Evidence map›Paper›PMID 29738534›Full record

ArticlePloS one2018

Low expression of neural cell adhesion molecule, CD56, is associated with low efficacy of bortezomib plus dexamethasone therapy in multiple myeloma.

Takashi Yoshida, Masaki Ri, Shiori Kinoshita, Tomoko Narita, Haruhito Totani, Reham Ashour, Asahi Ito, Shigeru Kusumoto, Takashi Ishida, Hirokazu Komatsu and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Evaluation of CD56 and CD117 Double-Positivity as a Predictor of Poor Prognosis in Multiple Myeloma Patients: A Retrospective AnalysisTurkish journal of haematology : official journal of Turkish Society of Haematology · 2024
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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

11 authors at 1 institution in 1 country.

Takashi YoshidaDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Masaki RiDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.ORCID 0000-0002-9617-486X
Shiori KinoshitaDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Tomoko NaritaDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Haruhito TotaniDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Reham AshourDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Asahi ItoDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Shigeru KusumotoDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Takashi IshidaDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Hirokazu KomatsuDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Shinsuke IidaDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Nagoya City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bortezomib (Btz) is an active agent used to treat multiple myeloma (MM). Not all patients who receive Btz-containing therapy show a favorable response. Interaction of cellular adhesion molecules with MM and bone marrow stromal cells is crucial for the survival of MM cells. However, little is known about the role of these molecules in the sensitivity of MM to Btz-containing therapy. Thus, we evaluated the correlation between the level of cellular adhesion molecules in MM cells and the efficacy of Btz plus dexamethasone (Bd) therapy. The expression of the neural cell adhesion molecule gene (NCAM, also known as CD56), ITGA4, CXCR4, and other genes were analyzed in 74 samples of primary MM cells collected from patients before they received Bd therapy. Of the eight genes tested, expression of NCAM was lower among patients who responded poorly to Bd therapy. In vitro expression of NCAM induced by transfection of MM cells enhanced their sensitivity to Btz treatment by causing accumulation of polyubiquitinated proteins. Our results indicate that expression of NCAM is associated with better response to Btz treatment and is a promising candidate biomarker for predicting response to therapies involving Btz.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsApoptosisBortezomibCD56 AntigenCell Line, TumorDexamethasoneDrug Resistance, NeoplasmEndoplasmic Reticulum StressGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMultiple MyelomaNeoplasm ProteinsProteasome InhibitorsRNA, MessengerRNA, NeoplasmBortezomibCD56 AntigenDexamethasoneNCAM1 protein, humanNeoplasm ProteinsProteasome InhibitorsRNA, MessengerRNA, NeoplasmUbiquitinated Proteins

Identifiers

PMID29738534
PMCPMC5940221
OpenAlexW2801357468

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.