Scientists at Nagoya University in Japan studied what happens when macrophages—a type of immune cell—encounter dying cancer cells in tumors and discovered a mechanism that accelerates tumor growth. When cancer cells begin to die within tumors, they expose signals on their surface that indicate they are dying. Macrophages then detect these signals and engage in phagocytosis, where they eat dying cancer cells. Using fruit flies as a model organism, the scientists found this triggers production of proteins called cytokines, which activate growth signals in remaining cancer cells. These cells then produce more cytokines, causing an unexpected chain reaction that promotes tumor growth.  

Some disposable, electronic cigarettes and vape pods release higher amounts of toxic metals than older e-cigarettes and traditional cigarettes, according to a UC Davis study.

Aggressive forms of acute myeloid leukemia (AML) remain challenging to treat, especially in patients with FLT3-ITD mutations. Researchers from Japan have identified SETD1B as a key epigenetic regulator that promotes leukemia cell growth by promoting MYC activation through H3K4me3 modification. Using laboratory models, they demonstrated that disrupting SETD1B significantly slows cancer cell proliferation. These findings offer promising new avenues for developing therapies against treatment-resistant AML.  

It’s common knowledge that preventing diabetes decreases the chance of mortality. But even within those with “normal” blood glucose levels, is there an optimal number for reducing the risk of other diseases such as heart disease or cancer? A small farming community in the Tohoku region may have provided medical researchers with the clues they have been looking for. 

Recent findings shed new light on the critical role of TET1, a pivotal player in epigenetic regulation, in the development and progression of various clinical diseases. As an enzyme responsible for DNA demethylation, TET1 influences gene expression by modifying methylcytosine levels, which are crucial for maintaining genomic stability and proper cellular function.

This new review article highlights the critical role of ribosome biogenesis in liver health and disease progression. As the center of protein synthesis, ribosomes influence liver regeneration, hepatitis C virus (HCV) infection, nonalcoholic fatty liver disease (NAFLD), liver fibrosis, cirrhosis, and hepatocellular carcinoma. The article explores how disruptions in this process contribute to disease and how targeted therapies could offer new treatment avenues.

A new review brings to light the pivotal role of ribonucleases (RNases) in shaping the molecular foundation of Mendelian disorders. These essential enzymes, known for maintaining RNA metabolism, are revealed as central players in a diverse spectrum of human diseases. When disrupted by genetic mutations, RNases lose their ability to regulate RNA dynamics, giving rise to neurological, growth-related, hematopoietic, and mitochondrial dysfunctions.