Evidence map›Paper›PMID 28558048›Full record

ArticlePloS one2017

DEK protein level is a biomarker of CD138positive normal and malignant plasma cells.

Zihni Onur Çalışkaner, Türkan Çakar, Emrah Özçelik, Ahmet Özdilek, Annette S Kim, Öner Doğan, Amma Bosompem, Gerard Grosveld, Bülent Saka, Ayten Kandilci

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

4 citing papers in PubMed, 7 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

10 authors at 4 institutions in 2 countries.

Zihni Onur ÇalışkanerDepartment of Molecular Biology and Genetics, Gebze Technical University, Gebze, Kocaeli, Turkey.
Türkan ÇakarDepartment of Molecular Biology and Genetics, Gebze Technical University, Gebze, Kocaeli, Turkey.
Emrah ÖzçelikDepartment of Molecular Biology and Genetics, Gebze Technical University, Gebze, Kocaeli, Turkey.
Ahmet ÖzdilekDepartment of Molecular Biology and Genetics, Gebze Technical University, Gebze, Kocaeli, Turkey.
Annette S KimDepartment of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, United States of America.
Öner DoğanDepartment of Pathology, Istanbul University, Istanbul Medical Faculty, Istanbul, Turkey.
Amma BosompemDepartment of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, United States of America.
Gerard GrosveldDepartment of Genetics, St Jude Children's Research Hospital, Memphis, Tennessee, United States of America.
Bülent SakaDepartment of Internal Medicine, Istanbul University, Istanbul Medical Faculty, Istanbul, Turkey.
Ayten KandilciDepartment of Molecular Biology and Genetics, Gebze Technical University, Gebze, Kocaeli, Turkey.ORCID http://orcid.org/0000-0003-4209-4992
Gebze Technical University · TRIstanbul University · TRVanderbilt University · USSt. Jude Children's Research Hospital · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI STACIE B DUSETZINA · 1995 to 2026
$172.8M
NCI NIH HHS P30 CA068485
6 · The paper itself

Abstract

Overexpression of DEK oncogene is associated with increased proliferation of carcinoma cells and it is observed in several solid tumors due to the amplification of the 6p22.3 chromosomal region where DEK locates. Although the same chromosomal amplification occurs in multiple myeloma (MM), a plasma cell neoplasm, whether the expression and the copy number of the DEK gene are affected in MM remains elusive. We show that despite the increased copy number in CD138positive MM cells (4 out of 41 MM samples), DEK mRNA expression was down-regulated compared with that in CD138negative bone marrow (BM) cells of the same patients (P<0.0001). DEK protein was not detectable by immunohistochemistry (IHC) in CD138positive normal plasma cells or in malignant plasma cells of MM patients (n = 56) whereas it was widely expressed in normal and neoplastic B-cells. Stable knockdown or overexpression of DEK in CD138positive MM cell lines did not affect the proliferation and viability of the cells profoundly in the presence or absence of chemotherapeutic agent melphalan whereas knockdown of DEK moderately but significantly increased the expression level of CD138 (p<0.01). Decreased DEK expression in plasma cells suggests a potential role of this gene in plasma cell development and lack of detectable DEK protein by IHC could be used as a biomarker for normal and malignant plasma cells.

Indexed as

BiomarkersCell LineCell Line, TumorCell ProliferationChromosomal Proteins, Non-HistoneHumansMultiple MyelomaOncogene ProteinsPlasma CellsPoly-ADP-Ribose Binding ProteinsRNA, MessengerSyndecan-1BiomarkersChromosomal Proteins, Non-HistoneDEK protein, humanOncogene ProteinsPoly-ADP-Ribose Binding ProteinsRNA, MessengerSDC1 protein, humanSyndecan-1

Identifiers

PMID28558048
PMCPMC5448761
OpenAlexW2618217657

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.