Polish Journal of Pathology最新文献

It has been reported that mismatch repair deficient (d-MMR) tumors show sensitivity to immune checkpoint inhibitors. We aimed to evaluate the correlation of d-MMR and PD-1/PD-L1 expression in invasive urothelial carcinoma of the bladder. Tissue microarray (TMA) tissues were stained PD-1/PD-L1 and MMR proteins. The expression ratio of these markers has been compared with histopathologic parameters. d-MMR tumors were more superficial muscle invasive (p = 0.012). When the d-MMR, and PD-1/PD-L1 expression ratios were examined, a significant correlation was obtained between the d-MMR and PD-L1 expression ratio of > 5% in both the tumor and immune cells (p = 0.02 and p = 0.004, respectively). The expression ratio was higher in the patients without MMR loss. PD-1 and PD-L1expression in those with MSH6 loss was one or none. When PD1/PDL1 expression was compared with histopathological parameters, a significant relationship was observed between tumor grade and depth of muscle invasion. PD-L1 expression was not observed in the superficial muscle invasive tumors. This study was shown the status of d-MMR and PD-1/PD-L1 in invasive urothelial cancers and their correlation with prognostic markers. PD-1/PD-L1 expression may contribute to the progression and poor prognosis of bladder cancer. However, further studies are required to research the clinical utility.

It has been demonstrated in many studies that angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism is related to Henoch-Schonlein purpura nephritis (HSPN) risk in children. However, this conclusion remains controversial. In this study, we systemically retrieved relevant studies in electronic databases such as PUBMED, CNKI, and EMBASE followed by calculation of odds ratios (OR) with 95% confidence intervals (CI). In addition, meta-package in STATA version 12.0 was used. Angiotensin-converting enzyme I/D polymorphism was related to HSPN susceptibility in children (D vs. I: OR 1.47, 95% CI: 1.13-1.93; DD vs. II: OR 2.29, 95% CI: 1.29-4.07; DI vs. II: OR 1.10, 95% CI: 0.82-1.48; dominant model: OR 1.44, 95% CI: 1.09-1.89; recessive model: OR 2.26, 95% CI: 1.67-3.06). In addition, subgroup analysis stratified according to ethnicity indicated a significant relationship between this polymorphism and HSPN susceptibility among Asians and Caucasians. The data extracted from HaploReg indicated that ACE I/D polymorphism was not in linkage disequilibrium with other variants in the ACE gene. The research shows that ACE I/D polymorphism is related to HSPN susceptibility in children.

The aim of this study is to make a differential diagnosis and prognosis of the ampullary adenocarcinoma subtypes. We also investigated the role of prognostic markers PD-1 and PD-L1, and epidermal growth factor receptor (EGFR). Local or locally advanced stage ampullary adenocarcinoma patients who had undergone pancreaticoduodenectomy at the time of diagnosis were included. MUC1, MUC2, MUC5AC, CDX2, CK7, CK20, PD-1, and PDL-1 were analysed immunohistochemically, and EGFR was analysed by real-time polymerase chain reaction. According to histopathological and immunohistochemical evaluation, we found 27 patients as pancreatobiliary type and 56 patients as intestinal type adenocarcinoma. The median survival of patients with intestinal and pancreatobiliary type adenocarcinoma was 23 months and 76 months ( p = 0.201), respectively. When the survival of PD1-positive ( n = 23) and PD-L1-positive ( n = 18) patients were compared with the patients with negative staining ( n = 60, n = 65), no significant difference was found. Epidermal growth factor receptor mutation was detected in a total of 6 patients, and 5 of these 6 mutations were shown in intestinal type tumours and one in a pancreatobiliary type tumour. A significant difference was determined in terms of overall survival for the patients with EGFR mutations compared to those without ( p = 0.008). In conclusion, we could reveal the prognostic significance of EGFR mutation, which is also a target molecule.

Acute leukaemia (AL) is a heterogeneous neoplastic disease that occurs by the growth of abnormal lymphoid and myeloid cells in the bone marrow and blood leading to acute myeloid leukaemia (AML) and acute lymphocytic leukaemia (ALL). Conventional cytogenetics is a characteristic technique to hunch chromosomal abnormalities, it helps in the diagnosis and therapeutic approach of the disease by the molecular cytogenetics technique of fluorescence in situ hybridization (FISH). Chromosomal abnormalities in AL are performed by karyotyping to confirm specific chromosomal abnormalities using FISH. The descriptive study included 42 clinically diagnosed AL patients. Karyotyping analysis was performed using the standard Giemsa banding procedure. To confirm specific chromosomal abnormalities and all culture failure (CF) cases, FISH was done. Among 42 cases, 29 (69.4%) males and 13 (30.9%) females, AML comprised 22 (52.38%) cases, ALL 14 (33.33%) cases, and AL 6 (14.2%) cases. Normal karyotype was found in 18 (42.85%), abnormal karyotype in 16 (39.09%), and 8 (19.09%) were CF. Specific abnormalities of t(15;17), hyperdiploidy; t(3;3) with monosomy 7 in; del(9q22); del(2p); del(17p); del(Xq); 1~2 dmin; der(3); +11, +13 and composite karyotype. Hypodiploidy was strongly associated with AL, which signifies the loss of chromosomes causing potential risk. Composite karyotype, rare t(3;3) double minutes, +11,+13, del(9q), and del(Xq) were the novel findings reported in the South Canara region of Karnataka. Despite other molecular techniques, conventional cytogenetics remains the baseline in the diagnosis of malignancies.

The aim of this study was to investigate the prognostic value of inscuteable spindle orientation adaptor protein (INSC) in colon cancer (CC). Firstly, transcriptional change of INSC was analysed using the data from public databases. Next, INSC protein expression was assessed by immunohistochemistry. Its correlation with clinicopathological features and the prognostic values of patients were also investigated. Then, an INSC-based nomogram was built to predict CC prognosis. Compared to normal tissues, INSC was significantly downregulated at the transcriptional level in CC tissues. A low INSC mRNA level not only positively correlated with TNM stage (tumour-nodus-metastases), advanced T stage, and N stage, but also with the shorter 5- and 8-year overall survival (OS) and disease-specific survival. Concerning protein level, INSC downregulation was confirmed in CC samples. In terms of the correlation with N stage and 5- and 8-year OS, it was also consistent with mRNA levels. Cox regression analysis indicated that INSC protein expression was an independent prognostic factor for OS. The nomogram showed better prognostic accuracy and clinical net benefit for 5-year OS than TNM staging. Altogether, downregulation of INSC is related to inferior clinicopathological features and patient outcomes, and it may be a novel independent prognostic biomarker in CC.

Single-minded homolog 2 (SIM2) has been identified as a potential contributor to the development of solid tumors. Despite this, there is a lack of comprehensive research regarding its biological role and underlying mechanism within pancreatic cancer (PC), as well as its prognostic impact. This study systematically evaluated the expression level and clinical significance of SIM2 in patients with PC using various databases, including The Cancer Genome Atlas, KM Plotter, and gene expression profiling interactive analysis. To investigate the relationship between SIM2 expression and immune cell infiltration, we conducted ESTIMATE and single-sample gene set enrichment analysis (ssGSEA) analyses. Single-minded homolog 2 was up-regulated in patients with PC. Pancreatic cancer patients with higher SIM2 expression had poorer overall survival rates. Gene set enrichment analysis results suggested that SIM2 may have a significant impact on the progression of PC and the regulation of immune responses. According to the ssGSEA algorithm, SIM2 has a negative correlation with the levels of infiltrating TFH, mast cells, and pDC. Our study demonstrated that SIM2 serves as a biomarker, and is associated with both prognosis and immune infiltration in PC. This provides a solid foundation for future investigations into the precise role of SIM2 in the carcinogenesis and progression of PC.

This study aims to determine the prognostic significance of programmed cell death ligand 1 (PD-L1) expression and tumour-infiltrating lymphocytes (TILs) in triple- negative breast cancer (TNBC). PD-L1 expression and TIL percentage were determined in TNBCs that did not receive neoadjuvant therapy. The relationship between PD-L1 expression and the percentage of TILs with survival was investigated. The presence of intratumoural PD-L1-positive tumour-infiltrating immune cells (TIICs) in tumours with ≥ 1% PD-L1 expression was identified as a new PD-L1 evaluation parameter. The presence of intratumoural PD-L1-positive TIICs as a new parameter in PD-L1-positive cases increased overall survival. The percentage of TILs increased in both overall and distant metastasis-free survival (p = 0.040 and p = 0.006, respectively). As a result, it was found that the risk of death was increased 5.18-fold (p = 0.013) in patients without intratumoural PD-L1-positive TIICs. This risk of death was calculated to be 5.40-fold higher in patients with TIL percentage ≤ 10% than in those with > 40% (p = 0.024), and the risk of distant metastasis was calculated to be 11.95 times higher. In our study, we discovered that the percentage of TILs made a statistically significant difference in TNBC survival. The presence of intratumoural PD-L1-positive TIICs in PD-L1-positive cases significantly increased survival.

Recent studies revealed that programmed cell death ligand 1 (PD-L1) expression was associated with unfavorable prognosis in various solid tumors, but its clinical relevance for pancreatic cancer has not yet been well established. This meta-analysis summarizes the potential prognostic value of PD-L1 in pancreatic cancer. A quantitative meta-analysis was performed by a systematic search of databases including PubMed, EMBASE, Web of Science, Cochrane library, Scopus and Ovid for eligible studies on the prognostic significance of PD-L1 in pancreatic cancer patients. Pooled hazard ratios (HRs) and their 95% confidence intervals (CIs) were calculated to evaluate the strength of the link between PD-L1 expression and clinical prognosis of patients. Seventeen eligible studies with 2669 patients were included in our study. A significant association was observed between PD-L1 abundance and poor overall survival (OS) of patients with pancreatic cancers, with a pooled hazard ratio (HR) of 1.902, 95% CI: 1.657-2.184. Sensitivity analysis confirmed the reliability of our results. Subgroup analysis shows that differences in regions and detection methods of PD-L1 did not change the overall predictive value of PD-L1 for poor prognosis in pancreatic cancer patients. This meta-analysis indicated that the expression of PD-L1 is associated with a worse OS in pancreatic cancer patients. Additionally, PD-L1 may act as a potential parameter for predicting poor prognosis and thus providing a promising target for anticancer therapy in pancreatic cancer.

Aim of the study: Aim of the study is To investigate the effect of lentinan on proliferation and apoptosis of human astrocytoma U251 cells. Lentinan was dissolved in DMEM complete medium to form different concentrations (0, 25, 50, 100, 200, 400, 500, 600 µg/ml). CCK8 was used to detect the effect of lentinan with different concentrations on proliferation of human astrocytoma U251 cells, and the expression of Ki-67 was detected by immunofluorescence. In addition, the effect of different concentrations of lentinan on apoptosis of human astrocytoma U251 cells was detected by flow cytometry. Compared with the blank control group, 50 and 100 µg/ml lentinan significantly promoted proliferation of human astrocytoma U251 cells. When the concentration is more than 100 µg/ml, the cell activity gradually decreases, and the cell activity is the lowest when the concentration is 600 µg/ml. In addition, the low concentration lentinan (25, 50, and 100 µg/ml) had no significant effect on apoptosis of human astrocytoma U251 cells. However, lentinan above 200 µg/ml significantly promoted apoptosis of human astrocytoma U251 cells and had a concentration gradient effect, and the highest apoptosis rate was at 600 µg/ml.

Conclusions: Lentinan can effectively inhibit proliferation and promote apoptosis of human astrocytoma U251 cells.