Thousands of biomarkers have been discovered to solve the mechanisms of cancer, but dynamic alterations in the parameters that affect cancer progression cause complex disease status. Therefore, it is essential when dealing with cancer to analyze all parameters, including pathway information, to understand the disease mechanism of action. In our study, we applied multi-omics data integration for microbiome, transcriptome, and microbial pathway datasets obtained from colorectal cancer patients. The Cldn7 gene and Fusobacteria, which both play roles in the stability of the intestinal barrier, were found to be highly associated with each other (r = 0.71). The Klf3 gene has been identified as a critical regulator in the activation of the WNT1 and WNT/β-catenin signaling pathways. Notably, it exhibited a strong positive correlation with the presence of Fusobacteria, which are also implicated in modulating these pathways. In addition, the glutaryl CoA degradation and p-cymene degradation pathways demonstrated a strong positive association with the expression of the Ahcy, Eis2s2, Hsp90ab1, Psma7, Lbr, Rpl7l1, Cse1l, Cbx3, Ncl, Hspd1, Tpx2, and Top2a genes (r > 0.65), suggesting their potential involvement in the regulation and metabolic integration of these pathways at the transcriptional level.

Background/Objectives: Coronary slow flow phenomenon (CSFP) is a cardiovascular condition characterized by delayed passage of contrast medium through the coronary arteries, predominantly affecting young male smokers admitted with acute coronary syndrome. Although over 80% of patients experience recurrent chest pain and more than 20% require readmission, the etiology of CSFP remains poorly understood. Given the emerging role of gut microbiome in cardiovascular diseases, this study investigates the microbial composition associated with CSFP. Methods: Stool samples were collected from patients diagnosed with CSFP and healthy control individuals. Microbiota profiling was performed using 16S rRNA sequencing. Taxonomic differences were evaluated to identify microbial markers potentially associated with CSFP. Results: The analysis revealed a notable enrichment of the genus Gemmiger and the species Anaerobutyricum in CSFP patients, specifically within the selenium metabolism pathway. This is of particular interest given the established link between selenium deficiency and heightened cardiovascular risk, suggesting a possible microbiome-mediated modulation of selenium bioavailability in CSFP pathophysiology. Moreover, a marked increase in taxa associated with the biosynthesis of trimethylamine (TMA), a proatherogenic metabolite implicated in the onset and progression of various cardiovascular disorders, was observed in the CSFP cohort, further supporting a potential mechanistic role of gut microbiota in the disease’s underlying etiology. Conclusions: Although statistical significance could not be established due to the limited sample size, the observed trends support the hypothesis that specific gut microbes and metabolic pathways, particularly those linked to selenium metabolism and TMA production, may serve as potential microbial indicators for CSFP. These preliminary findings warrant further investigation in larger cohorts.

Thousands of biomarkers have been discovered to solve the mechanism of cancer but dynamic alterations of the parameters affecting the cancer progression cause chaotic disease status. This is the reason why it is essential to deal with cancer with an eye to analyzing all parameters including pathway information to understand the molecular level of action. In our study, we applied multi-omics data integration method for microbiome, transcriptome and microbial pathway datasets obtained from colorectal cancer patients by including the transcriptome pathway information. Cldn7 gene and Fusobacteria were found to be highly associated, and they both take role in stability of intestinal barrier (r= 0.71). Klf3 was another gene that played a significant role in activation of WNT1 and WNT/β-catein pathways and it demonstrated high correlation with Fusobacteria which was also found to be involved in same pathways. In addition, The Glutaryl-CoA degradation and p-cymene degradation pathways demonstrated a strong positive association with the expression of Ahcy, Eis2s2, Hsp90ab1, Psma7, Lbr, Rpl7l1, Cse1l, Cbx3, Ncl, Hspd1, Tpx2, and Top2a genes (r > 0.65), suggesting their potential involvement in the regulation and metabolic integration of these pathways at the transcriptional level.

Gastrointestinal cancer is defined as the second leading cause of cancer related deaths in the world. In addition to many environmental and hereditary factors that cause cancer, recent studies have shown that many types of microorganisms can also cause cancer due to chronic infections, virulence factors and carcinogenic metabolites. Helicobacter pylori play a pivotal role in the initiation of gastric carcinogenesis, whereas Escherichia coli has been implicated in the progression of colorectal cancer. The aim of this research is to get more detailed information about the gastrointestinal cancer associated pathogens, to define the role of genotoxin producing Escherichia coli for the colon cancer and Helicobacter pylori virulence factors in Turkish population. For the purpose of this study, tumor tissue specimens were collected from patients diagnosed with colon and gastric cancer. In colon tumor tissues, the presence of colibactin was assessed by screening for the genes clbA, clbB, clbN, and clbQ. In gastric tumor tissues, Helicobacter pylori virulence factors including ureA, ureB, dupA, hpaA, napA, cagA, and vacA (s1/s2) were analyzed. Colibactin positivity (clb+) was detected in only four colon cancer patients, while H. pylori virulence factors were identified in three gastric cancer patients. Two clb+ colon tumor samples were cultured using the single-colony isolation technique. Whole-genome sequencing (WGS) was subsequently performed on isolates from these cultures to determine their species identity. The first sample yielded Escherichia coli Nissle, while the second was identified as Citrobacter braakii.