A recent study reveals that bacteria residing within colorectal tumors form distinct ecosystems closely linked to disease progression and patient outcomes. These “tissue-resident” microbes appear to play an integral role in shaping tumor biology, and can help predict patient survival more accurately than standard clinical factors alone.

A recent study published in the medical journal Gut has revealed a novel cancer-promoting mechanism of Streptococcus anginosus (Sa). The research shows that methionine metabolites produced by this bacterium can significantly contribute to the development of gastric cancer.

This finding deepens the understanding of the gut microbiome’s role in cancer and opens new paths for microbiota-targeted prevention strategies.

This study reveals how lipid metabolism dysregulation promotes colorectal cancer liver metastasis (CRLM) through a novel YTHDF3-mediated mechanism involving m⁶A RNA modification and liquid-liquid phase separation.

Gastric (stomach) cancer remains one of the most common and deadly cancers in East Asia, including Korea. Yet despite its high prevalence, it has received far less molecular attention than colorectal cancer, which is more common in Western countries. As a result, many of today’s models of gastric cancer biology are still based on assumptions borrowed from colorectal cancer research — often with limited success when applied to patients.

One of the biggest unanswered questions has concerned the very first steps of gastric cancer development: how do early cancer cells survive and grow when they should not?

Under normal conditions, cells lining the stomach cannot grow independently. They rely on constant signals from their surrounding tissue — known as the microenvironment — to tell them when to divide, when to rest, and when to die. Losing this dependence is one of the defining features of cancer. But in gastric cancer, researchers have long struggled to explain how this transition occurs.

This problem has been tackled by a joint international research team led by Dr. LEE Ji-Hyun, Dr. KOO Bon-Kyoung, and Dr. LEE Heetak at the Center for Genome Engineering within the Institute for Basic Science (IBS), in partnership with the laboratories of Prof. CHEONG Jae-Ho and Prof. KIM Hyunki (Yonsei University College of Medicine) and Prof. Daniel E. STANGE (TU Dresden / University Hospital Carl Gustav Carus). The team has identified a previously unknown mechanism that allows early gastric cancer cells to become self-sufficient. The findings provide a new framework for understanding how stomach cancer begins — and point to potential new targets for treatment.

Clostridioides difficile is best known for causing antibiotic-related diarrhea, but a new review from China suggests it may also promote gastrointestinal cancers, especially colorectal cancer (CRC). The authors summarize clinical data, epidemiology, and tumor models showing how recurrent infection, toxins, inflammation, metabolism, and biofilms could reshape the colonic microenvironment. They argue chronic C. difficile infection as a potential driver of colorectal tumorigenesis and a promising biomarker, offering new insights for effective CRC prevention and therapy.

Researchers from the B·ARGO at IGTP and ICO have conducted a comparative analysis of the impact of BRAF gene mutations in melanoma and colorectal cancer, published in the journal BBA Reviews on Cancer.