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Helicobacter pylori ( H. pylori ) infection has been considered as the main causal factor in gastric carcinogenesis, but other bacterial species may also play an important role in pathophysiology of gastric cancer. The aim of the study was to explore the link between gastric cancer prognosis and the mucosal microbial community in tumorous and adjacent gastric tissue. The bacterial profile was analysed using 16S sequencing (V1–V2 region). Microbial differences were mostly characterized by lower relative abundances of H. pylori in tumorous gastric tissues. Bacterial community and outcome data analysis revealed the genus Fusobacterium and Prevotella significantly associated with worse overall survival in gastric cancer patients. In particular, Fusobacterium was associated with significant increase in hazard ratio in both univariable and multivariable analysis and independently validated using TCMA data. Phylogenetic biodiversity of Fusobacterium species in the stomach revealed F. periodonticum as the most prevalent in healthy subjects, while F. nucleatum was most abundant in patients with gastric cancer. Bacterial community network analysis in gastric cancer suggests substantial complexity and a strong interplay between F. nucleatum and Prevotella. In summary, mucosal microbial community in the stomach was associated with worse overall survival in gastric cancer patients. Strongest negative impact on prognosis was linked to the abundance of F. nucleatum in tumorous specimens, suggesting its translational relevance in management of gastric cancer patients.

The rapid emergence of multidrug-resistant bacterial species poses a critical threat by reducing the efficacy of antibiotics and complicating infection treatment. Bacteriocins, such as klebicin KvarM, have emerged as promising alternatives to traditional antibiotics due to their targeted antimicrobial activity. In this study, we evaluated the therapeutic potential of Eudragit-coated klebicin KvarM in a mouse model of intestinal colonization, assessing both its antimicrobial effectiveness and impact on commensal gut microbiota. Antimicrobial activity of KvarM in comparison to conventional antibiotic therapy with ciprofloxacin was tested in murine models for gastrointestinal (GI) tract infection. The haemolysin gene ( ) was chosen as the qualitative marker for genus identification, and 16S rRNA gene sequencing of V1-V2 hypervariable region was performed for analyses of gut microbiota. Our results demonstrated that KvarM was highly effective in reducing colonization, showing the same efficacy as ciprofloxacin. Following inoculation, administration of KvarM resulted in a significant reduction in bacterial load indicating a 99% effectiveness. Furthermore, microbiome analysis of the gut microbiota revealed that KvarM therapy showed no significant changes in microbial composition compared with commensal microbiota composition, whereas administration of ciprofloxacin led to a significant decrease in microbial diversity. These findings demonstrate that klebicin KvarM therapy is highly effective for treating intestinal infections and it does not affect the integrity of the gut microbiota.

Canine mammary gland tumors (CMTs) are one of the most prevalent cancers in dogs and a good model for human breast cancer (BC), however gene expression analysis of CMTs is scarce. Although divergence of genes expression has been found in BC of different human races, no such research of different dog’s breeds has been done. The purpose of this study was to investigate expression of the VEGF-B, VEGF-A, FLT-1, KDR, ERBB2, EGFR, GRB2, RAC1, CDH1 and HYAL-1 genes of canine mammary carcinomas, compare the expression levels with clinicopathological parameters and analyze expression disparities between different breeds. Carcinomas and adjacent tissues were collected from female dogs to perform routine histopathology, immunohistochemistry (IHC) and quantitative real-time polymerase chain reaction (qRT-PCR). We found that VEGF-B and EGFR genes were overexpressed in the mammary gland carcinomas compared to adjacent tissue. VEGF-B gene expression had associations with different parameters (tumor size, grade, and absence of metastasis). Furthermore, differences in VEGF-B, FLT1, ERBB2, GRB2, RAC1, CDH1 and HYAL-1 genes expression have been found in different breed dogs (German Shepherd, Yorkshire Terrier) and mixed-breed dogs indicating that a dog’s breed could determine a molecular difference, outcome of cancer and should be accounted as a confounding factor in the future gene expression research.

Gastrointestinal (GI) tract cancers are considered one of the main public health problems with medical and economic burdens because of their high prevalence and mortality rate. Gastric cancer (GC) is the fourth and colorectal cancer (CRC) is the second most common cause of cancer-related death, with 750,000 and 1.23 million deaths per year, respectively [1–3]. Lithuania is one of the European countries with the highest incidence of GC. The relative prevalence of GC and CRC in Lithuania follows the global trend of being the third and fourth cause of death, respectively [4]. Due to the lack of symptoms in the early stages of both GC and CRC and limited treatment options, the prognosis of GC and CRC remains very poor. Many factors contribute to the development of both diseases, including diet, genetics, environment, and infection with microorganisms [3, 5].Bacteria are one of the most abundant and diverse life forms on the planet. Fossil evidence suggests that bacteria-like ancestors have existed on the Earth for at least 3.5 billion years [6]. Bacteria are ubiquitously present in the environment, air, soil, water, plants, and animals. For a long time, the main focus has been directed to human pathogenic bacteria; however, with time it became known, that bacteria coevolved with humans and are an integral part of human health and perform certain crucial functions.Over the past decade, extensive research has highlighted the important role of the microbiome in several diseases. Although the gut is the main habitat for microorganisms, other body compartments such as the stomach, mouth, respiratory tract, skin, genital tract, liver, and even the eyes are also colonized by microorganisms [7]. The changes in the microbiota composition and/or loss of bacterial diversity (dysbiosis) are the major features of the number of inflammatory and tumorous diseases [8].Studies have shown that some human bacteria may directly promote carcinogenesis or be involved in interactions with the human immune system or oncogenic factors. Studies using animal models have identified specific bacteria, such as Fusobacterium nucleatum, Bacteroides fragilis, Escherichia coli, and Helicobacter pylori, among others, that are associated with the development of CRC and GC [9, 10]. Knowledge about human health conditions association with bacterial profile changes could be useful for disease risk prediction or microbiome-based therapies [11, 12]. Although H. pyloriis a recognized risk factor for GC, only 1–3% of people with this bacterium develop GC [13].Most research on microbiota has been done using DNA genetic material; however, recent studies are analyzing RNA samples. In order to adopt a common standard for microbiota analysis, there is a lack of comparison between different methods. In addition, there is a lack of studies describing microbiota alterations in precancerous conditions [9].While the tissue and fecal microbiota have received most of the attention concerning various diseases, particularly gastrointestinal diseases, the presence, and significance of microbial genetic signatures in the bloodstream is a novel and intriguing area of research [14]. With the development of technological methods such as next-generation sequencing (NGS), it has been shown that blood contains circulating microbial cell-free DNA – bacterial genetic signatures.

Next-generation sequencing technologies have started a new era of respiratory tract research in recent years. Alterations in the respiratory microbiome between healthy and malignant conditions have been revealed. However, the composition of the microbiome varies among studies, even in similar medical conditions. Also, there is a lack of complete knowledge about lung–gut microbiome interactions in lung cancer patients. The aim of this study was to explore the lung–gut axis in non-small-cell lung cancer (NSCLC) patients and the associations between lung–gut axis microbiota and clinical parameters (CRP, NLR, LPS, CD8, and PD-L1). Lung tissue and fecal samples were used for bacterial 16S rRNA sequencing. The results revealed, for the first time, that the bacterial richness in lung tumor tissue gradually decreased with an increase in the level of PD-L1 expression (p < 0.05). An analysis of β-diversity indicated a significant positive correlation between the genera Romboutsia and Alistipes in both the lung tumor biopsies and stool samples from NSCLC patients (p < 0.05). Survival analysis showed that NSCLC patients with higher bacterial richness in their stool samples had prolonged overall survival (HR: 2.06, 95% CI: 1.025–4.17, p = 0.0426).

Intratumoral bacteria locally contribute to cellular and molecular tumor heterogeneity that support cancer stemness through poorly understood mechanisms. This study aims to explore how Colibactin-producing Escherichia coli (CoPEC) flexibly alters the tumor microenvironment in right-sided colorectal cancer (CRC). Metabolomic and transcriptomic spatial profiling uncovered that CoPEC colonization establishes a high-glycerophospholipid microenvironment within the tumor that is conducive to exhaustion of infiltrated CD8+ T cell and has a lowered prognostic value in right-sided CRC. Mechanistically, the accumulation of lipid droplets in infected cancer cells relied on the production of colibactin as a measure to limit genotoxic stress and supply with sufficient energy for sustaining cell survival and lowering tumor immunogenicity. Specifically, a heightened phosphatidylcholine remodeling of CoPEC-infected cancer cells by the enzyme of the Land’s cycle coincided with a lowered accumulation of proapoptotic ceramide and lysophosphatidylcholine. Consequently, a reduced infiltration of CD8+ T lymphocytes that produce the cytotoxic cytokines IFN-γ was found where invading bacteria have been geolocated. By contrast, such an immunosuppressive dysmetabolic process was not observed when human colon cancer cells were infected with the mutant strain that did not produce colibactin (11G5δClbQ). This work revealed an unexpected property of CoPEC on lipid overload within tumors that could locally provide an inflammatory environment leading to immunosuppressive mechanisms and tumor expansion. This may pave the way for improving chemoresistance and subsequently outcome of CRC patients who are colonized by CoPEC.