Evidence map›Paper›PMID 33095415›Full record

ArticleInternational journal of hematology2021

EWSR1 overexpression is a pro-oncogenic event in multiple myeloma.

Daichi Nishiyama, Yoshiaki Chinen, Reiko Isa, Yuto Fujibayashi, Saeko Kuwahara-Ota, Junko Yamaguchi, Tomoko Takimoto-Shimomura, Yayoi Matsumura-Kimoto, Taku Tsukamoto, Yuji Shimura and 5 more

Abstract read
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In one paragraph

Article in International journal of hematology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 31% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

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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

15 authors at 2 institutions in 1 country.

Daichi NishiyamaDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto, 602-8566, Japan.
Yoshiaki ChinenDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto, 602-8566, Japan.
Reiko IsaDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto, 602-8566, Japan.
Yuto FujibayashiDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto, 602-8566, Japan.
Saeko Kuwahara-OtaDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto, 602-8566, Japan.
Junko YamaguchiDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto, 602-8566, Japan.
Tomoko Takimoto-ShimomuraDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto, 602-8566, Japan.
Yayoi Matsumura-KimotoDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto, 602-8566, Japan.
Taku TsukamotoDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto, 602-8566, Japan.
Yuji ShimuraDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto, 602-8566, Japan.
Tsutomu KobayashiDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto, 602-8566, Japan.
Shigeo HoriikeDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto, 602-8566, Japan.
Masafumi TaniwakiCenter for Molecular Diagnostics and Therapeutics, Kyoto Prefectural Univesity of Medicine, Kyoto, Japan.
Hiroshi HandaDepartment of Hematology, Gunma University Graduate School of Medicine, Maebashi, Japan.
Junya KurodaDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto, 602-8566, Japan. junkuro@koto.kpu-m.ac.jp.ORCID http://orcid.org/0000-0001-6130-1550
Kyoto Prefectural University of Medicine · JPGunma University · JP

Funding

Japan Agency for Medical Research and Development JP16ck0106077h003Japan Agency for Medical Research and Development JP17ck0106348h0001Japan Agency for Medical Research and Development JP18ck0106348h0002Japan Agency for Medical Research and Development JP19ck0106348h0003Ministry of Education, Culture, Sports, Science and Technology 16K09856Ministry of Education, Culture, Sports, Science and Technology 18K08367Ministry of Health, Labour and Welfare H26-kakushin-teki-gan-ippan-074National Cancer Center Research and Development Funds 26-A-4National Cancer Center Research and Development Funds 29-A-3
6 · The paper itself

Abstract

Multiple myeloma (MM) is cytogenetically, genetically and molecularly heterogenous even among subclones in one patient, therefore, it is essential to identify both frequent and patient-specific drivers of molecular abnormality. Following previous molecular investigations, we in this study investigated the expression patterns and function of the Ewing sarcoma breakpoint region 1 (EWSR1) gene in MM. The EWSR1 transcriptional level in CD138-positive myeloma cells was higher in 36.4% of monoclonal gammopathy of undetermined significance, in 67.4% of MM patients compared with normal plasma cells, and significantly higher in ten human myeloma-derived cell lines (HMCLs) examined. EWSR1 gene knockdown caused growth inhibition with an increase of apoptotic cells in NCI-H929 and KMS-12-BM cells. Gene expression profiling using microarray analysis suggested EWSR1 gene knockdown caused transcriptional modulation of several genes associated with processes such as cell proliferation, cell motility, cell metabolism, and gene expression. Of particular, EWSR1 gene knockdown caused upregulation of let-7c and downregulation of its known targets K-RAS and AKT. Finally, our analysis using community database suggested that high EWSR1 expression positively associates with poor prognosis and advanced disease stage in MM. These findings suggest that EWSR1 overexpression is a pro-oncogenic molecular abnormality that may participate in MM progression.

Indexed as

ApoptosisCell DivisionCell Line, TumorCell MovementCell Transformation, NeoplasticClonal EvolutionDisease ProgressionGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansKaplan-Meier EstimateMicroRNAsMonoclonal Gammopathy of Undetermined SignificanceMultiple MyelomaNeoplasm ProteinsEWSR1 protein, humanMicroRNAsMIRNlet-7c microRNA, humanNeoplasm ProteinsRNA-Binding Protein EWSRNA, NeoplasmRNA, Small InterferingCell motilityCell proliferationEWSR1microRNAMultiple myeloma

Identifiers

PMID33095415
OpenAlexW3094453361

What OpenQuestion holds

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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.