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Background Neurofascin 155 autoimmune nodopathy (NF155 AN) is a recently recognised immune-mediated neuropathy distinct from chronic inflammatory demyelinating polyneuropathy. While adult-onset cases have been increasingly reported, the juvenile-onset form remains poorly characterised.

Methods We retrospectively analysed 36 patients with NF155 AN, focusing on detailed characterisation of 16 juvenile-onset cases. Their clinical and laboratory data were reviewed.

Results Juvenile-onset patients presented with sensorimotor neuropathy characterised by distal predominant weakness, tremor and sensory ataxia. Motor symptoms were the presenting feature in 75% of patients, which significantly differed from the adult cases (p=0.0015). Postural tremor was more frequent in juvenile patients (94%), while cranial nerve involvement was less common (19%).

Gou Young Koh & team establish ERG and Fli1 as core transcriptional regulators of lymphatic identity, integrity, and function, using human cells and mouse models:

The figure shows stasis of mesenteric lymphatic drainage for a tracer (red) in Prox1-GFP-mice lacking Erg/Fli1 specifically in lymphatic endothelial cells compared with Prox1-GFP-WT mice; with Prox1-GFP marking lymphatic structures (green).

¹Center for Vascular Research, Institute for Basic Science, Daejeon, South Korea.

²Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, South Korea.

Address correspondence to: Hyuek Jong Lee or Gou Young Koh, Center for Vascular Research, Institute for Basic Science, Daejeon 34,141, South Korea. Email: [email protected] (HJL); [email protected] (GYK).

Liver regeneration in chronic disease is incompletely understood. In this issue, Jia and coworkers identify a distinct population of hepatocytes expressing Setd4 as key contributors to liver regeneration after chronic injury. Using lineage-tracing and ablation strategies in mouse models of chronic liver damage due to thioacetamide or 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet, the authors show that Setd4+ cells are a long-lasting, dormant, injury-resistant hepatocyte population that survives chronic insults and get activated to support de novo regeneration. Quiescent Setd4+ cells show suppressed metabolic activity maintained by a chromatin state that promotes cellular dormancy and survival (H4K20me3-enriched heterochromatin). After chronic injury, chromatin accessibility remodelling occurs, leading to activation of the cells and initiating regeneration. Selective ablation of Setd4+ cells markedly impaired regenerative recovery, leading to increased fibrosis, higher transaminases, and shorter survival. Interestingly, Setd4+ cells appeared to be essential to initiate de novo regeneration under chronic but not acute conditions. Given the presented data, this newly identified dormant Setd4+ hepatocyte population might hold therapeutic potential to restore regeneration in chronic liver disease.

Full text here: https://www.journal-of-hepatology.eu/article/S0168-8278(…4/fulltext.

EASL — the home of hepatology.

Chronic liver injury and its progression to disease often extend beyond exposure to toxic metabolites or xenobiotics. Recovery from chronic injury, when achieved, depends on de novo regeneration, the underlying mechanisms of which remain poorly understood. Herein, we investigate a specific cell population proposed to be fundamental for de novo regeneration and recovery following chronic injury, aiming to elucidate its regulatory mechanisms.

Now online! Leigh syndrome is a severe and untreatable mitochondrial disease. Using patient-derived models in 2D and 3D, Zink and colleagues identify the PDE5 inhibitor sildenafil as a repurposable drug candidate, leading to lifespan extension in mammalian models and clinical improvement in six individuals with Leigh syndrome.

Zhang, S., Fu, Q., Yuan, X. et al. Reshaping the colorectal cancer immune microenvironment: insights from single-cell and spatial omics. Cancer Cell Int (2026). https://doi.org/10.1186/s12935-026-04245-y.

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New in practicalRO: radonc.

A dose-escalation trial of reirradiation (reRT) was conducted in patients with a diagnosis of recurrent glioblastoma (rGBM) to increase the total overall dose given to the tumor without increasing toxicity. The primary objective of this study was to establish the maximum tolerated dose (MTD) for reRT in patients with rGBM.

A new preclinical study in mice shows that precancerous cells in the pancreas can be eliminated before they have the chance to become tumors. Using an experimental therapy to target microscopic precancerous lesions in the pancreas nearly doubled survival in mouse models of pancreatic ductal adenocarcinoma (PDAC) compared to the same treatment given after cancer developed.

The research, published in Science, was led by physician-scientists in the Perelman School of Medicine at the University of Pennsylvania and Penn Medicine’s Abramson Cancer Center. It’s the first time scientists have shown that a medical intervention could stop growth of pre-cancerous lesions in the pancreas before they develop into pancreatic cancer, providing strong evidence for the burgeoning field of cancer interception.

“I’m convinced that cancer interception will become the next frontier of cancer therapy,” said co-corresponding author Robert Vonderheide, MD, DPhil, director of the Abramson Cancer Center.