Evidence map›Paper›PMID 29437589›Full record

ArticleBlood2018

Prolyl 4-hydroxylase 2 promotes B-cell lymphoma progression via hydroxylation of Carabin.

Wei Jiang, Xiaoyan Zhou, Zengxia Li, Kaiyu Liu, Weige Wang, Renke Tan, Xiaoji Cong, Jiaoyu Shan, Yanxia Zhan, Zhaomeng Cui and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.0field-weighted citation impact, top 30% 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

28 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Targeting collagen Prolyl 4-hydroxylase for cancer treatment.Medical oncology (Northwood, London, England) · 2025
    Review
  3. Article
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  6. Review
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  8. Article
  9. Haematologica · 2024
    Article
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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

20 authors at 7 institutions in 3 countries.

Wei JiangKey Laboratory of Metabolism and Molecular Medicine, The Ministry of Education, Department of Biochemistry and Molecular Biology, Shanghai Medical College, Fudan University, Shanghai, China.
Xiaoyan ZhouDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai, China.
Zengxia LiKey Laboratory of Metabolism and Molecular Medicine, The Ministry of Education, Department of Biochemistry and Molecular Biology, Shanghai Medical College, Fudan University, Shanghai, China.
Kaiyu LiuKey Laboratory of Metabolism and Molecular Medicine, The Ministry of Education, Department of Biochemistry and Molecular Biology, Shanghai Medical College, Fudan University, Shanghai, China.
Weige WangDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai, China.
Renke TanKey Laboratory of Metabolism and Molecular Medicine, The Ministry of Education, Department of Biochemistry and Molecular Biology, Shanghai Medical College, Fudan University, Shanghai, China.
Xiaoji CongDrug Discovery and Design Center, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
Jiaoyu ShanShanghai Institute of Immunology, Department of Immunology and Microbiology, Shanghai JiaoTong University School of Medicine, Shanghai, China.
Yanxia ZhanDepartment of Hematology.
Zhaomeng CuiKey Laboratory of Metabolism and Molecular Medicine, The Ministry of Education, Department of Biochemistry and Molecular Biology, Shanghai Medical College, Fudan University, Shanghai, China.
Lizhi JiangKey Laboratory of Metabolism and Molecular Medicine, The Ministry of Education, Department of Biochemistry and Molecular Biology, Shanghai Medical College, Fudan University, Shanghai, China.
Quanfu LiKey Laboratory of Metabolism and Molecular Medicine, The Ministry of Education, Department of Biochemistry and Molecular Biology, Shanghai Medical College, Fudan University, Shanghai, China.
Suqin ShenSchool of Life Science, Fudan University, Shanghai, China; and.
Meirong BaiCardiovascular Research Institute and.
Yunfeng ChengDepartment of Hematology.
Bin LiShanghai Institute of Immunology, Department of Immunology and Microbiology, Shanghai JiaoTong University School of Medicine, Shanghai, China.
Minjia TanDrug Discovery and Design Center, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
Dengke K MaCardiovascular Research Institute and.
Jun O LiuDepartment of Pharmacology and Molecular Sciences, The Johns Hopkins University School of Medicine, Baltimore, MD.
Yongjun DangKey Laboratory of Metabolism and Molecular Medicine, The Ministry of Education, Department of Biochemistry and Molecular Biology, Shanghai Medical College, Fudan University, Shanghai, China.ORCID 0000-0001-7237-1132
Shanghai Medical College of Fudan University · CNChinese Academy of Sciences · CNShanghai Jiao Tong University · CNUniversity of California, San Francisco · USZhongshan Hospital · CNFudan University · CNJohns Hopkins University · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
Dissecting a Novel Genetic Pathway for Fatty Acid Desaturation and Temperature AdaptationR01GM117461 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MA, DENGKE · 2016 to 2020
$1.6M
NCI NIH HHS P30 CA006973NIGMS NIH HHS R01 GM117461
6 · The paper itself

Abstract

B-cell lymphomas are heterogeneous blood disorders with limited therapeutic options, largely because of their propensity to relapse and become refractory to treatments. Carabin, a key suppressor of B-cell receptor signaling and proliferation, is inactivated in B-cell lymphoma by unknown mechanisms. Here, we identify prolyl 4-hydroxylase 2 (P4HA2) as a specific proline hydroxylase of Carabin. Carabin hydroxylation leads to its proteasomal degradation, thereby activating the Ras/extracellular signal-regulated kinase pathway and increasing B-cell lymphoma proliferation. P4HA2 is undetectable in normal B cells but upregulated in the diffuse large B-cell lymphoma (DLBCL), driving Carabin inactivation and lymphoma proliferation. Our results indicate that P4HA2 is a potential prognosis marker for DLBCL and a promising pharmacological target for developing treatment of molecularly stratified B-cell lymphomas.

Indexed as

Cell ProliferationMAP Kinase Signaling SystemAdaptor Proteins, Signal TransducingBiomarkers, TumorCell Line, TumorGTPase-Activating ProteinsHumansHydroxylationLymphoma, Large B-Cell, DiffuseNeoplasm ProteinsProlyl HydroxylasesProteasome Endopeptidase ComplexProteolysisAdaptor Proteins, Signal TransducingBiomarkers, TumorGTPase-Activating ProteinsNeoplasm ProteinsP4HA2 protein, humanProlyl HydroxylasesProteasome Endopeptidase ComplexTBC1D10C protein, human

Identifiers

PMID29437589
PMCPMC5865229
OpenAlexW2787048720

What OpenQuestion holds

Textmetadata
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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.