Evidence map›Paper›PMID 19744130›Full record

ArticleBritish journal of haematology2009

Evidence for a novel mechanism for gene amplification in multiple myeloma: 1q12 pericentromeric heterochromatin mediates breakage-fusion-bridge cycles of a 1q12 approximately 23 amplicon.

Jeffrey R Sawyer, Erming Tian, Edward Thomas, Mark Koller, Colin Stangeby, Gael Sammartino, Linda Goosen, Charles Swanson, Regina L Binz, Bart Barlogie and 1 more

Abstract read
In one paragraph

Article in British journal of haematology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–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

18 citing papers in PubMed.

  1. Complex/crypticGenes · 2023
    Article
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  15. Article
  16. Article
  17. Update on the role of autologous hematopoietic stem cell transplantation in multiple myeloma.Mediterranean journal of hematology and infectious diseases · 2012
    Article
  18. Many multiple myelomas: making more of the molecular mayhem.Hematology. American Society of Hematology. Education Program · 2011
    Review
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

11 authors.

Jeffrey R SawyerMyeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, Little Rock, AR 72204, USA. sawyerjeffreyr@uams.edu
Erming Tian
Edward Thomas
Mark Koller
Colin Stangeby
Gael Sammartino
Linda Goosen
Charles Swanson
Regina L Binz
Bart Barlogie
John Shaughnessy

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 CA055819NCI NIH HHS P01 CA55819
6 · The paper itself

Abstract

Gene amplification is defined as a copy number (CN) increase in a restricted region of a chromosome arm, and is a mechanism for acquired drug resistance and oncogene activation. In multiple myeloma (MM), high CNs of genes in a 1q12 approximately 23 amplicon have been associated with disease progression and poor prognosis. To investigate the mechanisms for gene amplification in this region in MM, we performed a comprehensive metaphase analysis combining G-banding, fluorescence in situ hybridization, and spectral karyotyping in 67 patients with gain of 1q. In six patients (9%), evidence for at least one breakage-fusion-bridge (BFB) cycle was found. In three patients (4%), extended ladders of 1q12 approximately 23 amplicons were identified. Several key structures that are predicted intermediates in BFB cycles were observed, including: equal-spaced organization of amplicons, inverted repeat organization of amplicons along the same chromosome arm, and deletion of sequences distal to the amplified region. The 1q12 pericentromeric heterochromatin region served as both a recurrent breakpoint as well as a fusion point for sister chromatids, and ultimately bracketed both the proximal and distal boundaries of the amplicon. Our findings provide evidence for a novel BFB mechanism involving 1q12 pericentromeric breakage in the amplification of a large number of genes within a 1q12 approximately 23 amplicon.

Indexed as

Chromosome BreakageChromosomes, Human, Pair 1Gene AmplificationGene FusionHeterochromatinHumansIn Situ Hybridization, FluorescenceKaryotypingMultiple MyelomaHeterochromatin

Identifiers

PMID19744130
PMCPMC3738438

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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.