Evidence map›Paper›PMID 38916435›Full record

ArticleProtein & cell2025

Lentivirus-modified hematopoietic stem cell gene therapy for advanced symptomatic juvenile metachromatic leukodystrophy: a long-term follow-up pilot study.

Zhao Zhang, Hua Jiang, Li Huang, Sixi Liu, Xiaoya Zhou, Yun Cai, Ming Li, Fei Gao, Xiaoting Liang, Kam-Sze Tsang and 13 more

Abstract read
In one paragraph

Article in Protein & cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

23 authors.

Zhao ZhangCord Blood Bank, Guangzhou Institute of Eugenics and Perinatology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Hua JiangDepartment of Haematology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Li HuangCord Blood Bank, Guangzhou Institute of Eugenics and Perinatology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.ORCID 0000-0002-1564-0110
Sixi LiuDepartment of Hematology and Oncology, Shenzhen Children's Hospital, Shenzhen 518026, China.
Xiaoya ZhouCord Blood Bank, Guangzhou Institute of Eugenics and Perinatology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Yun CaiDepartment of Haematology, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen University School of Medicine, Shenzhen University, Shenzhen 518060, China.
Ming LiDepartment of Haematology, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen University School of Medicine, Shenzhen University, Shenzhen 518060, China.
Fei GaoState Key Laboratory of Pharmaceutical Biotechnology, Department of Medicine, The University of Hong Kong, Hong Kong SAR 999077, China.
Xiaoting LiangState Key Laboratory of Pharmaceutical Biotechnology, Department of Medicine, The University of Hong Kong, Hong Kong SAR 999077, China.
Kam-Sze TsangDepartment of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, Hong Kong SAR 999077, China.
Guangfu ChenDepartment of Paediatrics, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen University School of Medicine, Shenzhen University, Shenzhen 518060, China.
Chui-Yan MaState Key Laboratory of Pharmaceutical Biotechnology, Department of Medicine, The University of Hong Kong, Hong Kong SAR 999077, China.
Yuet-Hung ChaiState Key Laboratory of Pharmaceutical Biotechnology, Department of Medicine, The University of Hong Kong, Hong Kong SAR 999077, China.
Hongsheng LiuDepartment of Radiology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 518026, China.
Chen YangCord Blood Bank, Guangzhou Institute of Eugenics and Perinatology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Mo YangScientific Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen 518107, China.
Xiaoling ZhangDepartment of Hematology and Oncology, Shenzhen Children's Hospital, Shenzhen 518026, China.
Shuo HanState Key Laboratory of Pharmaceutical Biotechnology, Department of Medicine, The University of Hong Kong, Hong Kong SAR 999077, China.
Xin DuDepartment of Haematology, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen University School of Medicine, Shenzhen University, Shenzhen 518060, China.
Ling ChenState Key Laboratory of Pharmaceutical Biotechnology, Department of Medicine, The University of Hong Kong, Hong Kong SAR 999077, China.
Wuh-Liang HwuDepartment of Paediatrics and Medical Genetics, Taiwan University Hospital, Taipei 110024, China.
Jiacai ZhuoDepartment of Haematology, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen University School of Medicine, Shenzhen University, Shenzhen 518060, China.
Qizhou LianCord Blood Bank, Guangzhou Institute of Eugenics and Perinatology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.ORCID 0000-0001-8189-7160

Funding

Poland Fundacja Siepomaga, JS Foundation
6 · The paper itself

Abstract

Metachromatic leukodystrophy (MLD) is an inherited disease caused by a deficiency of the enzyme arylsulfatase A (ARSA). Lentivirus-modified autologous hematopoietic stem cell gene therapy (HSCGT) has recently been approved for clinical use in pre and early symptomatic children with MLD to increase ARSA activity. Unfortunately, this advanced therapy is not available for most patients with MLD who have progressed to more advanced symptomatic stages at diagnosis. Patients with late-onset juvenile MLD typically present with a slower neurological progression of symptoms and represent a significant burden to the economy and healthcare system, whereas those with early onset infantile MLD die within a few years of symptom onset. We conducted a pilot study to determine the safety and benefit of HSCGT in patients with postsymptomatic juvenile MLD and report preliminary results. The safety profile of HSCGT was favorable in this long-term follow-up over 9 years. The most common adverse events (AEs) within 2 months of HSCGT were related to busulfan conditioning, and all AEs resolved. No HSCGT-related AEs and no evidence of distorted hematopoietic differentiation during long-term follow-up for up to 9.6 years. Importantly, to date, patients have maintained remarkably improved ARSA activity with a stable disease state, including increased Functional Independence Measure (FIM) score and decreased magnetic resonance imaging (MRI) lesion score. This long-term follow-up pilot study suggests that HSCGT is safe and provides clinical benefit to patients with postsymptomatic juvenile MLD.

Indexed as

Genetic TherapyHematopoietic Stem Cell TransplantationLentivirusLeukodystrophy, MetachromaticAdolescentCerebroside-SulfataseChildChild, PreschoolFemaleFollow-Up StudiesHematopoietic Stem CellsHumansMalePilot ProjectsCerebroside-Sulfataseadvanced symptomaticefficacyHSCGTjuvenilemetachromatic leukodystrophypatientssafety

Identifiers

PMID38916435
PMCPMC11700595

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.