A new study published today in Science Translational Medicine by researchers at The University of Texas MD Anderson Cancer Center details a therapeutic vulnerability in  patients with an aggressive subtype of triple-negative breast cancer.

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.

BUFFALO, NY — December 23, 2025 — A new research paper was published in Volume 12 of Oncoscience on October 14, 2025, titled “Bridging clinical insight and laboratory model in high-grade serous ovarian carcinoma (HGSOC) using DNA sequencing-based profiling of TP53.”

New research reveals that disrupting our internal body clock weakens immune defenses and fuels aggressive cancer — while pointing to a promising new treatment.

Multiple myeloma is an incurable plasma cell malignancy despite major therapeutic advances. A recent review by Chinese researchers highlights how immunotherapy is reshaping its treatment landscape. The article summarizes immune mechanisms driving disease progression and explores emerging targets, such as BCMA, GPRC5D, and FcRL5. It also presents promising approaches—antibody–drug conjugates, CAR-T cells, and bispecific antibodies—offering new opportunities for overcoming drug resistance and achieving durable, personalized cancer immunotherapy.

The 2024 report on China’s gastroenterology and digestive endoscopy, based on national databases, highlights increased early cancer detection, optimized care for priority diseases, and enhanced endoscopy quality, with mixed cost trends for inflammatory bowel disease.

A study by the Mildred Scheel Early Career Center group led by Dr. Mohamed Elgendy at the TUD Faculty of Medicine provides fundamental insights into cancer biology. Published in the renowned journal Nature Communications, the study shows for the first time that the protein MCL1 not only inhibits programmed cell death, but also plays a central role in tumor metabolism.