Evidence map›Paper›PMID 21887346›Full record

ArticlePloS one2011

SMURF1 amplification promotes invasiveness in pancreatic cancer.

Kevin A Kwei, A Hunter Shain, Ryan Bair, Kelli Montgomery, Collins A Karikari, Matt van de Rijn, Manuel Hidalgo, Anirban Maitra, Murali D Bashyam, Jonathan R Pollack

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Smurf1 Modulates Smad Signaling Pathway in Fibrotic Cataract Formation.Investigative ophthalmology & visual science · 2024
    Article
  4. Review
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  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. SMURF1 facilitates estrogen receptor ɑ signaling in breast cancer cells.Journal of experimental & clinical cancer research : CR · 2018
    Article
  13. Article
  14. Article
  15. Dysregulation of ubiquitin ligases in cancer.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2015
    Review
  16. Article
  17. Article
  18. Article
  19. Article
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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

10 authors at 4 institutions in 3 countries.

Kevin A KweiDepartment of Pathology, Stanford University, Stanford, California, United States of America.
A Hunter Shain
Ryan Bair
Kelli Montgomery
Collins A Karikari
Matt van de Rijn
Manuel Hidalgo
Anirban Maitra
Murali D Bashyam
Jonathan R Pollack
Stanford University · USJohns Hopkins University · USCentre for DNA Fingerprinting and Diagnostics · INSpanish National Cancer Research Centre · ES

Funding

Tumor Antigens for Individual Signatures and TherapyP50CA062924 · NCI · JOHNS HOPKINS UNIVERSITY · PI LENNON, ANNE MARIE · 1993 to 2022
$54.6M
Spectrum Stanford Center for clinical and Translational Research and EducationUL1TR001085 · NCATS · STANFORD UNIVERSITY · PI CULLEN, MARK RICHARD, GREENBERG, HARRY BERNARD · 2013 to 2017
$37.1M
Stanford Center for Clinical and Translational Education and Research (SCCTER)UL1UL1RR025744 · NCRR · STANFORD UNIVERSITY · PI GREENBERG, HARRY BERNARD · 2008 to 2011
$22.4M
TUMOR BIOLOGYT32CA009151 · NCI · STANFORD UNIVERSITY · PI CLEARY, MICHAEL L · 1985 to 2014
$5.5M
Gene Amplification and Deletion in Pancreatic CancerR01CA112016 · NCI · STANFORD UNIVERSITY · PI POLLACK, JONATHAN R · 2006 to 2010
$1.4M
NCATS NIH HHS UL1 TR001085NCI NIH HHS CA09151NCI NIH HHS CA112016NCI NIH HHS CA62924NCI NIH HHS P50 CA062924NCI NIH HHS R01 CA112016NCI NIH HHS T32 CA009151NCRR NIH HHS UL1 RR025744
6 · The paper itself

Abstract

Pancreatic cancer is a deadly disease, and new therapeutic targets are urgently needed. We previously identified DNA amplification at 7q21-q22 in pancreatic cancer cell lines. Now, by high-resolution genomic profiling of human pancreatic cancer cell lines and human tumors (engrafted in immunodeficient mice to enrich the cancer epithelial fraction), we define a 325 Kb minimal amplicon spanning SMURF1, an E3 ubiquitin ligase and known negative regulator of transforming growth factor β (TGFβ) growth inhibitory signaling. SMURF1 amplification was confirmed in primary human pancreatic cancers by fluorescence in situ hybridization (FISH), where 4 of 95 cases (4.2%) exhibited amplification. By RNA interference (RNAi), knockdown of SMURF1 in a human pancreatic cancer line with focal amplification (AsPC-1) did not alter cell growth, but led to reduced cell invasion and anchorage-independent growth. Interestingly, this effect was not mediated through altered TGFβ signaling, assayed by transcriptional reporter. Finally, overexpression of SMURF1 (but not a catalytic mutant) led to loss of contact inhibition in NIH-3T3 mouse embryo fibroblast cells. Together, these findings identify SMURF1 as an amplified oncogene driving multiple tumorigenic phenotypes in pancreatic cancer, and provide a new druggable target for molecularly directed therapy.

Indexed as

AnimalsCell CommunicationCell LineCell Line, TumorGene AmplificationHumansIn Situ Hybridization, FluorescenceMiceNeoplasm InvasivenessOncogenesPancreatic NeoplasmsUbiquitin-Protein LigasesSMURF1 protein, humanUbiquitin-Protein Ligases

Identifiers

PMID21887346
PMCPMC3161761
OpenAlexW1980321000

What OpenQuestion holds

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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.