Evidence map›Paper›PMID 28203307›Full record

ReviewClinical epigenetics2017

Epigenetic strategies to reverse drug resistance in heterogeneous multiple myeloma.

Mark E Issa, Farnaz Sedigheh Takhsha, Chandra Sekhar Chirumamilla, Claudina Perez-Novo, Wim Vanden Berghe, Muriel Cuendet

Open access · goldAbstract readReview
In one paragraph

Review in Clinical epigenetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

54 citing papers in PubMed, 80 citations in OpenAlex.

  1. Epigenetic alterations in head and neck cancer: a brief update.Virchows Archiv : an international journal of pathology · 2026
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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

6 authors at 2 institutions in 2 countries.

Mark E Issa *School of Pharmaceutical Sciences, University of Geneva, University of Lausanne, Rue Michel-Servet 1, CH-1211 Geneva 4, Switzerland.
Farnaz Sedigheh Takhsha *Laboratory of Protein Science, Proteomics and Epigenetic Signaling (PPES), Department of Biomedical sciences, University of Antwerp, Campus Drie Eiken, Universiteitsplein 1, Wilrijk, Belgium.
Chandra Sekhar ChirumamillaLaboratory of Protein Science, Proteomics and Epigenetic Signaling (PPES), Department of Biomedical sciences, University of Antwerp, Campus Drie Eiken, Universiteitsplein 1, Wilrijk, Belgium.
Claudina Perez-NovoLaboratory of Protein Science, Proteomics and Epigenetic Signaling (PPES), Department of Biomedical sciences, University of Antwerp, Campus Drie Eiken, Universiteitsplein 1, Wilrijk, Belgium.
Wim Vanden Berghe *Laboratory of Protein Science, Proteomics and Epigenetic Signaling (PPES), Department of Biomedical sciences, University of Antwerp, Campus Drie Eiken, Universiteitsplein 1, Wilrijk, Belgium.ORCID 0000-0003-0161-7355
Muriel Cuendet *School of Pharmaceutical Sciences, University of Geneva, University of Lausanne, Rue Michel-Servet 1, CH-1211 Geneva 4, Switzerland.
University of Antwerp · BEUniversity of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma (MM) is a hematological malignancy, which remains incurable because most patients eventually relapse or become refractory to current treatments. Due to heterogeneity within the cancer cell microenvironment, cancer cell populations employ a dynamic survival strategy to chemotherapeutic treatments, which frequently results in a rapid acquisition of therapy resistance. Besides resistance-conferring genetic alterations within a tumor cell population selected during drug treatment, recent findings also reveal non-mutational mechanisms of drug resistance, involving a small population of "cancer stem cells" (CSCs) which are intrinsically more refractory to the effects of a variety of anticancer drugs. Other studies have implicated epigenetic mechanisms in reversible drug tolerance to protect the population from eradication by potentially lethal exposures, suggesting that acquired drug resistance does not necessarily require a stable heritable genetic alteration. Clonal evolution of MM cells and the bone marrow microenvironment changes contribute to drug resistance. MM-CSCs may not be a static population and survive as phenotypically and functionally different cell types via the transition between stem-like and non-stem-like states in local microenvironments, as observed in other types of cancers. Targeting MM-CSCs is clinically relevant, and different approaches have been suggested to target molecular, metabolic and epigenetic signatures, and the self-renewal signaling characteristic of MM CSC-like cells. Here, we summarize epigenetic strategies to reverse drug resistance in heterogeneous multiple myeloma.

Indexed as

AnimalsAntineoplastic AgentsDrug Resistance, MultipleDrug Resistance, NeoplasmEpigenesis, GeneticHumansMultiple MyelomaNeoplastic Stem CellsTumor MicroenvironmentAntineoplastic AgentsCombination therapyDrug resistanceEpigenetic drugsMicroenvironmentMultiple myelomaStem cellsTreatment

Identifiers

PMID28203307
PMCPMC5303245
OpenAlexW2587548185

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.