Polish Journal of Pathology最新文献

Each breast cancer is a heterogeneous tumour with different clinicopathological feature, and thus they all have different prognoses. Tumour budding (TB), considered as the first step in tumour metastasis, is the most critical factor for poor prognosis and is associated with the epithelial-mesenchymal transition (EMT). Tumour budding and its clinicopathological features in invasive breast carcinoma of no special type (NST). Patients who underwent surgery for invasive breast carcinoma (NST) between January 2018 and 2022 were retrospectively reviewed from the database, haematoxylin and eosin-stained slides were retrieved and reevaluated. The study included 200 patients. The mean number of TB was 12.8 ±9.6. The number of TB was significantly lower in patients who underwent neoadjuvant chemotherapy treatment ( p = 0.002). There was a weak positive correlation between TB count and tumour size ( r = 0.177). Triple-negative patients had significantly lower TB counts ( p = 0.001). No significant difference was observed between histological grade, nuclear grade, presence of ductal carcinoma in situ , stromal tumour-infiltrating lymphocytes, perineural invasion, lymph node metastasis, and number of TB ( p > 0.05). The number of TB was higher in oestrogen receptor positive tumours ( p = 0.015). There were more TB in patients with angiolymphatic invasion, which supports the pathophysiological relationship between tumour budding, metastasis, and EMT. Clarification of the mechanism of TB with more studies is promising in terms of treatment options.

Thyroid cancers are the most common endocrine organ cancers. Encapsulated follicular variant papillary thyroid carcinomas (EFVPTC) are quite slow (indolent). Non-invasive follicular thyroid neoplasm with papillary nuclear feature (NIFTP) is a new entity identified as a result of studies in recent years. If the patient instead of EFVPTC develops NIFTP, cancer will not be recognized and the treatment will change. Three groups, in which CD44, p53, Ki-67, p27, HBME-1, galectin-3, cytokeratin-19, CD56 were used as markers, were evaluated. Nuclear score assessment was also conducted in the NIFTP group. The results were compared with each other. Significant differences were detected in the intensities and percentages of CK19, HBME-1, CD56, CD44 staining and galectin-3 staining intensity. In group 1, cytokeratin-19, galectin-3, HBME-1 and CD44 expression were not as low as in the other groups, while CD56 staining was detected more frequently. p53, p27 and Ki-67 staining showed no obvious expression differences between the groups. The NIFTP group showed different IHC results compared to encapsulated invasive FVPTC and common invasive FVPTC. When evaluating whether the IHC expression patterns used in PTCs differ in NIFTP cases, it was found that CD44 could serve as an additional IHC stain that may guide pathologists during the diagnosis.

Mutations in the KRAS gene in non-small cell lung cancer (NSCLC) are common drivers. Gene expression and mutation data of NSCLC were collected from the TCGA dataset. DEGs between KRAS mutations and wild type were identified, and enrichment analysis was performed. The differences in immune cell infiltration between the 2 groups were evaluated using ssGSEA, and TIDE scoring, immune checkpoint therapy sensitivity, and drug treatment sensitivity analysis were performed. The expression of PD-L1 and CTLA-4 in tumour tissues was detected by western blot. CD8+PD-1 and CD8+CTLA-4 cells were detected by flow cytometry. The frequencies of KRAS-G12C, KRAS-G12V, and KRAS-G12D mutations were the highest. A total of 1323 DEGs were predominantly enriched in the PI3K-Akt signalling pathway, cell adhesion molecules, and metabolism of xenobiotics by cytochrome P450. Additionally, most immune cell infiltration levels in KRAS mutations were lower than in KRAS wild type. Sensitivity to immune checkpoint inhibitors and drug treatments increased in KRAS mutations. Western blot revealed significantly higher expressions of PD-L1 and CTLA-4 in KRAS mutations compared to KRAS wild type. The infiltration of CD8+PD-1+ T cells and CD8+CTLA-4+ T cells was higher in KRAS mutations than in KRAS wild type. KRAS-G12C, KRAS-G12V, and KRAS-G12D mutations may enhance NSCLC drug resistance through immunosuppression.

The IgG4-associated autoimmune hepatitis (IgG4-AIH) is a newly proposed disease entity characterised by the accumulation of the IgG4-expressing plasma cells in the liver. Its pathophysiology and clinical significance remain unclear and have poor evidence in the paediatric population. Thus, our study aims at comparing the group of paediatric patients with classical AIH and the IgG4-AIH. We carried out a retrospective analysis of 23 children (median age 8.5 years) diagnosed with AIH, who were compared according to the presence of IgG4-positive plasma cells in the liver biopsy. IgG4-AIH was defined if 10 or more IgG4 positive plasma cells/high-power field were found in the biopsy. The presence of the IgG4 component seems to be clinically insignificant. That is why, the conventional immunosuppressive protocol should be considered the standard treatment in the case of the IgG4-associated AIH.

Prostatic paraganglia (PP) can simulate adenocarcinoma's fused gland pattern, and a differential diagnostic panel is developed. Their differential diagnosis with benign prostatic lesions has been largely unreported. Intraprostatic adipose tissue (IPAT) is seen extremely rarely in prostatic specimens, but it must be known, to avoid false positive results for extraprostatic fat carcinomatous invasion in needle biopsy specimens.  We present one case from 100 randomly selected radical prostatectomy specimens in which our diagnosis evolved from IPAT to PP-hyperplasia, after additional immunohistochemical investigations. The presence of PP-hyperplasia, with both parenchymal and neurovascular bundle location, and its differential diagnosis with IPAT has not been previously reported.

The incidence and prevalence of neuroendocrine neoplasms (NENs) in many organs are increasing. Although such NENs have similar grades, they may exhibit quite different behaviors. In this multicenter study, we aimed to investigate the prevalence and distribution of different morphological NEN variants in the non-pancreatic gastrointestinal (GI) tract and determine whether they can guide prognosis prediction. Two hundred and fifty-six patients diagnosed with NENs originating from the GI tract from 7 different centers were included in the study. In 89 (36.6%) cases, different morphological variants were detected. When the variants were grouped according to their aggressiveness as described in the literature, a statistically significant relationship between aggressiveness and the variables organ and age was found ( p < 0.05). The oncocytic variant was found to metastasize more than the other aggressive types (42.9%). The paraganglioma-like variant was found to have a smaller size, lower proliferation index, and a more benign clinical course. This study demonstrated that well-differentiated GI neuroendocrine tumors (GI-NETs) have considerable morphological diversity. Generally, case reports of rare morphological variants of GI-NETs are available in the literature. We believe that our study contributes to a better understanding of the prevalence, localization, and significance of morphological variations in GI-NETs.

Although BRCA genes are well-known breast cancer genes, the clinicopathological features of breast cancer patients carrying BRCA1/2 pathogenic variants have not been adequately defined. The goals of this study were to determine the distribution of BRCA1/2 variants in the Turkish population and its correlation with clinicopathological features. Clinical data of 151 women who underwent BRCA1/2 gene testing at Mersin University Medical Faculty Hospital between 2016 and 2019 were retrospectively analyzed. BRCA1/2 variants were detected as pathogenic (n = 11), variants of uncertain significance (n = 5), likely benign (n = 3), and benign (n = 81) in breast cancer cases. The BRCA1/2 pathogenic variant carriers had a higher histological grade, rate of triple- negative type, Ki-67 proliferation index, and rate of no special type carcinoma than the group without mutation (p = 0.03, 0.01, 0.04, and 0.02 respectively). We analyzed the distribution of variants we detected in women living in our region and found that pathogenic variants in patients with breast cancer were associated with high histological grade, triple-negative type, high Ki-67 proliferation index, and histological type. Studies in diverse populations are needed to establish a clinicopathological relationship with variants more easily.

Small cell lung carcinoma (SCLC) is characterized by rapid growth and an aggressive clinical course. Standard therapy regimes have limited effects on disease course; therefore the prognosis of SCLC is poor. In the current study, the frequency of programmed death ligand 1 (PD-L1) expression in SCLC and its correlation with clinico-pathological features were evaluated. The study included 100 cases of SCLC wherein testing for PD-L1 was done with the SP263 clone on the Ventana benchmark XT system. Cases with > 1% PD-L1 expression in tumour cells or immune cells were categorized as positive. PD-L1 expression was identified in 14% of cases using the cut-off of ≥ 1%. The tumour proportion score was 10% and the immune proportion score was 9.78% using a cut-off of ≥ 1%. PD-L1 positive expression was more frequent in the male population with age > 40 years. All the patients with positive PD-L1 expression were smokers. In the PD-L1 positive group, presence of necrosis was identified in 71.4% of cases and when compared with the PD-L1 negative subgroup this finding was statistically significant (p = 0.010). Personalized targeted therapy for cases of SCLC is still under evaluation. The use of immunotherapeutic targets, such as PD-L1, may help to define a new treatment strategy for SCLC. Development of new treatment strategies may improve prognosis and survival.

Colorectal cancer is the third most common cancer worldwide and the second cause of death from malignant tumors. Colorectal cancers are treated with surgery, chemotherapy, gene therapy and immunotherapy. PD-1 and PD-L1 proteins have recently been considered as potential targets of anticancer therapy in colorectal cancer. The aim of this study was to evaluate the association of immunohistochemical expression of PD-1 and PD-L1 proteins in colorectal cancer patients with selected clinical and morphological parameters and their survival. Ninety-eight cases of colorectal cancer were studied. Immunohistochemistry was used to evaluate the expression of PD-1 and PD-L1 proteins. Correlations were found between the expression of PD-L1 protein in lymphocytes and lack of lymph node metastases and a lower clinical stage. There was also a correlation between PD-L1 protein expression in cancer cells and a higher grade of histological malignancy.