Evidence map›Paper›PMID 22308418›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Integrated cross-species transcriptional network analysis of metastatic susceptibility.

Ying Hu, Gang Wu, Michael Rusch, Luanne Lukes, Kenneth H Buetow, Jinghui Zhang, Kent W Hunter

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

44 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. SMARCD1 is a "Goldilocks" metastasis modifier.bioRxiv : the preprint server for biology · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Investigation of miRNA and mRNA Co-expression Network in Ependymoma.Frontiers in bioengineering and biotechnology · 2020
    Article
  17. Article
  18. Article
  19. Article
  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

7 authors at 3 institutions in 2 countries.

Ying HuLaboratory of Population Genetics, and Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Insitute, National Institutes of Health, Bethesda, MD 20892, USA.
Gang Wu
Michael Rusch
Luanne Lukes
Kenneth H Buetow
Jinghui Zhang
Kent W Hunter
St. Jude Children's Research Hospital · USLaboratory of Molecular Genetics · PLNational Institutes of Health · US

Funding

Genetic Modifiers of Intitiation and Progression of Mammary CancerZIABC011255 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HUNTER, KENT WILLIAM · 2010 to 2025
$33.2M
Intramural NIH HHS
6 · The paper itself

Abstract

Metastatic disease is the proximal cause of mortality for most cancers and remains a significant problem for the clinical management of neoplastic disease. Recent advances in global transcriptional analysis have enabled better prediction of individuals likely to progress to metastatic disease. However, minimal overlap between predictive signatures has precluded easy identification of key biological processes contributing to the prometastatic transcriptional state. To overcome this limitation, we have applied network analysis to two independent human breast cancer datasets and three different mouse populations developed for quantitative analysis of metastasis. Analysis of these datasets revealed that the gene membership of the networks is highly conserved within and between species, and that these networks predicted distant metastasis free survival. Furthermore these results suggest that susceptibility to metastatic disease is cell-autonomous in estrogen receptor-positive tumors and associated with the mitotic spindle checkpoint. In contrast, nontumor genetics and pathway activities-associated stromal biology are significant modifiers of the rate of metastatic spread of estrogen receptor-negative tumors. These results suggest that the application of network analysis across species may provide a robust method to identify key biological programs associated with human cancer progression.

Indexed as

Disease SusceptibilityAnimalsBreast NeoplasmsCell Cycle ProteinsCell Line, TumorDatabases, GeneticDisease ProgressionFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGene Regulatory NetworksHumansKaplan-Meier EstimateMiceMicrotubule-Associated ProteinsNeoplasm MetastasisCell Cycle ProteinsMicrotubule-Associated ProteinsNuclear ProteinsReceptors, EstrogenTetraspanin 25TPX2 protein, human

Identifiers

PMID22308418
PMCPMC3286991
OpenAlexW1992387879

What OpenQuestion holds

Textmetadata
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.