Evidence map›Paper›PMID 39462545›Full record

ArticleJournal of clinical and experimental hematopathology : JCEH2024

Transcriptome analysis of the cytokine storm-related genes among the subtypes of idiopathic multicentric Castleman disease.

Asami Nishikori, Midori Filiz Nishimura, Shuta Tomida, Ryota Chijimatsu, Himawari Ueta, You Cheng Lai, Yuri Kawahara, Yudai Takeda, Sayaka Ochi, Tomoka Haratake and 4 more

Abstract read
In one paragraph

Article in Journal of clinical and experimental hematopathology : JCEH, 2024. 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

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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.

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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

14 authors.

Asami NishikoriDepartment of Molecular Hematopathology, Okayama University Graduate School of Health Sciences, Okayama, Japan.
Midori Filiz NishimuraDepartment of Molecular Hematopathology, Okayama University Graduate School of Health Sciences, Okayama, Japan.
Shuta TomidaCenter for Comprehensive Genomic Medicine, Okayama University Hospital, Okayama, Japan.
Ryota ChijimatsuCenter for Comprehensive Genomic Medicine, Okayama University Hospital, Okayama, Japan.
Himawari UetaDepartment of Molecular Hematopathology, Okayama University Graduate School of Health Sciences, Okayama, Japan.
You Cheng LaiDepartment of Medical Biotechnology and Laboratory Science, Chang Gung University, Taoyuan, Taiwan.
Yuri KawaharaDepartment of Molecular Hematopathology, Okayama University Graduate School of Health Sciences, Okayama, Japan.
Yudai TakedaDepartment of Molecular Hematopathology, Okayama University Graduate School of Health Sciences, Okayama, Japan.
Sayaka OchiDepartment of Molecular Hematopathology, Okayama University Graduate School of Health Sciences, Okayama, Japan.
Tomoka HaratakeDepartment of Molecular Hematopathology, Okayama University Graduate School of Health Sciences, Okayama, Japan.
Daisuke EnnishiCenter for Comprehensive Genomic Medicine, Okayama University Hospital, Okayama, Japan.
Naoya NakamuraDepartment of Pathology, Tokai University School of Medicine, Isehara, Japan.
Shuji MomoseDepartment of Pathology, Saitama Medical Center, Saitama Medical University, Saitama, Japan.
Yasuharu SatoDepartment of Molecular Hematopathology, Okayama University Graduate School of Health Sciences, Okayama, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic multicentric Castleman disease (iMCD) is a type of Castleman disease unrelated to the Kaposi sarcoma-associated herpesvirus/human herpesvirus type 8 (KSHV/HHV8) infection. Presently, iMCD is classified into iMCD-IPL (idiopathic plasmacytic lymphadenopathy), iMCD-TAFRO (thrombocytopenia, anasarca, fever, reticulin fibrosis/renal insufficiency, and organomegaly), and iMCD-NOS (not otherwise specified). The most common treatment for iMCD is using IL-6 inhibitors; however, some patients resist IL-6 inhibitors, especially for iMCD-TAFRO/NOS. Nevertheless, since serum IL-6 levels are not significantly different between the iMCD-IPL and iMCD-TAFRO/NOS cases, cytokines other than IL-6 may be responsible for the differences in pathogenesis. Herein, we performed a transcriptome analysis of cytokine storm-related genes and examined the differences between iMCD-IPL and iMCD-TAFRO/NOS. The results demonstrated that counts per million of STAT2, IL1R1, IL1RAP, IL33, TAFAIP1, and VEGFA (P < 0.001); STAT3, JAK2, MAPK8, IL17RA, IL18, TAFAIP2, TAFAIP3, PDGFA, VEGFC, CXCL10, CCL4, and CXCL13 (P < 0.01); and STAT1, STAT6, JAK1, MAPK1, MAPK3, MAPK6, MAPK7, MAPK9, MAPK10, MAPK11, MAPK12, MAPK14, NFKB1, NFKBIA, NFKBIB, NFKBIZ, MTOR, IL10RB, IL12RB2, IL18BP, TAFAIP6, TNFAIP8L1, TNFAIP8L3, CSF2RBP1, PDGFB, PDGFC, and CXCL9 (P < 0.05) were significantly increased in iMCD-TAFRO/NOS. Particularly, upregulated IL33 expression was demonstrated for the first time in iMCD-TAFRO/NOS. Thus, inflammatory signaling, such as JAK-STAT and MAPK, may be enhanced in iMCD-TAFRO/NOS and may be a cytokine storm.

Indexed as

Castleman DiseaseGene Expression ProfilingAdultAgedCytokine Release SyndromeCytokinesFemaleHumansMaleMiddle AgedTranscriptomeCytokinescytokine stormidiopathic multicentric Castleman diseasetranscriptome analysis

Identifiers

PMID39462545
PMCPMC11786152

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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.