Evidence map›Paper›PMID 22383169›Full record

ArticleGenes, chromosomes & cancer2012

The miR-17-92 cluster and its target THBS1 are differentially expressed in angiosarcomas dependent on MYC amplification.

Antoine Italiano, Rachael Thomas, Matthew Breen, Lei Zhang, Aimee M Crago, Samuel Singer, Raya Khanin, Robert G Maki, Aleksandra Mihailovic, Markus Hafner and 2 more

Open access · greenAbstract read
In one paragraph

Article in Genes, chromosomes & cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. THBS1 (thrombospondin-1).Atlas of genetics and cytogenetics in oncology and haematology · 2020
    Article
  15. Review
  16. JAK2/PD-L1/PD-L2 (9p24.1) amplifications in renal cell carcinomas with sarcomatoid transformation: implications for clinical management.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2019
    Article
  17. Review
  18. Review
  19. Role of Nerve Growth Factor (NGF) and miRNAs in Epithelial Ovarian Cancer.International journal of molecular sciences · 2017
    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

12 authors at 4 institutions in 2 countries.

Antoine ItalianoDepartment of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA. italiano@bergonie.org
Rachael Thomas
Matthew Breen
Lei Zhang
Aimee M Crago
Samuel Singer
Raya Khanin
Robert G Maki
Aleksandra Mihailovic
Markus Hafner
Tom Tuschl
Cristina R Antonescu
Memorial Sloan Kettering Cancer Center · USHoward Hughes Medical Institute · USNorth Carolina State University · USIcahn School of Medicine at Mount Sinai · US

Funding

SOFT TISSUE SARCOMA PROGRAM PROJECTP01CA047179 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI LADANYI, MARC · 1989 to 2010
$17.3M
SPORE in Soft Tissue SarcomaP50CA140146 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI SPRIGGS, DAVID R · 2010 to 2014
$11.1M
NCI NIH HHS P01 CA047179NCI NIH HHS P01 CA047179-15A2NCI NIH HHS P50 CA140146NCI NIH HHS P50 CA 140146-01
6 · The paper itself

Abstract

Angiosarcomas (ASs) represent a heterogeneous group of malignant vascular tumors that may occur spontaneously as primary tumors or secondarily after radiation therapy or in the context of chronic lymphedema. Most secondary ASs have been associated with MYC oncogene amplification, whereas the role of MYC abnormalities in primary AS is not well defined. Twenty-two primary and secondary ASs were analyzed by array-comparative genomic hybridization (aCGH) and by deep sequencing of small RNA libraries. By aCGH and subsequently confirmed by fluorescence in situ hybridization, MYC amplification was identified in three out of six primary tumors and in 8 out of 12 secondary AS. We have also found MAML1 as a new potential oncogene in MYC-amplified AS. Significant upregulation of the miR-17-92 cluster was observed in MYC-amplified AS compared to AS lacking MYC amplification and the control group (other vascular tumors, nonvascular sarcomas). Moreover, MYC-amplified ASs were associated with a significantly lower expression of thrombospondin-1 (THBS1) than AS without MYC amplification or controls. Altogether, our study implicates MYC amplification not only in the pathogenesis of secondary AS but also in a subset of primary AS. Thus, MYC amplification may play a crucial role in the angiogenic phenotype of AS through upregulation of the miR-17-92 cluster, which subsequently downregulates THBS1, a potent endogenous inhibitor of angiogenesis.

Indexed as

Gene AmplificationGenes, mycAdultAgedAged, 80 and overComparative Genomic HybridizationDNA-Binding ProteinsFemaleGene Expression Regulation, NeoplasticHemangiosarcomaHumansIn Situ Hybridization, FluorescenceMaleMicroRNAsMiddle AgedProto-Oncogene Proteins c-mycDNA-Binding ProteinsMAML1 protein, humanMicroRNAsMIR17HG, humanProto-Oncogene Proteins c-mycRNA, Long NoncodingThrombospondin 1Transcription Factors

Identifiers

PMID22383169
PMCPMC3360479
OpenAlexW2050152766

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.