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Melanoma ‘cellular compass’ discovery could help curb metastasis

Researchers have discovered a protein which is critical for steering melanoma cancer cells as they spread throughout the body. The malignant cells become dependent on this protein to migrate, pointing to new strategies for impeding metastasis.

The protein eIF2A is generally thought to spring into action when a cell is under stress, helping ribosomes launch protein synthesis. But according to a study published in the journal Science Advances, eIF2A has a completely different role in melanoma, helping control movement.

“Malignant cells that metastasize need to make their way through tissues in order to invade proximal or distant organs. Targeting eIF2A could be a new strategy to impede melanoma breaking free and seeding tumors elsewhere,” says Dr. Fátima Gebauer, corresponding author of the study and researcher at the Center for Genomic Regulation (CRG) in Barcelona.

The 0.05% RNA Process That Makes Cancer Self-Destruct

A group of Australian scientists has uncovered a new way to fight some of the toughest cancers by targeting an overlooked cellular process called minor splicing. This tiny but vital mechanism turns out to be essential for the growth of certain tumors, especially those driven by KRAS mutations — a common but hard-to-treat culprit in cancer. By blocking minor splicing, researchers triggered DNA damage and activated the body’s own cancer-defense system, killing cancer cells while sparing healthy ones. The results in animal and human cell models are so promising that drug development is now underway, potentially paving the way for more effective and less toxic treatments across multiple cancer types.

Sugar layer on beta cells prevents immune system from causing type 1 diabetes

Scientific breakthroughs in one disease don’t always shed light on treating other diseases. But that’s been the surprising journey of one Mayo Clinic research team. After identifying a sugar molecule that cancer cells use on their surfaces to hide from the immune system, the researchers have found the same molecule may eventually help in the treatment of type 1 diabetes, once known as juvenile diabetes.

Type 1 diabetes is a chronic autoimmune condition in which the immune system errantly attacks that produce insulin. The disease is caused by genetic and other factors and affects an estimated 1.3 million people in the U.S.

In their studies, the Mayo Clinic researchers took a cancer mechanism and turned it on its head. Cancer cells use a variety of methods to evade , including coating themselves in a known as sialic acid. The researchers found in a preclinical model of type 1 diabetes that it’s possible to dress up beta cells with the same sugar molecule, enabling the immune system to tolerate the cells.

Scientists shrink the genetic code of E. coli to contain only 57 of its usual 64 codons

The DNA of nearly all life on Earth contains many redundancies, and scientists have long wondered whether these redundancies served a purpose or if they were just leftovers from evolutionary processes. Both DNA and RNA contain codons, which are sequences of three nucleotides that either provide information about how to form a protein with a specific amino acid or tell the cell to stop (a stop signal) during protein synthesis.

Serotonin receptor signaling insights may pave way for next-gen mental health drugs

In a discovery that could guide the development of next-generation antidepressants and antipsychotic medications, researchers at the Icahn School of Medicine at Mount Sinai have developed new insights into how a critical brain receptor works at the molecular level and why that matters for mental health treatments.

The study, published in the online issue of Science Advances, focuses on the 5-HT1A , a major player in regulating mood and a common target of both traditional antidepressants and newer therapies such as psychedelics. The paper is titled “Structural determinants of G protein subtype selectivity at the serotonin receptor 5-HT1A.”

Despite its clinical importance, this receptor has remained poorly understood, with many of its molecular and pharmacological properties largely understudied—until now.

The hidden mental health cost of climate distress

A new Stanford-led study sheds light on “an emerging psychological health crisis” that disproportionately affects girls. Published July 30 in The Lancet Planetary Health, the study is among the first to quantify how repeated climate stressors impact the psychological well-being and future outlook of adolescents in low-resource settings.

Researchers from Stanford’s schools of Medicine, Law, and Sustainability partnered with in Bangladesh to survey more than 1,000 teenagers and conduct focus groups across two regions with starkly different flood exposure.

“What we found really lifts the voices of frontline —a group whose perspectives and are so rarely investigated and communicated,” said lead author Liza Goldberg, an incoming Earth system science Ph.D. student in the Stanford Doerr School of Sustainability.

Lactate infusion improves cardiac function in a porcine model of ischemic cardiogenic shock

Cardiogenic shock (CS) is associated with high mortality and medical therapies have failed to improve survival. Treatment with lactate is associated with improved cardiac function which may benefit this condition. Comprehensive hemodynamic assessment of lactate administration in CS is lacking, and the mechanisms underlying the cardiovascular effects of lactate in CS have not yet been elucidated. In this study we aimed to study the cardiovascular and cardiometabolic effects of treatment with lactate in experimental ischemic CS.

In a randomized, blinded design, 20 female pigs (60 kg) were studied. Left main coronary artery microsphere injections were used to cause CS, defined as a 30% reduction in CO or mixed venous saturation (SvO2). Subjects were randomized to receive either intravenous exogenous lactate or euvolemic, equimolar saline (control) for 180 min. Positive inotropic control with dobutamine was administered on top of ongoing treatment after 180 min. Extensive hemodynamic measurements were obtained from pulmonary artery and left ventricular (LV) pressure–volume catheterization. Furthermore, endomyocardial biopsies were analyzed for mitochondrial function and arterial, renal vein, and coronary sinus blood samples were collected. The primary endpoint was change in CO during 180 min of treatment.

Arterial lactate levels increased from 2.4 ± 1.1 to 7.7 ± 1.1 mmol/L (P 0.001) during lactate infusion. CO increased by 0.7 L/min (P 0.001) compared with control, due to increased stroke volume (P = 0.003). Notably, heart rate and mean arterial pressure did not differ significantly between treatments. End-systolic elastance (load independent contractility) was enhanced during lactate infusion (P = 0.048), together with LV ejection fraction (P = 0.009) and dP/dt(max) (P = 0.041). Arterial elastance (afterload) did not differ significantly (P = 0.12). This resulted in improved ventriculo-arterial coupling efficiency (P = 0.012). Cardiac mechanical efficiency (P = 0.003), diuresis (P = 0.016), and SvO2 (P = 0.018) were increased during lactate infusion. Myocardial mitochondrial complex I respiration was enhanced during lactate infusion compared with control (P = 0.04).

Potential chemo-induced cognitive changes discovered in cancer survivors

Researchers at The City College of New York have linked chemotherapy treatment to lasting cognitive changes in rats—potentially shedding light, for the first time, on cognitive problems some cancer survivors experience long after treatment ends.

Titled “Chemotherapy treatment alters DNA methylation patterns in the of female rat brain,” the study appears in the journal Scientific Reports.

“Our study explored how chemotherapy affects the brain at the using an ,” said Karen Hubbard, professor of biology in CCNY’s Division of Science, who co-led the study.