Exercise finds improvements in pain and function may fall short of what patients would notice in daily life, but more studies are needed to make firm conclusions, a new Cochrane review finds.

Enhancers are pieces of DNA that act like switches, regulating when genes are turned on and off and how strongly they are activated. Scientists know these switches play a critical role in cancer and other diseases, but they have yet to fully understand how enhancers work together to control gene activity. A new study, which focused on the DNA switches of prostate cancer cells, reveals new insights into enhancers that become active during cancer development and turn on genes linked to the disease. The study found that enhancers work cooperatively in 3D networks, rather than as isolated switches. Some enhancers function as “central hubs” that control many genes, while others play a supporting role. Rhie's lab focuses on chromatin interactions, a specialized area of research that investigates how DNA folds and interacts to regulate gene expression. Using 201 datasets from both prostate tumor samples and healthy prostate tissue, her team identified 3,216 key enhancers specific to prostate cancer. They then zoomed in on one region of the genome and used an advanced technique known as Region Capture Micro-C to map physical interactions between enhancers and genes at extremely high resolution. They found that in prostate cancer cells, enhancers formed an interconnected 3D network that did not exist in normal prostate cells. Next, they used the gene-editing tool CRISPR to delete enhancers one at a time and observe how this affected enhancer activity, chromatin interactions, gene expression and cancer cell growth. Deleting some enhancers had little effect. Deleting other “central” enhancers disrupted the entire network, reducing the activity of other enhancers, switching off many cancer-promoting genes and slowing cancer cell growth. The discovery that some enhancers serve as key control points could inform future cancer therapies. Rather than targeting individual genes, gene-editing therapies could one day edit these master switches to control multiple cancer-promoting genes at the same time.

As the need for new physician-scientists grows, the Texas Tech University Health Sciences Center (TTUHSC) Medical Student Summer Research Program (MSSRP) provides opportunities to build foundational skills. New research on the program shows promising results for a research-ready physician workforce.

A national study led by the Keck School of Medicine of USC analyzed more than 42,000 U.S. death certificates and found significant disparities in multiple sclerosis (MS) mortality by race, age and geography. Black patients with MS died younger than white patients, with death rates peaking a decade earlier, while co-occurring conditions like high blood pressure and cardiac arrest emerged as growing contributors to mortality. The findings, published in Neurology, also revealed that MS death rates rose steadily over the 12-year study period despite treatment advances, and were highest in parts of the northern and midwestern U.S. The researchers say the results point to a need for earlier diagnosis and more comprehensive care that addresses cardiovascular health alongside MS treatment.

Three studies presented today at the Society of NeuroInterventional Surgery’s (SNIS) 23rd Annual Meeting found that racial, geographic and socioeconomic disparities continue to influence stroke treatment and outcomes across the United States. Together, the findings suggest that while advances in stroke care have improved survival and expanded treatment options, not all patients are benefiting equally.

Researchers at the Society of NeuroInterventional Surgery (SNIS) 23rd Annual Meeting presented an experimental neurointerventional technique designed to treat severe back pain, a leading cause of disability and opioid use, by delivering medication directly through the arteries supplying the painful area. The approach uses catheter-based procedures commonly used for stroke treatment to target the source of pain in the spine.