Evidence map›Paper›PMID 16332260›Full record

ArticleBMC cancer2005

Increased staining for phospho-Akt, p65/RELA and cIAP-2 in pre-neoplastic human bronchial biopsies.

Jay W Tichelaar, Yu Zhang, Jean C leRiche, Paul W Biddinger, Stephen Lam, Marshall W Anderson

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 34 citations in OpenAlex.

  1. Early Diagnosis and Screening for Lung Cancer.Cold Spring Harbor perspectives in medicine · 2021
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. LCL161 increases paclitaxel-induced apoptosis by degrading cIAP1 and cIAP2 in NSCLC.Journal of experimental & clinical cancer research : CR · 2016
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Natural history of bronchial preinvasive lesions.Cancer metastasis reviews · 2010
    Review
  12. Article
  13. Article
  14. Epithelial NF-kappaB activation promotes urethane-induced lung carcinogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2007
    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

6 authors at 2 institutions in 2 countries.

Jay W TichelaarDepartment of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA. Jay.Tichelaar@uc.edu
Yu Zhang
Jean C leRiche
Paul W Biddinger
Stephen Lam
Marshall W Anderson
University of Cincinnati Medical Center · USBC Cancer Agency · CA

Funding

Chemoprevention of Lung CancerP01CA096964 · NCI · UNIVERSITY OF CINCINNATI · PI ANDERSON, MARSHALL W · 2003 to 2008
$13.1M
A Phase II Trial of ACAPHA in Former Smokers with IEN.U01CA096109 · NCI · BRITISH COLUMBIA CANCER AGENCY · PI LAM, STEPHEN C · 2002 to 2006
$4.6M
NCI NIH HHS CA096964NCI NIH HHS CA96109NCI NIH HHS P01 CA096964NCI NIH HHS U01 CA096109
6 · The paper itself

Abstract

backgroundThe development of non-small cell lung carcinoma proceeds through a series of well-defined pathological steps before the appearance of invasive lung carcinoma. The molecular changes that correspond with pathology changes are not well defined and identification of the molecular events may provide clues on the progression of intraepithelial neoplasia in the lung, as well as suggest potential targets for chemoprevention. The acquisition of anti-apoptotic signals is critical for the survival of cancer cells but the pathways involved are incompletely characterized in developing intra-epithelial neoplasia (IEN).

methodsWe used immunohistochemistry to determine the presence, relative levels, and localization of proteins that mediate anti-apoptotic pathways in developing human bronchial neoplasia.

resultsBronchial epithelial protein levels of the phosphorylated (active) form of AKT kinase and the caspase inhibitor cIAP-2 were increased in more advanced grades of bronchial IEN lesions than in normal bronchial epithelium. Additionally, the percentage of biopsies with nuclear localization of p65/RELA in epithelial cells increased with advancing pathology grade, suggesting that NF-kappaB transcriptional activity was induced more frequently in advanced IEN lesions.

conclusionOur results indicate that anti-apoptotic pathways are elevated in bronchial IEN lesions prior to the onset of invasive carcinoma and that targeting these pathways therapeutically may offer promise in prevention of non-small cell lung carcinoma.

Indexed as

ApoptosisBiopsyCarcinoma in SituCarcinoma, Non-Small-Cell LungCell SurvivalHumansImmunohistochemistryInhibitor of Apoptosis ProteinsLung NeoplasmsNeoplasm InvasivenessOncogene Protein v-aktSignal TransductionTranscription Factor RelAInhibitor of Apoptosis ProteinsOncogene Protein v-aktRELA protein, humanTranscription Factor RelA

Identifiers

PMID16332260
PMCPMC1325242
OpenAlexW2156633409

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.