Evidence map›Paper›PMID 32391356›Full record

ArticleFrontiers in cell and developmental biology2020

A Dual TLR7/TLR9 Inhibitor HJ901 Inhibits ABC-DLBCL Expressing the MyD88 L265P Mutation.

Beiying An, Shan Zhu, Tete Li, Jing Wu, Guoxia Zang, Xinping Lv, Yuan Qiao, Jing Huang, Yan Shao, Jiuwei Cui and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 44% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. The Role of Neutrophils in the Pathogenesis of Chronic Lymphocytic Leukemia.International journal of molecular sciences · 2021
    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

12 authors at 2 institutions in 1 country.

Beiying AnInstitute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Shan ZhuInstitute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Tete LiInstitute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Jing WuInstitute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Guoxia ZangInstitute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Xinping LvInstitute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Yuan QiaoInstitute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Jing HuangDepartment of Clinical Laboratory, The First Hospital of Jilin University, Changchun, China.
Yan ShaoChangchun Huapu Biotechnology Co., Ltd., Changchun, China.
Jiuwei CuiCancer Center, The First Hospital of Jilin University, Changchun, China.
Yong-Jun LiuInstitute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Jingtao ChenInstitute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Jilin University · CNFirst Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diffuse large B cell lymphoma (DLBCL) is associated with aggressive clinical cases and poor prognosis despite recent advances in disease treatment. In activated B-cell-like (ABC)-DLBCL, the most severe damaged signaling pathways converge to aberrantly activate the Toll-like receptor (TLR) 7/9/MyD88 pathways, leading to the avoidance of cell death and resistance to chemotherapy. A gain of function mutation in MyD88 (MyD88 L265P) enhanced the NF-κB and JAK-STAT signaling pathways and was associated with dysregulation of TLR signaling in the pathogenesis of ABC-DLBCL. Therefore, inhibition of the TLR signaling network may improve clinical outcomes. In this study, we designed a

Indexed as

ABC DLBCLantagonistMyD88 mutationsignaling pathwayTLR7TLR9

Identifiers

PMID32391356
PMCPMC7188833
OpenAlexW3018089423

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.