Evidence map›Paper›PMID 22729835›Full record

ArticlePathology oncology research : POR2012

RUNX3 downregulation in human lung adenocarcinoma is independent of p53, EGFR or KRAS status.

Mohd Feroz Mohd Omar, Kosei Ito, Min En Nga, Ross Soo, Bee Keow Peh, Tuty Muliana Ismail, Bhavin Thakkar, Richie Soong, Yoshiaki Ito, Manuel Salto-Tellez

Registry-linked trialAbstract read
PubMed Publisher
In one paragraph

Article in Pathology oncology research : POR, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02416739 (Randomized Double-blinded Comparative Trial to Study the Add-on Activity of Combination Treatment of Nicotinamide on Progression Free Survival for EGFR Mutated Lung Cancer Terminal Stage Patients Being Treated With Gefitinib or Erlotinib), which is not on this map. Cited by 9 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 2 pooled it
1.7field-weighted citation impact, top 15% 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.

NCT02416739 phase2 / phase3unknown statusnot on this mapstarted 2015, after this paper: background citation

Randomized Double-blinded Comparative Trial to Study the Add-on Activity of Combination Treatment of Nicotinamide on Progression Free Survival for EGFR Mutated Lung Cancer Terminal Stage Patients Being Treated With Gefitinib or Erlotinib

TypeinterventionalSponsorIl Yeong Park, Ph.D.Ran2015 to 2020Enrolled110ConditionsNon-Small-Cell Lung CarcinomaArmsNicotinamide
3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 2 syntheses or guidelines pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Epigenetics of lung cancer.Translational research : the journal of laboratory and clinical medicine · 2015
    Review
  7. Article
  8. The Tumor Suppressor Roles of miR-433 and miR-127 in Gastric Cancer.International journal of molecular sciences · 2013
    Article
  9. 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

10 authors at 5 institutions in 4 countries.

Mohd Feroz Mohd OmarCancer Science Institute of Singapore, Centre for Translational Medicine, National University of Singapore, #12-01, 14 Medical Drive, Singapore, 117599, Singapore.
Kosei Ito
Min En Nga
Ross Soo
Bee Keow Peh
Tuty Muliana Ismail
Bhavin Thakkar
Richie Soong
Yoshiaki Ito
Manuel Salto-Tellez
National University of Singapore · SGClinical Nutrition Research Centre · SGNational University Hospital · SGNagasaki University · JPNational University Cancer Institute, Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RUNX3 aberrations play a pivotal role in the oncogenesis of breast, gastric, colon, skin and lung tissues. The aim of this study was to characterize further the expression of RUNX3 in lung cancers. To achieve this, a lung cancer tissue microarray (TMA), frozen lung cancer tissues and lung cell lines were examined for RUNX3 expression by immunohistochemistry, while the TMA was also examined for EGFR and p53 expression. RUNX3 promoter methylation status, and EGFR and KRAS mutation status were also investigated. Inactivation of RUNX3 was observed in 70% of the adenocarcinoma samples, and this was associated with promoter hypermethylation but not biased to EGFR/KRAS mutations. Our results suggest a central role of RUNX3 downregulation in pulmonary adenocarcinoma, which may not be dependent of other established cancer-causing pathways and may have important diagnostic and screening implications.

Indexed as

AdenocarcinomaAdenocarcinoma of LungCarcinoma, Squamous CellCell Line, TumorCore Binding Factor Alpha 3 SubunitDNA MethylationDNA Mutational AnalysisDown-RegulationErbB ReceptorsHumansImmunohistochemistryLung NeoplasmsMutationProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsCore Binding Factor Alpha 3 SubunitEGFR protein, humanErbB ReceptorsKRAS protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsRunx3 protein, humanTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID22729835
OpenAlexW2071550970

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.