The latest discoveries in Endocrinology
Science Briefing
Sciencebriefing.com A concise briefing on the most relevant research developments in your field, curated for clarity and impact. sign Up and get -40%. USE CODE: CHRISTMAS50
A common enzyme, a stubborn cancer drug: the resistance circuit comes into focus
This study reports a mechanism of chemotherapy resistance in pancreatic cancer centered on ENO1. The authors link ENO1 to increased deoxycytidine synthesis and show that ENO1 stabilizes RRM2, a key component of nucleotide metabolism, in a way that supports resistance to gemcitabine. By connecting metabolic rewiring to a specific, drug-relevant node (RRM2), the work highlights actionable biology that could be exploited to restore gemcitabine sensitivity.
Why it might matter to you: Treatment resistance is often a downstream consequence of altered metabolism, and this paper provides a concrete, testable pathway that could inform biomarker selection and combination-therapy strategies. If similar nucleotide-supply mechanisms operate across hormone-influenced or gynecologic malignancies, the ENO1–RRM2 axis may help frame how to anticipate (and potentially prevent) loss of response during systemic therapy.
The skin’s repair switch: a new target for chronic wounds
This translational study identifies HDAC5 activity as a key regulator of skin re-epithelialization, reporting that HDAC5 deacetylates cytosolic ACTN4 during wound repair. By tying a specific deacetylation event to the mechanics of tissue closure, the work positions HDAC5 as a potential therapeutic target in chronic, non-healing wounds. The findings offer a molecular handle on a clinically persistent problem: how to reliably shift stalled wounds back into an effective repair program.
Why it might matter to you: Impaired wound healing intersects with metabolic and hormonal states that clinicians frequently manage, making mechanistically grounded targets valuable for risk stratification and future adjunct therapies. This work may also sharpen how you interpret skin and surgical-site healing complications by pointing to a druggable epigenetic control point rather than a purely “local” wound issue.
The brain’s glutamine supply chain isn’t local—and that changes the playbook
This paper describes how SLC38A3 functions at the blood–brain barrier as a critical transporter for blood-derived glutamine needed for normal brain development. In a mouse model with endothelial deletion of Slc38a3, reduced glutamine influx lowered brain glutamine, disrupted downstream neurotransmitter metabolism (glutamate and GABA pathways), and produced progressive microcephaly with neurologic and behavioral abnormalities. Notably, glutamine supplementation replenished brain glutamine and prevented key phenotypes, supporting a causal, potentially treatable “BBB aminoacidopathy.”
Why it might matter to you: The findings strengthen the concept that fetal and neonatal neurodevelopment can be constrained by specific, addressable nutrient-transport bottlenecks rather than only global malnutrition or placental insufficiency. For clinical pathways that involve developmental risk counseling or multidisciplinary perinatal care, this work adds a compelling example of a supplementation-responsive mechanism that could influence future screening and targeted intervention discussions.