Evidence map›Paper›PMID 25051404›Full record

ArticleBritish journal of cancer2014

Chromatin structure, transcriptional activity and DNA repair efficiency affect the outcome of chemotherapy in multiple myeloma.

M Gkotzamanidou, P P Sfikakis, S A Kyrtopoulos, C Bamia, M A Dimopoulos, V L Souliotis

RetractedErratum issuedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

M Gkotzamanidou1] Department of Medical Oncology, Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA [2] Department of Clinical Therapeutics, University of Athens School of Medicine, 11528 Athens, Greece.
P P SfikakisFirst Department of Propedeutic Medicine, University of Athens School of Medicine, 11527 Athens, Greece.
S A KyrtopoulosInstitute of Biology, Medicinal Chemistry and Biotechnology, National Hellenic Research Foundation, 48 Vassileos Constantinou Avenue, 11635 Athens, Greece.
C BamiaDepartment of Hygiene, Epidemiology and Medical Statistics, University of Athens School of Medicine, 11527 Athens, Greece.
M A DimopoulosDepartment of Clinical Therapeutics, University of Athens School of Medicine, 11528 Athens, Greece.
V L SouliotisInstitute of Biology, Medicinal Chemistry and Biotechnology, National Hellenic Research Foundation, 48 Vassileos Constantinou Avenue, 11635 Athens, Greece.
National and Kapodistrian University of Athens · GRNational Hellenic Research Foundation · GRHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMelphalan is one of the most active chemotherapeutic agents in the treatment of multiple myeloma (MM). However, the mechanism underlying differential patient responses to melphalan therapy is unknown.

methodsChromatin structure, transcriptional activity and DNA damage response signals were examined following ex vivo treatment with melphalan of both malignant bone marrow plasma cells (BMPCs) and peripheral blood mononuclear cells (PBMCs) of MM patients, responders (n=57) or non-responders (n=28) to melphalan therapy. PBMCs from healthy controls (n=25) were also included in the study.

resultsIn both BMPCs and PBMCs, the local chromatin looseness, transcriptional activity and repair efficiency of the transcribed strand (TS) were significantly higher in non-responders than in responders and lowest in healthy controls (all P<0.05). Moreover, we found that melphalan-induced apoptosis inversely correlated with the repair efficiency of the TS, with the duration of the inhibition of mRNA synthesis, phosphorylation of p53 at serine 15 and apoptosis rates being higher in responders than in non-responders (all P<0.001).

conclusionsOur findings provide a mechanistic basis for the link between DNA repair efficiency and response to melphalan therapy. Interestingly, the observation of these phenomena in PBMCs provides a novel approach for the prediction of response to anti-myeloma therapy.

Indexed as

DNA RepairTranscription, GeneticAdultAgedAntineoplastic Agents, AlkylatingApoptosisCase-Control StudiesChromatinDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticHumansLeukocytes, MononuclearMaleMelphalanMiddle AgedAntineoplastic Agents, AlkylatingChromatinMelphalan

Identifiers

PMID25051404
PMCPMC4183844
OpenAlexW2012630722

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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Registered trials

None linked

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.