Evidence map›Paper›PMID 27531699›Full record

ReviewNature reviews. Clinical oncology2017

Genomic complexity of multiple myeloma and its clinical implications.

Salomon Manier, Karma Z Salem, Jihye Park, Dan A Landau, Gad Getz, Irene M Ghobrial

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Clinical oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 357 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
357citing papers in PubMed, 5 pooled it
28.4field-weighted citation impact, top 1% 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

357 citing papers in PubMed, 5 syntheses or guidelines pooled it, 547 citations in OpenAlex.

  1. Pooled it
  2. International Myeloma Society/International Myeloma Working Group Consensus Recommendations on the Definition of High-Risk Multiple Myeloma.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2025
    Guideline
  3. Pooled it
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  5. Pooled it
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  19. Piercing myeloma's Achilles' heel.Nature chemical biology · 2026
    Article
  20. Article

297 more citing papers are in PubMed but not listed here.

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 4 institutions in 1 country.

Salomon ManierMedical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, HIM 237, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA.
Karma Z SalemMedical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, HIM 237, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA.
Jihye ParkMedical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, HIM 237, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA.
Dan A LandauNew York Genome Center, 101 Avenue of the Americas, Room 621, New York, New York 10013, USA.
Gad GetzCancer Program, Broad Institute of MIT and Harvard, 415 Main Street, Cambridge, Massachusetts 02142, USA.
Irene M GhobrialMedical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, HIM 237, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA.
Broad Institute · USHarvard University · USDana-Farber Cancer Institute · USNew York Genome Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma (MM) is a genetically complex disease that evolves from pre-malignant stages, such as monoclonal gammaopathy of undetermined significance and smouldering multiple myeloma, and progresses to symptomatic MM; this continuum provides a unique framework to study the sequential genomic evolution of MM. In the past 5 years, results from large-scale whole-exome sequencing studies have provided new insights into the clonal heterogeneity and evolution of the disease. Moreover, the recurrent co-occurrence of genomic events helps to dissect the genomic complexity underlying tumour progression. According to the primary genetic events involved in tumorigenesis, MM tumours are hierarchically subdivided into hyperdiploid and non-hyperdiploid subtypes; subsequently, secondary genetic events lead to tumour progression. In this Review, we describe the 'driver' gene alterations involved in the development and progression of MM, with a focus on the sequential acquisition of the main genomic aberrations. We also provide valuable insight into the clonal heterogeneity and clonal evolution of the disease, as well as into the therapeutic implications of a comprehensive understanding of the genomic complexity of MM.

Indexed as

Chromosome DeletionClonal EvolutionDiploidyDNA Copy Number VariationsGenetic HeterogeneityGenetic MarkersGenome, HumanGenomicsHumansMultiple MyelomaMutationPolymorphism, Single NucleotidePrognosisTranslocation, GeneticGenetic Markers

Identifiers

PMID27531699
OpenAlexW2511571730

What OpenQuestion holds

Textmetadata
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.