Evidence map›Paper›PMID 22498740›Full record

ArticleBlood2012

Clonal competition with alternating dominance in multiple myeloma.

Jonathan J Keats, Marta Chesi, Jan B Egan, Victoria M Garbitt, Stephen E Palmer, Esteban Braggio, Scott Van Wier, Patrick R Blackburn, Angela S Baker, Angela Dispenzieri and 7 more

Abstract read
In one paragraph

Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 335 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
335citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

335 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  15. Molecular Insights and Novel Therapies for Lymphoproliferative Disorders.International journal of molecular sciences · 2026
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275 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors.

Jonathan J KeatsComprehensive Cancer Center, Mayo Clinic Arizona, Scottsdale, AZ 85259, USA.
Marta Chesi
Jan B Egan
Victoria M Garbitt
Stephen E Palmer
Esteban Braggio
Scott Van Wier
Patrick R Blackburn
Angela S Baker
Angela Dispenzieri
Shaji Kumar
S Vincent Rajkumar
John D Carpten
Michael Barrett
Rafael Fonseca
A Keith Stewart
P Leif Bergsagel

Funding

CHROMOSOMAL ABNORMALITIES IN MYELOMA AS DETECTED BY FISHR01CA083724 · NCI · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI FONSECA, RAFAEL · 2000 to 2013
$4.0M
Mouse models of age-associated monoclonal gammopathyR01AG020686 · NIA · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI BERGSAGEL, PETER LEIF · 2003 to 2014
$3.3M
Molecular Pathogenesis of Multiple MyelomaR01CA133966 · NCI · MAYO CLINIC ARIZONA · PI BERGSAGEL, PETER LEIF · 2009 to 2013
$1.6M
Comparative Pharmaco-oncogenomics of Myeloma Drug ResistanceR01CA136671 · NCI · MAYO CLINIC ARIZONA · PI BERGSAGEL, PETER LEIF · 2009 to 2013
$1.6M
A Genome Wide RNAi Vulnerability Map for MyelomaR01CA133115 · NCI · MAYO CLINIC ARIZONA · PI STEWART, ALEXANDER KEITH · 2008 to 2012
$1.3M
NCI NIH HHS CA133115NCI NIH HHS CA133966NCI NIH HHS CA136671NCI NIH HHS R01 CA083724NCI NIH HHS R01 CA133115NCI NIH HHS R01 CA133966NCI NIH HHS R01 CA136671NIA NIH HHS R01 AG020686
6 · The paper itself

Abstract

Emerging evidence indicates that tumors can follow several evolutionary paths over a patient's disease course. With the use of serial genomic analysis of samples collected at different points during the disease course of 28 patients with multiple myeloma, we found that the genomes of standard-risk patients show few changes over time, whereas those of cytogenetically high-risk patients show significantly more changes over time. The results indicate the existence of 3 temporal tumor types, which can either be genetically stable, linearly evolving, or heterogeneous clonal mixtures with shifting predominant clones. A detailed analysis of one high-risk patient sampled at 7 time points over the entire disease course identified 2 competing subclones that alternate in a back and forth manner for dominance with therapy until one clone underwent a dramatic linear evolution. With the use of the Vk*MYC genetically engineered mouse model of myeloma we modeled this competition between subclones for predominance occurring spontaneously and with therapeutic selection.

Indexed as

DNA Copy Number VariationsAnimalsCells, CulturedClonal EvolutionCluster AnalysisDisease ProgressionGene Expression ProfilingGene Expression Regulation, NeoplasticGenes, DominantHumansMiceMice, Inbred C57BLMice, TransgenicMicroarray AnalysisModels, BiologicalMultiple Myeloma

Identifiers

PMID22498740
PMCPMC3412330

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.