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Decoding 3D chromatin architecture reveals distinct enhancer classes underlying hierarchical gene regulation in prostate cancer

The transcription process is controlled by non-coding regulatory elements, more than 70% of which are putative enhancers. These enhancers comprise over 600,000 regions and are marked by histone modifications. However, the mechanisms by which altered enhancers in cancer cooperate within the three-dimensional chromatin architecture to drive oncogenic programs remain poorly understood.

By integrating 201 H3K27ac ChIP-seq datasets from prostate, we identify 3,216 high-confidence prostate cancer-specific putative enhancers. Ultra-high-resolution chromatin interaction profiling by Region Capture Micro-C at a representative chr6q24.1 locus reveals that these enhancers form cancer-specific, highly nested interactions with promoters that coalesce into a multi-connected hub absent in normal prostate cells. CRISPR/Cas9 perturbations of these enhancers, examined one by one, distinguish enhancer classes within the hub. Deletion of a central enhancer collapses hub-wide enhancer activities and architecture, leading to the downregulation of target genes, impaired proliferation, and reduced clonogenic growth. In contrast, deletion of a redundant enhancer results in minimal transcriptional changes, as neighboring enhancers rescue cancer signaling through compensatory architectural rewiring that strengthens alternative enhancer-promoter interactions.

A study in mice and human tissue shows that the antioxidant glutathione feeds cancer cells

Glutathione is considered an antioxidant due to its ability to repair cellular damage. The body produces it naturally, but it is also sold as an antioxidant supplement. A study in mice and human tissue, published in Nature, shows that cancer cells can break it down and use it as fuel—particularly the cysteine it contains—promoting tumour growth and survival. “Depriving tumours of extracellular glutathione or inhibiting its breakdown is potentially a viable therapeutic strategy for cancer patients,” the authors state.

Yeast βglucan supplementation supports immunometabolic antitumor responses and reverses obesityinduced dysfunction via trained hematopoiesis

Obesity is associated with profound immune dysregulation, driving chronic inflammation while compromising host defense against tumors. While trained immunity can enhance innate effector functions, it has thus far required parenteral administration of microbial ligands. Here, we show that incorporating a yeast-derived β-glucan supplement in mouse diets induces trained immunity via reprogramming of hematopoietic stem and progenitor cells. This dietary intervention leads to sustained production of metabolically enhanced monocytes and macrophages that rescue anti-tumor immunity in high-fat diet-induced obese mice, and corrects immune dysfunction sustained after weight loss. Our work reveals that yeast β-glucans act as functional “immuno-nutrients,” which remodel innate immunity and identifies the mucosal/bone-marrow axis as a target for dietary manipulations to restore immune resilience without impacting metabolism.

Keywords: CP: immunology; beta-glucan; dietary supplementation; hematopoiesis; immunometabolism; innate immunity; macrophage; monocyte; obesity; trained immunity; tumor immunity.

Copyright © 2026 The Authors. Published by Elsevier Inc. All rights reserved.

Newly discovered microprotein linked to type 2 diabetes, shows promise as a precision treatment

A previously unknown microprotein hidden within the human mitochondrial genome may help explain certain forms of type 2 diabetes and could point toward a new precision medicine approach to treating it, according to a new USC study.

Obesity and type 2 diabetes are among the fastest-growing threats to human health, yet their genetic underpinnings remain only partly understood. While most disease-gene research focuses on the larger set of DNA found in the nucleus within cells, the much smaller genome found in mitochondria—cells’ energy factories—is now known to encode a family of microproteins with wide-ranging biological effects.

The new study adds a striking example to that list, said Pinchas Cohen, the study’s senior author, USC Distinguished Professor and dean of the USC Leonard Davis School of Gerontology. The findings were published in the journal Theranostics.

Obstructive sleep apnea in people with epilepsy: Modifying risk

Obstructive sleep apnea (OSA) is a common but underdiagnosed and undertreated sleep disorder among people with epilepsy (PWE). In PWE, this sleep disorder is often managed as a comorbid condition rather than a contributor to epilepsy outcomes. For many years, OSA has been associated with higher seizure burden and interictal epileptiform discharges. Emerging evidence links OSA to late onset epilepsy (LOE) and increased risk markers for sudden unexpected death in epilepsy (SUDEP). This evidence also suggests that treating OSA with continuous positive airway pressure may improve seizure control. This critical review of the literature posits that OSA should be viewed as a modifiable risk factor for PWE. We apply the Bradford Hill criteria for causation as a framework to appraise the evidence connecting OSA with seizure severity, incident LOE, and SUDEP risk.

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