Prostate cancer treatment is currently based on surgical removal, radiotherapy, and hormone therapy. In recent years, another therapeutic method has emerged—immunological treatment. Immunotherapy modulates and strengthens one’s immune responses against cancer. Neoplastic cells naturally escape from the control of the immune system, and the main goal of immune therapy is to bring the control back. Satisfying outcomes after treatment of advanced melanoma and lung cancer suggest a great potential of immunotherapy as an approach for other tumors’ treatment, especially in patients primarily introduced to palliative care. After initial clinical trials, immunotherapy seems to have different side effects than chemotherapy. Prostate cancer was the first neoplasm in which a specific vaccine significantly improved survival. There is a tremendous potential for synergistic combinations of immunotherapy with conventional cancer treatments. A combination of several drugs or methods can be a key in radical treatment of metastatic prostate cancer as demonstrated by preliminary studies.

Purpose We propose a treatment algorithm for PDAC with particular emphasis on BRCA1 or 2 mutation-positive patients. Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest diseases in the United States and Europe. BRCA1 and BRCA2 are among the most common of the known genetic mutations involved in familial PDAC. The optimal chemotherapy regimen to use for BRCA1 or 2 mutation carriers with PDAC is not yet established. As new treatment options emerge, algorithms must balance the need to give the best drugs first with ensuring that there are still beneficial options available for later. Methods We conducted a review of the literature for data on possible therapies in BRCA-positive and BRCA-negative pancreatic cancer. Results There is accumulating evidence of increased sensitivity to platinum-based therapy and poly-ADP-ribose polymerase inhibitors (PARPi) in BRCA-associated PDAC. There are no studies relating to borderline BRCA-associated PDAC and, therefore, same treatment as for sporadic PDAC seems appropriate. Treatment of unresectable PDAC varies depending on stage of the disease. Patients with BRCA-associated locally advanced PDAC can benefit from targeted therapy with PARPi (olaparib) as a second-line therapy after antimetabolite treatment failure. Patients with unresectable metastatic BRCA-positive PDAC may benefit from platinum-based therapy. Conclusion Targeted therapies are shifting the treatment paradigms and increasing survival for patients with PDAC, a group that used to have a grim prognosis.

Available biomarkers for pancreatic adenocarcinoma (PAC) are inadequate to guide individual patient prognosis or therapy. Therefore, herein we aimed to verify the hypothesis that differences in the expression of KIF11 and KIF14, i.e., molecular motor proteins being primarily implicated in cell division events could account for the differences in the clinical outcome of PAC patients. In-house immunohistochemistry was used to evaluate the protein expressions of KIF11 and KIF14 in PAC, whereas RNA-seq datasets providing transcript expression data were obtained from public sources. IHC and mRNA results were correlated with clinicopathological features and overall survival (OS). Furthermore, the genes co-expressed with KIF11 or KIF14 were predicted and functionally annotated. In our series, malignant ducts displayed more intense but less abundant KIF11 staining than normal-appearing ducts. The former was also true for KIF14, whereas the prevalence of positive staining was similar in tumor and normal adjacent tissues. Based on categorical immunoreactive scores, we found KIF11 and KIF14 to be frequently downregulated or upregulated in PAC cases, respectively, and those with elevated levels of either protein, or both together, were associated with better prognosis. Specifically, we provide the first evidence that KIF11 or KIF14 proteins can robustly discriminate between patients with better and worse OS, independently of other relevant clinical risk factors. In turn, mRNA levels of KIF11 and KIF14 were markedly elevated in tumor tissues compared to normal tissues, and this coincided with adverse prognosis, even after adjusting for multiple confounders. Tumors with low predicted KIF11 or KIF14 expression were seen to have enrichment for circadian clock, whereas those with high levels were enriched for the genomic instability-related gene set. KIF11 and KIF14 were strongly correlated with one another, and CEP55, ASPM, and GAMT were identified as the main hub genes. Importantly, the combined expression of these five genes emerged as the most powerful independent prognostic indicator associated with poor survival outcome compared to classical clinicopathological factors and any marker alone. In conclusion, our study identifies novel prognostic biomarkers for PAC, which await validation.

Low-grade ovarian cancers represent up to 8% of all epithelial ovarian carcinomas (EOCs). Recent studies demonstrated that epithelial-mesenchymal transition (EMT) is crucial for the progression of EOCs. EMT plays a key role in cancer invasion, metastasis formation and chemotherapy resistance. An array of novel EMT transcription factors from the zinc finger protein family have been described recently, among them zinc finger protein 143 (ZNF143) and zinc finger protein 281 (ZNF281). The study included tissue specimens from 42 patients. Based on histopathological examination of surgical specimens, eight lesions were classified as serous borderline ovarian tumors (sBOTs) and 34 as low-grade EOCs. The proportions of the ovarian tumors that tested positively for ZNF143 and ZNF281 were 90 and 57%, respectively. No statistically significant differences were found in the expressions of ZNF143 and ZNF281 transcription factors in SBOTs and low-grade EOCs. Considering the expression patterns for ZNF143 and ZNF281 identified in this study, both sBOTs and low-grade EOCs might undergo a dynamic epithelial-mesenchymal interconversion. The lack of statistically significant differences in the expressions of the zinc finger proteins in sBOTs and low-grade serous EOCs might constitute an evidence for common origin of these two tumor types.

Chronic rhinosinusitis is a process involving a number of adverse changes in the mucosa of the paranasal sinuses and nasal polyps. The main histological features of tissue remodeling are changes in epithelial structure, oedema, degradation of ECM (extracellular matrix), angiogenesis, and subepithelial fibrosis. In this study, patients were divided into two groups: group 1—patients with CRSwNP (chronic rhinosinusitis with nasal polyps) taking a nasal steroid and an oral steroid in the preoperative period, and group 2—patients with CRSwNP taking only the nasal steroid in the preoperative period. All samples were subject to histopatologic evaluation. The aim of this study was to investigate the effect of oral corticosteroids and topical steroids on the tissue of paranasal sinuses. We have shown statistically significant decreases in tissue eosinophilia per 5HPF and decreased fibrosis in group 1. No significant differences were presented in the percentage of total tissue oedema, epithelium, neutrophils, basement membrane thickening and vessels. Using systemic administration of 40 mg of prednisone for seven days decreased the counts of eosinophils and decreased fibrosis in the nasal polyps tissue in CRSwNP.

Prostate cancer (PCa) is the second most commonly diagnosed malignant tumor and the fifth leading cause of cancer death in men in the world. The most common types of tumors are adenocarcinomas. Prostate cancer is a slow‐growing cancer. The incidence increases with age. Evaluation of proinflammatory factors such as IL‐17A, IL‐17F, IL‐17RA, and IL‐17RC expression makes it possible to assess the impact of inflammatory process on progression of PCa. The aim of the study was to retrospectively assess the histological material of PCa divided into few groups using the Gleason score. Studies were carried out on archival tissue material in the form of paraffin blocks of 40 men with PCa after radical prostatectomy. The control group was composed of 10 men with benign prostatic hyperplasia (BPH). The material was obtained by the transurethral resection of the prostate (TURP). Immunohistochemistry was performed on prepared material using specific primary antibodies against IL‐17A, IL‐17F, IL‐17RA, and IL‐17RC. Expression of the antibody to be examined using light microscopy and the Remmele‐Stegner score (IRS) in cancer staining was then evaluated. Expression of IL‐17 RA was not shown in a group of patients with PCa and in the control group. In the group of patients with Gleason score 8 and 9 PCa, the expression of IL‐17A was higher compared to that of IL‐17F. In addition, in PCa with an increased grade of Gleason scale, a decrease in the expression of the study inflammatory parameters was found. The inflammatory process has an impact on PCa. A study on IL‐17 may become a starting point for further research on an attempt to use, for example, immunotherapy in PCa.