Evidence map›Paper›PMID 21059853›Full record

ArticleThe Journal of experimental medicine2010

Gain of MYC underlies recurrent trisomy of the MYC chromosome in acute promyelocytic leukemia.

Letetia Jones, Guangwei Wei, Sabina Sevcikova, Vernon Phan, Sachi Jain, Angell Shieh, Jasmine C Y Wong, Min Li, Joshua Dubansky, Mei Lin Maunakea and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

46 citing papers in PubMed, 71 citations in OpenAlex.

  1. Trial
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  5. Missense Mutations in Myc Box I Influence Nucleocytoplasmic Transport to Promote Leukemogenesis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
  6. Article
  7. Disentangling the roles of aneuploidy, chromosomal instability and tumour heterogeneity in developing resistance to cancer therapies.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023
    Review
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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

17 authors at 5 institutions in 2 countries.

Letetia JonesHelen Diller Family Comprehensive Cancer Center and Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA 94143, USA.
Guangwei Wei
Sabina Sevcikova
Vernon Phan
Sachi Jain
Angell Shieh
Jasmine C Y Wong
Min Li
Joshua Dubansky
Mei Lin Maunakea
Rachel Ochoa
George Zhu
Thelma R Tennant
Kevin M Shannon
Scott W Lowe
Michelle M Le Beau
Scott C Kogan
Institute of Biomedical Science · GBUniversity of California, San Francisco · USUCSF Helen Diller Family Comprehensive Cancer Center · USUniversity of Chicago · USHoward Hughes Medical Institute · US

Funding

MOUSE MODELS OF MYELOID LEUKEMIAU01CA084221 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SHANNON, KEVIN M. · 1999 to 2009
$8.7M
Translational Investigation of KRas & NF1 in Myeloid LeukemiaR37CA072614 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SHANNON, KEVIN M. · 2007 to 2016
$3.4M
Molecular Mechanisms of Leukemogenesis by PMLRAR alphaR01CA095274 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KOGAN, SCOTT C. · 2002 to 2013
$2.7M
NCI NIH HHS CA84221NCI NIH HHS CA95274NCI NIH HHS R01 CA095274NCI NIH HHS R37 CA072614NCI NIH HHS U01 CA084221
6 · The paper itself

Abstract

Gain of chromosome 8 is the most common chromosomal gain in human acute myeloid leukemia (AML). It has been hypothesized that gain of the MYC protooncogene is of central importance in trisomy 8, but the experimental data to support this are limited and controversial. In a mouse model of promyelocytic leukemia in which the MRP8 promoter drives expression of the PML-RARA fusion gene in myeloid cells, a Myc allele is gained in approximately two-thirds of cases as a result of trisomy for mouse chromosome 15. We used this model to test the idea that MYC underlies acquisition of trisomy in AML. We used a retroviral vector to drive expression of wild-type, hypermorphic, or hypomorphic MYC in bone marrow that expressed the PML-RARA transgene. MYC retroviruses cooperated in myeloid leukemogenesis and suppressed gain of chromosome 15. When the PML-RARA transgene was expressed in a Myc haploinsufficient background, we observed selection for increased copies of the wild-type Myc allele concomitant with leukemic transformation. In addition, we found that human myeloid leukemias with trisomy 8 have increased MYC. These data show that gain of MYC can contribute to the pathogenic effect of the most common trisomy of human AML.

Indexed as

Chromosomes, Human, Pair 8Genes, mycTrisomyAnimalsCells, CulturedDisease Models, AnimalHumansLeukemia, Promyelocytic, AcuteMiceOncogene Proteins, FusionRecurrenceOncogene Proteins, Fusionpromyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein

Identifiers

PMID21059853
PMCPMC2989761
OpenAlexW2155464138

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.