## 8 Conclusions  
Gastrointestinal cancers, that is, esophageal, stomach, liver, biliary tract, pancreas, and colon cancers, account for one-third of total cancer incidence and mortality in developing countries. Commensal microbiota is believed to have a beneficial influence on human health; however, numbers of studies aim to demonstrate if changes in gut microbiota contribute to the pathogenesis of gastrointestinal malignancies. A lot of interest is set on the link between microbiota and cancer. Microbiota is believed to contribute to cancer development through various mechanisms, such as (a) tissue homeostasis disruption through over amplification of the immune response, (b) activation of epithelial proliferation, and (c) breakdown of the integrity of the barrier. In this review article, we have illustrated microbial signatures in GI cancers (Table 8). It is worth noticing that few phyla are common for almost all GI malignancies. An increase in members of Proteobacteria, Acinetobacteria, and Fusobacteria phyla in gut microbiota was reported in almost all GI cancers. Proteobacteria has been linked to various human diseases, especially inflammation-related [148]. Studies reveal that impairments in the innate immune system promote the outgrowth of Proteobacteria, and that increases in the Proteobacteria number enhance the immune response in the host gut, which might lead to systemic inflammation development [57; 58]. Members of Acinetobacteria phylum are opportunistic pathogens. A direct link between Acinetobacteria phyla with cancer development was not reported, however, infections with these bacteria are common among cancer patients [149; 150]. Members of Fusobacteria phylum were reported to be related to GI cancer development. _F. nucleatum_ has been suggested by a considerable number of studies as a potential marker for CRC detection [150]. _Leptotrichia_ spp. infections are common among cancer patients [151]. Certain strains of _Escherichia coli_, _Streptococcus bovis_, _Helicobacter pylori_, _Bacteroides fragilis_, and _Enterococcus_ spp., as well as some members of the _Enterobacteriaceae_ family, were reported to exhibit direct cancerogenic activity on host cells. Those strains, by direct induction of proliferation of epithelial cells, can lead to hyperplasia. Moreover, changes in gastrointestinal microbiota are reported to occur in various gastrointestinal cancers. Nonetheless, despite the ever-increasing amount of data on human microbiome, there are still questions lacking answers. Why microbiota undergo changes in cancer environment? Are changes in microbiota diversity a cause or a result of cancer neoplastic transformation? Do changes in microbiota community increase or enhance cancer development? Answers to those questions might provide more information about the relation between cancer and host microbiota. An obstacle in the complete analysis of microbiota composition is also a huge number of bacterial genomes that could not be recognized and still fall into the dark matter. Moreover, all studies that were quoted in this review article present data obtained by 16s sequencing, while this method is cheap and provides enough information about taxonomic diversity of microbiota, it lacks data about metabolic changes occurring in the microbial community, which is also crucial. Furthermore, it is also crucial to include environmental factors into statistical analysis in order to evaluate the authentic role of microbiota in GI cancer development. **Author Contributions:** Conceptualization, Z.K. and B.K. ; methodology, Z.K. ; validation, B.K., J.S. ; formal analysis, Z.K. ; resources, B.K. ; writing--original draft preparation, Z.K. ; writing--review and editing, B.K., J.S. ; supervision, B.K., J.S. ; project administration, X.X. ; funding acquisition, B.K. All authors have read and agreed to the published version of the manuscript. **Funding:** This research received no external funding. **Acknowledgments:** This study was supported by the Medical University of Lodz (503/3-045-02/503-31-001-19-00).