Evidence map›Paper›PMID 37705009›Full record

ArticleClinical proteomics2023

Proteome analysis of CD5-positive diffuse large B cell lymphoma FFPE tissue reveals downregulation of DDX3X, DNAJB1, and B cell receptor signaling pathway proteins including BTK and Immunoglobulins.

Takuya Hiratsuka, Shinji Ito, Rika Sakai, Tomoyuki Yokose, Tatsuya Endo, Yataro Daigo, Yohei Miyagi, Tatsuaki Tsuruyama

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical proteomics, 2023. 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
1.3field-weighted citation impact, top 20% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. 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

8 authors at 5 institutions in 1 country.

Takuya HiratsukaDepartment of Drug Discovery Medicine, Pathology Division, Kyoto University Graduate School of Medicine, Kyoto, Japan. hiratsuka.takuya.65s@st.kyoto-u.ac.jp.
Shinji ItoMedical Research Support Center, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Rika SakaiDepartment of Oncology, Kanagawa Cancer Center Research Institute, Yokohama, Japan.
Tomoyuki YokoseDepartment of Pathology, Kanagawa Cancer Center Research Institute, Yokohama, Japan.
Tatsuya EndoDepartment of Physics, Graduate School of Science, Tohoku University, Sendai, Japan.
Yataro DaigoDepartment of Medical Oncology, Cancer Center, and Center for Advanced Medicine Against Cancer, Shiga University of Medical Science, Otsu, Japan.
Yohei MiyagiMolecular Pathology and Genetics Division, Kanagawa Cancer Center Research Institute, Yokohama, Japan.
Tatsuaki TsuruyamaDepartment of Drug Discovery Medicine, Pathology Division, Kyoto University Graduate School of Medicine, Kyoto, Japan. tsuruyam@kuhp.kyoto-u.ac.jp.
Kanagawa Prefectural Hospital Organization · JPKyoto University · JPTohoku University · JPKanagawa Cancer CenterUniversity of Tokyo Hospital · JP

Funding

Ministry of Education, Culture, Sports, Science and Technology 17K08719
6 · The paper itself

Abstract

backgroundThe molecular pathology of diffuse large B cell lymphoma (DLBCL) has been extensively studied. Among DLBCL subtypes, the prognosis of CD5-positive DLBCL is worse than that of CD5-negative DLBCL, considering the central nervous system relapse and poor response to R-CHOP therapy. However, the molecular mechanisms underlying the tumorigenesis and progression of CD5-positive DLBCL remain unknown.

methodsTo identify molecular markers that can be targeted for treating DLBCL, a proteomic study was performed using liquid chromatography-mass spectrometry with chemically pretreated formalin-fixed paraffin-embedded specimens from CD5-positive (n = 5) and CD5-negative DLBCL patients (n = 6).

resultsTwenty-one proteins showed significant downregulation in CD5-positive DLBCL compared to CD5-negative DLBCL. Principal component analysis of protein expression profiling in CD5-positive and CD5-negative DLBCL revealed that DNAJB1, DDX3X, and BTK, which is one of the B cell phenotypic proteins, were the most significantly downregulated proteins and served as biomarkers that distinguished both groups. Additionally, a set of immunoglobulins, including IgG4, exhibited significant downregulation. Immunohistochemistry analysis for BTK demonstrated reduced staining in CD5-positive DLBCL compared to CD5-negative DLBCL.

conclusionsIn conclusion, DNAJB1 and DDX3X, BTK, and a set of immunoglobulins are promising biomarkers. Probably, the suppression of BCR signaling is the unique phenotype of CD5-positive DLBCL. This formalin-fixed paraffin-embedded (FFPE)-based profiling may help to develop novel therapeutic molecularly targeted drugs for treating DLBCL.

Indexed as

BiomarkersBruton tyrosine kinaseCD5-positive Diffuse large B cell lymphomaDDX3XDNAJB1Formalin-fixed paraffin-embedded specimenImmunoglobulinProteomics

Identifiers

PMID37705009
PMCPMC10498596
OpenAlexW4386695723

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.