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Cancer creates an immunosuppressive environment that hampers immune responses, allowing tumors to grow and resist therapy. One way the immune system fights back is by inducing ferroptosis, a type of cell death, in tumor cells through CD8 + T cells. This involves lipid peroxidation and enzymes like lysophosphatidylcholine acyltransferase 3 (Lpcat3), which makes cells more prone to ferroptosis. However, the mechanisms by which cancer cells avoid immunotherapy-mediated ferroptosis are unclear. Our study reveals how cancer cells evade ferroptosis and anti-tumor immunity through the upregulation of fatty acid-binding protein 7 (Fabp7).

To explore how cancer cells resist immune cell-mediated ferroptosis, we used a comprehensive range of techniques. We worked with cell lines including PD1-sensitive, PD1-resistant, B16F10, and QPP7 glioblastoma cells, and conducted in vivo studies in syngeneic 129 Sv/Ev, C57BL/6, and conditional knockout mice with Rora deletion specifically in CD8+ T cells, Cd8 cre; Rorafl mice. Methods included mass spectrometry-based lipidomics, targeted lipidomics, Oil Red O staining, Seahorse analysis, quantitative PCR, immunohistochemistry, PPARγ transcription factor assays, ChIP-seq, untargeted lipidomic analysis, ROS assay, ex vivo co-culture of CD8+ T cells with cancer cells, ATAC-seq, RNA-seq, Western blotting, co-immunoprecipitation assay, flow cytometry and Imaging Mass Cytometry.

PD1-resistant tumors upregulate Fabp7, driving protective metabolic changes that shield cells from ferroptosis and evade anti-tumor immunity. Fabp7 decreases the transcription of ferroptosis-inducing genes like Lpcat3 and increases the transcription of ferroptosis-protective genes such as Bmal1 through epigenetic reprogramming. Lipidomic profiling revealed that Fabp7 increases triglycerides and monounsaturated fatty acids (MUFAs), which impede lipid peroxidation and ROS generation. Fabp7 also improves mitochondrial function and fatty acid oxidation (FAO), enhancing cancer cell survival. Furthermore, cancer cells increase Fabp7 expression in CD8+ T cells, disrupting circadian clock gene expression and triggering apoptosis through p53 stabilization. Clinical trial data revealed that higher FABP7 expression correlates with poorer overall survival and progression-free survival in patients undergoing immunotherapy.

Senescent skin cells, often referred to as zombie cells because they have outlived their usefulness without ever quite dying, have existed in the human body as a seeming paradox, causing inflammation and promoting diseases while also helping the immune system to heal wounds.

New findings may explain why: Not all senescent cells are the same.

Researchers from Johns Hopkins University have identified three subtypes of senescent skin cells with distinct shapes, biomarkers, and functions—an advance that could equip scientists with the ability to target and kill the harmful types while leaving the helpful ones intact.

Brain cell-derived extracellular vesicles (EVs) in the blood, carrying diverse cargoes, represent a valuable source of predictive, diagnostic, prognostic, disease-monitoring and treatment-response biomarkers for neurological disorders. This Review summarizes key aspects of EV biology and provides a critical overview of EV biomarker research and therapeutic development in neurology.

Shark fin electrocardiographic (ECG) pattern, also known as ‘Lambda-wave’, ‘giant R waves’, or ‘triangular QRS-ST-T waveform’ is a dangerous ECG pattern associated with ST-elevation myocardial infarction (STEMI). It is formed by the fusion of QRS, ST, and T waves and predicts the high risk of mortality due to cardiogenic shock and ventricular fibrillation. The management should be aggressive with reperfusion via thrombolysis or percutaneous intervention, ideally in the intensive care unit with ventricular assist devices. This ECG pattern may be misdiagnosed as wide complex tachycardia or the ECG changes of hyperkalemia. Thus, differentiating it from other conditions causing similar ECG changes and prompt management is highly important to save the patient from serious complications.

A scientific revolution is underway as researchers push to bring atomic-level precision, once reserved for small molecule drugs, into the realm of nanomedicine. By tightly controlling the structure of nanoscale therapies, they’re creating more effective vaccines and treatments for cancer, infecti

A new study found that a gene recently recognized as a biomarker for Alzheimer’s disease is actually a cause of it, due to its previously unknown secondary function. Researchers at the University of California San Diego used artificial intelligence to help both unravel this mystery of Alzheimer’s disease and discover a potential treatment that obstructs the gene’s moonlighting role.

The research team published their results on April 23 in the journal Cell.

About one in nine people aged 65 and older has Alzheimer’s disease, the most common cause of dementia. While some particular , when mutated, can lead to Alzheimer’s, that connection only accounts for a small percentage of all Alzheimer’s patients. The vast majority of patients do not have a mutation in a known disease-causing gene; instead, they have “spontaneous” Alzheimer’s, and the causes for that are unclear.

In today’s interconnected world, infectious diseases pose an escalating threat, as demonstrated by the coronavirus pandemic and outbreaks of H1N1, SARS, Ebola, Zika, and H5N1 (bird flu) viruses—all of which have had significant global health and economic impacts.

But more common viral diseases also contribute to global health challenges and economic costs. For example, seasonal influenza epidemics occur annually, causing a substantial global disease burden and economic losses exceeding $11.2 billion each year in the United States alone. Meanwhile, herpes simplex virus-1 (HSV-1), spread primarily through oral contact, infects over two-thirds of the global population and is the leading cause of infectious blindness in Western countries.

Low vaccination rates for influenza viruses and the lack of an HSV vaccine underscore the need for a new approach—one that targets reducing viral loads at the sites where transmission occurs. And for viruses like these, which are transmitted more efficiently through the mouth than the nose, this means focusing on the oral cavity.