While the gut microbiome is composed of numerous bacteria, specific bacteria within the gut may play a significant role in carcinogenesis, progression, and metastasis of colorectal carcinoma (CRC). Certain microbial species are known to be associated with specific cancers; however, the interrelationship between bacteria and metastasis is still enigmatic. Mounting evidence suggests that bacteria participate in cancer organotropism during solid tumor metastasis. A critical review of the literature was conducted to better characterize what is known about bacteria populating a distant site and whether a tumor depends upon the same microenvironment during or after metastasis. The processes of carcinogenesis, tumor growth and metastatic spread in the setting of bacterial infection were examined in detail. The literature was scrutinized to discover the role of the lymphatic and venous systems in tumor metastasis and how microbes affect these processes. Some bacteria have a potent ability to enhance epithelial–mesenchymal transition, a critical step in the metastatic cascade. Bacteria also can modify the microenvironment and the local immune profile at a metastatic site. Early targeted antibiotic therapy should be further investigated as a measure to prevent metastatic spread in the setting of bacterial infection.

Gastric cancer metastasis is a process in which the tumor microenvironment may carry significant influence. Helicobacter pylori (H. pylori) infection is well-established as a contributor to gastric carcinoma. However, the role that these bacteria and others may play in gastric carcinoma metastasis is a current focus of study. A review of the literature was conducted to elucidate the process by which gastric adenocarcinoma metastasizes, including its ability to utilize both the lymphatic system and the venous system to disseminate. Studies that investigate the tumor microenvironment at both the primary and secondary sites were assessed in detail. H. pylori and Mycoplasma hyorhinis (M. hyorhinis) were found to be important drivers of the pathogenesis of gastric adenocarcinoma by modifying various steps in cell metastasis, including epithelial–mesenchymal transition, cell migration, and cell invasion. H. pylori is also a known driver of MALT lymphoma, which is often reversible simply with the eradication of infection. M. hyorhinis has been implicated in gastric neoplasia via β-catenin stabilization and subsequent activation of the WNT-signaling pathway, promoting gastric cancer cell motility and inciting cancer progression. Fusobacterium nucleatum (F. nucleatum) and its association with worse prognosis in diffuse-type gastric adenocarcinoma are also reviewed. Recognition of the roles that bacteria play within the metastatic cascade is vital in gastrointestinal adenocarcinoma treatment and potential reoccurrence. Further investigation is needed to establish potential treatment for metastatic gastric carcinoma by targeting the tumor microenvironment.

Table 1. Results of comparison of technical success, clinical success, and rate of adverse events between the transgastric and transduodenal/transjejunal approach METHOD 1-Including studies with patients in both arms N of studies Pooled odds ratio (TG vs. TD/TJ) 95% CI p-value Adverse events 6 1.58 0.46-5.45 0.47 Clinical success 3 0.30 0.06-1.48 0.14 Technical success 3 0.30 0.05-1.89 0.20 METHOD 2-: Including all the studies N of Studies (TG vs TD/TJ) AE(%) 95% CI p-value Adverse events 9 vs 15 27.5% vs 15.2% 17.1%-41.1%) vs (9.5%-23.6%) 0.07 Clinical success 6 vs 13 83.3% vs 91.7% (71.0%-91.0%) vs (82.4%-96.3%) 0.16 Technical success 9 vs 15 91.3% vs 95.6% 83.6%-95.6%) vs 90.7%-97.7%) 0.22 S1118 Safety and Efficacy of the Novel EndoRotor Device for the Treatment of Walled-Off Pancreatic Necrosis (WOPN): A Systematic Review and Meta-Analysis

Pancreatic neuroendocrine neoplasms (PNETs) are rare but can be associated with significant morbidity and mortality. PNETs can be difficult to diagnose and have a propensity for metastasis before their diagnosis is established. To this end, many PNETs do not become apparent until late in their clinical course. Endoscopic ultrasound (EUS) has become the modality of choice for detecting these lesions due to its high tumor detection rate. Additionally, therapeutic techniques have arisen from EUS which allow for the treatment of PNETs. Overall, EUS has become a powerful diagnostic and therapeutic modality for addressing pancreatic lesions such as PNETs. In this perspective article, we provide an overview of the therapeutic potentials of EUS in the management of PNETs.