Evidence map›Paper›PMID 28234347›Full record

ArticleBlood cancer journal2017

Bi-allelic inactivation is more prevalent at relapse in multiple myeloma, identifying RB1 as an independent prognostic marker.

S S Chavan, J He, R Tytarenko, S Deshpande, P Patel, M Bailey, C K Stein, O Stephens, N Weinhold, N Petty and 18 more

Open access · goldAbstract read
In one paragraph

Article in Blood cancer journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. iScience · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Genomic Classification and Individualized Prognosis in Multiple Myeloma.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2024
    Article
  12. Article
  13. Recent Advances in The Definition of the Molecular Alterations Occurring in Multiple Myeloma.Mediterranean journal of hematology and infectious diseases · 2024
    Review
  14. LAMP5 may promote MM progression by activating p38.Pathology oncology research : POR · 2023
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article
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

28 authors at 4 institutions in 1 country.

S S ChavanThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
J HeFoundation Medicine Inc., Cambridge, MA, USA.
R TytarenkoThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
S DeshpandeThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
P PatelThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
M BaileyFoundation Medicine Inc., Cambridge, MA, USA.
C K SteinThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
O StephensThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
N WeinholdThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
N PettyThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
D StewardThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
L RascheThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
M BauerThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
C AshbyThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
E PetersonThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
S AliFoundation Medicine Inc., Cambridge, MA, USA.
J RossFoundation Medicine Inc., Cambridge, MA, USA.
V A MillerFoundation Medicine Inc., Cambridge, MA, USA.
P StephensFoundation Medicine Inc., Cambridge, MA, USA.
S ThanendrarajanThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
C SchinkeThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
M ZangariThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
F van RheeThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
B BarlogieThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
T I MughalFoundation Medicine Inc., Cambridge, MA, USA.
F E DaviesThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
G J MorganThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
B A WalkerThe Myeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
University of Arkansas for Medical Sciences · USFoundation Medicine (United States)Albany Medical Center Hospital · USIcahn School of Medicine at Mount Sinai · US

Funding

Tumor Cell-Microenvironment Interactions in the Molecular Pathogenesis of MultiplP01CA055819 · NCI · UNIV OF ARKANSAS FOR MED SCIS · PI BELLAMY, WILLIAM T · 1993 to 2013
$49.7M
NCI NIH HHS P01 CA055819
6 · The paper itself

Abstract

The purpose of this study is to identify prognostic markers and treatment targets using a clinically certified sequencing panel in multiple myeloma. We performed targeted sequencing of 578 individuals with plasma cell neoplasms using the FoundationOne Heme panel and identified clinically relevant abnormalities and novel prognostic markers. Mutational burden was associated with maf and proliferation gene expression groups, and a high-mutational burden was associated with a poor prognosis. We identified homozygous deletions that were present in multiple myeloma within key genes, including CDKN2C, RB1, TRAF3, BIRC3 and TP53, and that bi-allelic inactivation was significantly enriched at relapse. Alterations in CDKN2C, TP53, RB1 and the t(4;14) were associated with poor prognosis. Alterations in RB1 were predominantly homozygous deletions and were associated with relapse and a poor prognosis which was independent of other genetic markers, including t(4;14), after multivariate analysis. Bi-allelic inactivation of key tumor suppressor genes in myeloma was enriched at relapse, especially in RB1, CDKN2C and TP53 where they have prognostic significance.

Indexed as

HumansMultiple MyelomaNeoplasm Recurrence, LocalPrognosisRetinoblastoma Binding ProteinsRetinoblastoma ProteinUbiquitin-Protein LigasesRB1 protein, humanRetinoblastoma Binding ProteinsRetinoblastoma ProteinUbiquitin-Protein Ligases

Identifiers

PMID28234347
PMCPMC5386330
OpenAlexW2590839512

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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.