Molecular biologist Yali Dou, PhD, holder of the Marion and Harry Keiper Chair in Cancer Research and professor of medicine and cancer biology at the Keck School of Medicine of USC, has been elected a fellow of the American Association for the Advancement of Science (AAAS). She is one of seven USC faculty members in the 2025 cohort of new fellows. Dou, the associate director for basic research at USC Norris Comprehensive Cancer Center, is a recognized leader in the study of epigenetics, the mechanisms that enable the singular instructions in DNA to be expressed as myriad cell and tissue types. She has made major contributions to the fundamental understanding of a family of enzymes that plays a vital role in fetal development by altering the coiled chromatin, which packages DNA to fit in the chromosomes of a cell’s nucleus, so that genes are activated. Because mutations of the founding member of this family of enzymes can also spur leukemia, they are known as mixed-lineage leukemia proteins, or MLL. MLL enzymes are among the most frequently mutated genes in cancer.

Cancer remains a leading cause of death globally, with lung cancer being particularly lethal. Despite advancements in diagnostics and therapies, the five-year survival rates for advanced tumors have seen minimal improvement, largely due to therapeutic resistance. This resistance can be genetic or nongenetic, with the latter being less understood but increasingly recognized for its role in treatment failure. Non-genetic resistance is associated with resistant cancer cells that have innate or acquired drug resistance traits. These cells are often found in heterogeneous tumors and include cancer stem-like cells (CSCs), cells undergoing epithelial-to-mesenchymal transition (EMT), partial EMT cells, and drug-tolerant persisters (DTPs). NOTCH signaling plays a crucial role in tumorigenesis and therapeutic resistance, with its activation linked to drug resistance in various cancers.

Using cutting-edge spatial and genetic tools, Singapore scientists have uncovered two gastric cancer tumour subgroups, characterising their unique cellular states, immune responses and interactions with their surroundings. Their discoveries can potentially revolutionise stomach cancer therapy by unveiling new targets for precision diagnostics and treatment.

The mechanism of anticancer activity of a pigment OR3 from Streptomyces coelicolor is explored in in vitro and in vivo metastatic breast cancer models.

The University of Texas MD Anderson Cancer Center today announced that Jeffrey E. Lee, M.D., an internationally regarded leader in the field of oncology, has been appointed chief medical executive (CME) effective April 1. Prior to his appointment, Lee served as CME ad interim, demonstrating strength as a leader committed to advancing the institution’s efforts in research, patient care, prevention and education. Assuming the role of CME is the culmination of Lee’s 34-year tenure at the institution, where he has made substantial contributions in the field of oncology and served in multiple leadership roles

A tiny magnetic robot which can take 3D scans from deep within the body, that could revolutionise early cancer detection, has been developed by researchers. 

The team, led by engineers from the University of Leeds, say this is the first time it has been possible to generate high-resolution three-dimensional ultrasound images taken from a probe deep inside the gastrointestinal tract, or gut. 

Research conducted by the National Cancer Research Centre (CNIO), published today in ‘Nature’, reveals a mechanism in mice that is triggered just minutes after acute liver damage occurs.

This finding opens up avenues for future treatments of serious liver damage to include a diet enriched with the amino acid glutamate.

Glutamate supplementation can promote liver regeneration and benefit patients in recovery following hepatectomy or awaiting a transplant, the authors write in ‘Nature’.

Activating liver regeneration is key to treating diseases that involve severe liver damage, which are becoming increasingly frequent and are associated with poor dietary habits and alcohol consumption.

The body’s cells respond to stress—toxins, mutations, starvation or other assaults—by pausing normal functions to focus on conserving energy, repairing damaged components and boosting defenses.

If the stress is manageable, cells resume normal activity; if not, they self-destruct.

Scientists have believed for decades this response happens as a linear chain of events: sensors in the cell “sound an alarm” and modify a key protein, which then changes a second protein that slows or shuts down the cell’s normal function.

But in a new study published today in the journal Nature, researchers at Case Western Reserve University have discovered a cell’s response is more nuanced and compartmentalized—not fixed or rigid, as previously thought.