Evidence map›Paper›PMID 40546725›Full record

Trial reportBlood neoplasia2025

JAK1/2 inhibitor ruxolitinib for the treatment of systemic chronic active Epstein-Barr virus disease: a phase 2 study.

Yu Uemura, Masahide Yamamoto, Masataka Ishimura, Hirokazu Kanegane, Akihisa Sawada, Akihiro Hirakawa, Ken-Ichi Imadome, Mayumi Yoshimori, Masashi Nagata, Kouhei Yamamoto and 3 more

Erratum issuedAbstract readClinical Trial
In one paragraph

Trial report in Blood neoplasia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors.

Yu UemuraDepartment of Hematology and Oncology, St. Marianna University School of Medicine, Kawasaki, Japan.
Masahide YamamotoDepartment of Hematology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Tokyo, Japan.
Masataka IshimuraDepartment of Pediatrics, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Hirokazu KaneganeDepartment of Child Health and Development, Institute of Science Tokyo, Tokyo, Japan.
Akihisa SawadaDepartment of Hematology/Oncology, Osaka Women's and Children's Hospital, Izumi, Japan.
Akihiro HirakawaDepartment of Clinical Biostatistics, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Tokyo, Japan.
Ken-Ichi ImadomeDepartment of Advanced Medicine for Viral Infections, National Center for Child Health and Development, Tokyo, Japan.
Mayumi YoshimoriDepartment of Hematology and Biophysical Systems Analysis, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Tokyo, Japan.
Masashi NagataDepartment of Pharmacy, Institute of Science Tokyo Hospital, Tokyo, Japan.
Kouhei YamamotoDepartment of Human Pathology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Tokyo, Japan.
Norio ShimizuDivision of Advanced Multidisciplinary Research, Center for Stem Cell and Regenerative Medicine, Institute of Science Tokyo, Tokyo, Japan.
Ryuji KoikeHealth Science Research and Development Center, Institute of Science Tokyo Hospital, Tokyo, Japan.
Ayako AraiDepartment of Hematology and Oncology, St. Marianna University School of Medicine, Kawasaki, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic chronic active Epstein-Barr virus disease (sCAEBV) is a rare intractable EBV-positive T-cell or natural killer (NK)-cell lymphoid neoplasm with systemic inflammation. The only curative treatment is allogeneic hematopoietic stem cell transplantation (allo-HSCT). Disease activity defined by multiple inflammatory symptoms is associated with poor survival. In sCAEBV, signal transducer and activator of transcription 3 (STAT3) is constitutively activated in EBV-infected T and NK cells and promotes their activation and survival. Ruxolitinib, a Janus kinase 1/2 inhibitor, suppresses the STAT3 activation in vitro, suggesting its clinical potential. We conducted a phase 2, multicenter, open-label study to investigate the effects of ruxolitinib on disease activity of sCAEBV. Complete response (CR) and partial response were defined as complete and partial resolution of disease activity, respectively. Nine patients received ruxolitinib, and 7 patients completed the study. The primary end point, CR rate (%) 56 days after the administration or at early termination as defined in the protocol, was 22.2% (2/9). No patient showed hematopoietic toxicity nor disease progression. Notably, 71.4% (5/7) of patients who completed the study were treated at our outpatient clinic. One patient developed a severe adverse event of oral bleeding due to lesion shrinkage during the treatment, and ruxolitinib was discontinued. EBV-DNA levels in whole blood did not change significantly whether the treatment was effective or not. After ruxolitinib treatment, 7 patients received allo-HSCT, and 5 of them achieved CR with undetectable EBV-DNA levels in whole blood. Ruxolitinib is a potent treatment drug that may improve allo-HSCT outcomes by suppressing disease activity of sCAEBV. The trial was registered at University hospital Medical Information Network (UMIN), numbered UMIN000035121.

Identifiers

PMID40546725
PMCPMC12182833

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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.