The gut microbiota plays an essential role in maintaining immune homeostasis and influencing the immune landscape within the tumor microenvironment. This review aims to elucidate the interactions between gut microbiota and tumor immune dynamics, with a focus on colorectal cancer (CRC). The review spans foundational concepts of immuno-microbial interplay, factors influencing microbiome composition, and evidence linking gut microbiota to cancer immunotherapy outcomes. Gut microbiota modulates anti-cancer immunity through several mechanisms, including enhancement of immune surveillance and modulation of inflammatory responses. Specific microbial species and their metabolic byproducts can significantly influence the efficacy of cancer immunotherapies. Furthermore, microbial diversity within the gut microbiota correlates with clinical outcomes in CRC, suggesting potential as a valuable biomarker for predicting response to immunotherapy. Conclusions: Understanding the relationship between gut microbiota and tumor immune responses offers potential for novel therapeutic strategies and biomarker development. The gut microbiota not only influences the natural history and treatment response of CRC but also serves as a critical modulator of immune homeostasis and anti-cancer activity. Further exploration into the microbiome’s role could enhance the effectiveness of existing treatments and guide the development of new therapeutic modalities.

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Objective: The molecular mechanisms of bladder cancer development and progression are not clear. Bladder cancer is an important focus for epidemiological studies and understanding clinical implications. Goal: The primary aim of prevention is achieved by limiting exposure to non-genetic risk factors such as smoking, diet, arsenic in drinking water, or aromatic amines at work or elsewhere. Current therapies for bladder cancer are affected by tumor morphology and associated acquired genetic mutations. Methods: A literature search was performed using PubMed, Scopus, ResearchGate, Google, MEDLINE, and ScienceDirect databases to find studies of bladder cancer published between 1984 and early 2020. The focus was articles that address epidemiological risk factors and underlying pathophysiological mechanism. Articles were selected that enabled our review of these factors as well as molecular and structural patterns. Results: There are multiple views of bladder cancer. The literature offers a number of novel insights regarding the development and progression of bladder cancer and possible biomarkers that may be useful in clinical and diagnostic practice. Conclusion: There are several molecular pathways associated with bladder cancer that are frequently updated. In addition, genetic subtypes of bladder tumors are not distinguished clearly that requires future more detailed analysis.

Introduction. Colorectal cancer (CRC) is one of the most common oncological diseases, the pathogenesis of which is closely associated with the development of inflammation. The study of inflammation regulation, including the balance of pro- and antiinflammatory cytokines, is a promising topic for research, allowing for a deeper understanding of the pathogenesis of CRC and improving clinical approaches to the treatment for and diagnosis of this disease. This study investigates the altered secretion of proinflammatory cytokines, i.e., TNF-α and IL-1β, in CRC patients, aiming to elucidate immune dysregulation mechanisms. We sought to investigate the secretion characteristics of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β), in patients with CRC. Materials and methods. We enrolled 25 newly diagnosed CRC patients and 20 age- and sex-matched controls. Monocytes were isolated from the peripheral blood of participants using magnetic separation based on the CD14 marker. The isolated monocytes were cultured and subjected to dual stimulation with bacterial lipopolysaccharide at 24 hours and 7 days, followed by quantitative measurement of basal and stimulated cytokine levels using an enzyme-linked immunosorbent assay (ELISA). Results. We revealed a significant reduction in TNF-α secretion in CRC monocytes after initial LPS stimulation, with no subsequent recovery upon restimulation. In contrast, IL-1β secretion elevated markedly in CRC patients, particularly after restimulation. These results suggest an impaired TNF-α response and an exacerbated IL-1β response in CRC, indicating a potential immune tolerance mechanism that may contribute to tumor progression. The distinct cytokine dynamics observed point at complex immune dysregulation within the CRC microenvironment. Conclusion. The observed cytokine secretion patterns may indicate immune dysregulation in the microenvironment of CRC. Our study underscores the importance of understanding the specific roles of cytokines in CRC pathogenesis and highlights the potential for targeted therapeutic interventions to modulate these immune responses. Further research is necessary to explore the underlying signaling pathways and the broader implications of these findings for CRC treatment strategies. This work provides critical insights into the pro-inflammatory cytokine profiles in CRC, advancing our understanding of the immune landscape in cancer and opening new avenues for therapeutic exploration. Keywords: colorectal cancer, cytokines, tumor necrosis factor-alpha, interleukin-1 beta, immune tolerance

Cardiac involvement is the most important factor determining prognosis in patients with systemic amyloidosis. This retrospective observational study of 98 patients with amyloidosis was undertaken to assess the amyloid types that are most likely to affect the heart, describe histopathological and clinical features of cardiac amyloidosis, and estimate the number of cases not diagnosed clinically prior to death. All cases were divided into two groups based on the method of examination. The first group included 46 patients with cardiac amyloidosis revealed via endomyocardial biopsies (EMBs), and the second group included 52 amyloidosis patients who did not undergo EMBs, in whom cardiac involvement was identified only at autopsy. The EMBs demonstrated that AL amyloidosis was detected in 21 (46%) specimens, ATTR amyloid in 24 cases (52%), and AA amyloid in 1 case (2%). The autopsy reports defined 15 (46%) cases of AL amyloidosis, 21 (40%) of ATTR and 16 (31%) of AA amyloidosis. It should be noted that a clinical diagnosis of ATTR amyloidosis was made only in 9.5% of patients from the autopsy group, suggesting that ATTR may be an underdiagnosed cause of heart failure in elderly patients. The most intense amyloid deposits were determined in biopsy and autopsy specimens of patients with AL kappa amyloidosis, underlying a poorer prognosis.

In the course of the serrated pathway of carcinogenesis, there are changes in the expression of mucins with a characteristic immunophenotypic sign, such as a late loss of intestinal differentiation and an increase in gastric differentiation. To comparatively assess the expression of Muc 2, Muc 5AC, and Muc 6 in hyperplastic polyps (HPs), sessile serrated adenomas (SSAs) and traditional serrated adenomas (TSAs) of the colon for determination of their role in differential diagnosis. Sixty-five serrated masses from 52 patients were examined. Among them, there were 26 SSAs, 26 HPs, and 13 TSAs. A histological examination was done using hematoxylin and eosin staining; periodic acid-Schiff reaction in combination with alcian blue, as well as immunohistochemistry with anti-Muc 2, anti-Muc 5AC, and anti-Muc 6 antibodies were used. Genetic testing of the specimens for KRAS and BRAF mutations was also carried out. All the serrated neoplasms of the colon exhibited a pronounced expression of Muc 2. A marked Muc 6 expression in the dilated crypt bases was found in 76.9% of SSAs, while no reaction was seen in 92.3% of HPs and in 100% of TSAs. SSAs were characterized by an intense Muc 5AC expression in the whole length of the crypts and in the surface epithelium in contrast with HPs and TSAs, where the expression of the marker was focal. Comparison of the response of the markers and the presence of gene mutations identified that the SSAs with BRAF mutation intensely expressed along the length of the crypt for Muc 5AC and Muc 6; and the TSAs with KRAS mutation had a moderate focal Muc 5AC expression in the crypt bases in 100% of cases. For differential diagnosis of the types of serrated adenomas of the colon, it is useful for a pathologist to apply the immunohistochemical markers Muc 2, Muc 5AC, and Muc 6 in his/her practice.