Evidence map›Paper›PMID 22328562›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2012

Integrative genomics identified RFC3 as an amplified candidate oncogene in esophageal adenocarcinoma.

William W Lockwood, Kelsie L Thu, Lin Lin, Larissa A Pikor, Raj Chari, Wan L Lam, David G Beer

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 41 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Polymorphisms inFrontiers in veterinary science · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Key Molecular Events in Cervical Cancer Development.Medicina (Kaunas, Lithuania) · 2019
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

7 authors at 2 institutions in 2 countries.

William W LockwoodIntegrative Oncology, British Columbia Cancer Research Centre, Vancouver, British Columbia, Canada. william.lockwood@nih.gov
Kelsie L Thu
Lin Lin
Larissa A Pikor
Raj Chari
Wan L Lam
David G Beer
Occupational Cancer Research Centre · CAUniversity of Michigan–Ann Arbor · US

Funding

CIHRIntramural NIH HHS Z99 HG999999Intramural NIH HHS Z99 HL999999Intramural NIH HHS Z99 MH999999Wellcome Trust
6 · The paper itself

Abstract

purposeEsophageal adenocarcinoma (EAC) is a lethal malignancy that can develop from the premalignant condition, Barrett's esophagus (BE). Currently, there are no validated simple methods to predict which patients will progress to EAC. A better understanding of the genetic mechanisms driving EAC tumorigenesis is needed to identify new therapeutic targets and develop biomarkers capable of identifying high-risk patients that would benefit from aggressive neoadjuvant therapy. We employed an integrative genomics approach to identify novel genes involved in EAC biology that may serve as useful clinical markers. EXPERIMENTAL

designWhole genome tiling-path array comparative genomic hybridization was used to identify significant regions of copy number alteration in 20 EACs and 10 matching BE tissues. Copy number and gene expression data were integrated to identify candidate oncogenes within regions of amplification and multiple additional sample cohorts were assessed to validate candidate genes.

resultsWe identified RFC3 as a novel, candidate oncogene activated by amplification in approximately 25% of EAC samples. RFC3 was also amplified in BE from a patient whose EAC harbored amplification and was differentially expressed between nonmalignant and EAC tissues. Copy number gains were detected in other cancer types and RFC3 knockdown inhibited proliferation and anchorage-independent growth of cancer cells with increased copy number but had little effect on those without. Moreover, high RFC3 expression was associated with poor patient outcome in multiple cancer types.

conclusionsRFC3 is a candidate oncogene amplified in EAC. RFC3 DNA amplification is also prevalent in other epithelial cancer types and RFC3 expression could serve as a prognostic marker.

Indexed as

AdenocarcinomaAdultAgedAged, 80 and overCell LineCell Line, TumorCell ProliferationCohort StudiesComparative Genomic HybridizationDNA Copy Number VariationsEsophageal NeoplasmsFemaleGene AmplificationGene Expression ProfilingGenetic Predisposition to DiseaseHEK293 CellsReplication Protein CRFC3 protein, human

Identifiers

PMID22328562
PMCPMC3523177
OpenAlexW2124890939

What OpenQuestion holds

Textmetadata
LicenceTDM
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.