%, 96.7% and 86.7% of the cases of WHO grades II & III meningiomas respectively. The relation was statistically highly significant (p- value: <0.001). As regards cases with brain invasion the expression of HGF, cMET and HGF/cMET co-expression was found in 92.9%, 100.0% and 92.9% respectively in comparison with 50.0%, 54.3% and 47.8% in the rest of the cases of meningiomas respectively; the relation was statistically significant (p- value: 0.004). Conclusion The results suggest that HGF/cMET pathway may play a role in the progression of meningiomas from WHO grade I to higher grades II & III.
Background Systemic lupus erythematosus (SLE) is an immune-mediated disease, due to exposure of self-antigens, through impairment of apoptosis and failure of lymphocytic tolerance. Impaired regulation of the pro- and anti-apoptotic gene products which coordinate programmed cell death may result in autoreactive B and T cells and autoimmunity. Genetically engineered mice that over-express the anti-apoptotic molecule Bcl-2, B cell lymphoma 2 (Bcl2) in B-lymphocytes advance a lupus-like illness. Lupus nephritis (LN) is one of the most serious manifestations of this autoimmune disorder. Glomerulonephritis (GN) is caused by either impaired regulation of apoptosis and/or clearance of apoptotic cells leading to a T cell-mediated autoimmune reaction with initiation of pathological immune complex deposits. Objective To evaluate the correlation between Bcl2 glomerular and tubular expression and pathological findings and laboratory data in different types of SLE GN. Results Compared to the control group, patients with lupus nephritis have significantly higher glomerular, interstitial and tubular expression level (P value < 0.001). BCL2 expression was positively correlated with serum anti-ds-DNA, urine 24-h protein and with the chronicity index. All LN patients had significant glomerular, interstitial and tubular deposits of BCL2, P value < 0.001, P value 0.004, and P value 0.03, respectively. Conclusion The intrinsic pathway of apoptosis interferes not only with the pathogenesis of lupus glomerulonephritis but also interferes with the pathogenesis of tubulointerstitial lupus nephritis. tubulointerstitial lesions may not only be a result of glomerular injury but also a significant factor in lupus nephritis.
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