Scientists have discovered a key protein that helps cancer cells avoid detection by the immune system during a type of advanced therapy.

By creating a new drug that blocks this protein, researchers hope to make cancer treatments more effective, especially for hard-to-treat blood cancers. This breakthrough could lead to better survival rates and fewer relapses for patients.

Scientists at City of Hope, one of the leading cancer research and treatment centers in the U.S., have uncovered a key factor that allows cancer cells to evade CAR T cell therapy.

HPH-15, a compound developed by Kumamoto University, reduces blood glucose and fat accumulation more effectively than metformin, with added benefits like antifibrotic properties and a safer profile. This innovation may revolutionize diabetes treatment.

Scientists at Kumamoto University have unveiled a novel compound, HPH-15, which has dual effects: reducing blood glucose levels and combating fat accumulation. This breakthrough represents a significant advancement in diabetes treatment innovation.

Type 2 diabetes, a condition affecting millions worldwide, is often accompanied by complications such as fatty liver and insulin resistance, posing challenges for current treatment methods. The research team, led by Visiting Associate Professor Hiroshi Tateishi and Professor Eiichi Araki, has identified HPH-15 as a promising alternative to existing medications like metformin.

A research team led by Prof. Wang Haoyi from the Institute of Zoology (IOZ) of the Chinese Academy of Sciences has developed a chimeric antigen receptor T (CAR-T) cell exhaustion model and a functional screening platform for identifying compounds that can rejuvenate exhausted T cells.

Using this innovative platform, the team identified the small-molecule compound miltefosine, which significantly enhances the tumor-killing activity of CAR-T cells. This study was published in Cell Reports Medicine on December 9.

T cell exhaustion is a differentiation state that arises when T cells are exposed to persistent antigen stimulation. This state is characterized by a progressive loss of effector functions, sustained expression of inhibitory receptors, impaired proliferation, and compromised mitochondrial respiration and glycolysis capacity.