Evidence map›Paper›PMID 39919265›Full record

ArticleBlood2025

The JAK2 46/1 haplotype influences PD-L1 expression.

Gonzalo Carreño-Tarragona, María Tiana, Raquel Rouco, Alejandra Leivas, Jesús Victorino, Roberto García-Vicente, Andrew J Chase, Andrea Maidana, William J Tapper, Rosa Ayala and 3 more

Abstract read
In one paragraph

Article in Blood, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Homozygosity of germ lineBlood neoplasia · 2026
    Article
  2. Article
  3. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors.

Gonzalo Carreño-TarragonaHematology Department, Hospital Universitario 12 de Octubre, I+12, Centro Nacional de Investigaciones Oncológicas, Complutense University, Centro de Investigación Biomédica en Red de Oncología, Madrid, Spain.ORCID 0000-0002-9570-5542
María TianaTissue and Organ Homeostasis Program, Centro de Biología Molecular Severo Ochoa, Centro Superior de Investigaciones Científicas-Universidad Autónoma de Madrid, Madrid, Spain.ORCID 0000-0003-0678-1154
Raquel RoucoFunctional Genomics Group, Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid, Spain.ORCID 0000-0002-0657-0704
Alejandra LeivasHematology Department, Hospital Universitario 12 de Octubre, I+12, Centro Nacional de Investigaciones Oncológicas, Complutense University, Centro de Investigación Biomédica en Red de Oncología, Madrid, Spain.
Jesús VictorinoFunctional Genomics Group, Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid, Spain.ORCID 0000-0002-5871-5813
Roberto García-VicenteHematology Department, Hospital Universitario 12 de Octubre, I+12, Centro Nacional de Investigaciones Oncológicas, Complutense University, Centro de Investigación Biomédica en Red de Oncología, Madrid, Spain.ORCID 0000-0002-4796-9391
Andrew J ChaseDepartment of Human Genetics, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Andrea MaidanaTissue and Organ Homeostasis Program, Centro de Biología Molecular Severo Ochoa, Centro Superior de Investigaciones Científicas-Universidad Autónoma de Madrid, Madrid, Spain.
William J TapperDepartment of Human Genetics, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Rosa AyalaHematology Department, Hospital Universitario 12 de Octubre, I+12, Centro Nacional de Investigaciones Oncológicas, Complutense University, Centro de Investigación Biomédica en Red de Oncología, Madrid, Spain.ORCID 0000-0002-2699-8353
Nicholas C P CrossDepartment of Human Genetics, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.ORCID 0000-0001-5481-2555
Joaquín Martínez-LópezHematology Department, Hospital Universitario 12 de Octubre, I+12, Centro Nacional de Investigaciones Oncológicas, Complutense University, Centro de Investigación Biomédica en Red de Oncología, Madrid, Spain.
Miguel ManzanaresTissue and Organ Homeostasis Program, Centro de Biología Molecular Severo Ochoa, Centro Superior de Investigaciones Científicas-Universidad Autónoma de Madrid, Madrid, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

abstractAlthough described more than a decade ago, the mechanism by which the JAK2 46/1 haplotype increases the risk of developing JAK2-mutated myeloproliferative neoplasms (MPNs) remains unexplained. Inflammation and immunity are linked to MPN development and thus could be relevant to the mechanism by which 46/1 mediates its effect. Here, we show that programmed death-1 receptor ligand (PD-L1) expression is elevated in 46/1 haplotype, both in healthy carriers and in CD34+ cells from patients with MPN. Using circular chromosome conformation capture, we observed that PD-L1 and the neighboring PD-L2 loci physically interact with JAK2 in a manner that differs between 46/1 and nonrisk haplotypes. CRISPR/Cas9 genome editing identified a region within JAK2 intron 2 that influences both JAK2 and PD-L1 expression. We suggest that increased PD-L1 expression may be relevant to the mechanism by which 46/1 leads to an increased inherited risk of developing MPN.

Indexed as

B7-H1 AntigenHaplotypesJanus Kinase 2Myeloproliferative DisordersHumansProgrammed Cell Death 1 Ligand 2 ProteinB7-H1 AntigenCD274 protein, humanJAK2 protein, humanJanus Kinase 2Programmed Cell Death 1 Ligand 2 Protein

Identifiers

PMID39919265
PMCPMC12105720

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.