Evidence map›Paper›PMID 29289756›Full record

ReviewBiology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation2018

The Role of Janus Kinase Signaling in Graft-Versus-Host Disease and Graft Versus Leukemia.

Mark A Schroeder, Jaebok Choi, Karl Staser, John F DiPersio

Open access · bronzeAbstract readReview
In one paragraph

Review in Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 3 pooled it
5.4field-weighted citation impact, top 4% of its field
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

60 citing papers in PubMed, 3 syntheses or guidelines pooled it, 108 citations in OpenAlex.

  1. Pooled it
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  11. Advances in treatment of chronic graft-versus-host disease.International journal of hematology · 2026
    Review
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  18. Graft-Versus-Host Disease Mouse Models: A Clinical-Translational Perspective.Methods in molecular biology (Clifton, N.J.) · 2025
    Review
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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

4 authors at 1 institution in 1 country.

Mark A SchroederWashington University School of Medicine, Division of Oncology, Section of Stem Cell Transplantation, St. Louis, Missouri. Electronic address: markschroeder@wustl.edu.
Jaebok ChoiWashington University School of Medicine, Division of Oncology, Section of Stem Cell Transplantation, St. Louis, Missouri.
Karl StaserWashington University School of Medicine, Division of Oncology, Section of Stem Cell Transplantation, St. Louis, Missouri.
John F DiPersioWashington University School of Medicine, Division of Oncology, Section of Stem Cell Transplantation, St. Louis, Missouri.
Washington University in St. Louis · US

Funding

Specimen Acquistition and Expression ProfilingP01CA101937 · NCI · WASHINGTON UNIVERSITY · PI LINK, DANIEL C · 2003 to 2023
$58.8M
Targeting the Bone Marrow Microenvironment In Acute Lymphocytic LeukemiaP50CA171963 · NCI · WASHINGTON UNIVERSITY · PI Daniel C Link · 2013 to 2026
$31.6M
Optimizing Hematopoietic Stem Cell Transplantation For The Treatment Of Hematological MalignanciesR35CA210084 · NCI · WASHINGTON UNIVERSITY · PI John F. Dipersio · 2017 to 2026
$7.8M
RETARGETING AGENTS TO TREAT AMLR01CA194552 · NCI · WASHINGTON UNIVERSITY · PI DIPERSIO, JOHN F. · 2015 to 2017
$1.1M
NCI NIH HHS P01 CA101937NCI NIH HHS P50 CA171963NCI NIH HHS R01 CA194552NCI NIH HHS R35 CA210084
6 · The paper itself

Abstract

For patients with hematologic malignancies, allogeneic hematopoietic cell transplantation (alloHCT) offers a potential curative treatment option, primarily due to an allogeneic immune response against recipient tumor cells (ie, graft-versus-leukemia [GVL] activity). However, many recipients of alloHCT develop graft-versus-host disease (GVHD), in which allogeneic immune responses lead to the damage of healthy tissue. GVHD is a leading cause of nonrelapse mortality and a key contributor to morbidity among patients undergoing alloHCT. Therefore, improving alloHCT outcomes will require treatment strategies that prevent or mitigate GVHD without disrupting GVL activity. Janus kinases (JAKs) are intracellular signaling molecules that are well positioned to regulate GVHD. A variety of cytokines that signal through the JAK signaling pathways play a role in regulating the development, proliferation, and activation of several immune cell types important for GVHD pathogenesis, including dendritic cells, macrophages, T cells, B cells, and neutrophils. Importantly, despite JAK regulation of GVHD, preclinical evidence suggests that JAK inhibition preserves GVL activity. Here we provide an overview of potential roles for JAK signaling in the pathogenesis of acute and chronic GVHD as well as effects on GVL activity. We also review preclinical and clinical results with JAK inhibitors in acute and chronic GVHD settings, with added focus on those actively being evaluated in patients with acute and chronic GVHD.

Indexed as

Graft vs Leukemia EffectGraft vs Host DiseaseHematopoietic Stem Cell TransplantationHumansJanus KinasesSignal TransductionTransplantation, HomologousJanus KinasesGraft-versus-host diseaseHematopoietic cell transplantationJanus kinase

Identifiers

PMID29289756
PMCPMC5993569
OpenAlexW2778252021

What OpenQuestion holds

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Registered trials

None linked

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.