Evidence map›Paper›PMID 30166698›Full record

ArticleTransactions of the American Clinical and Climatological Association2018

TARGETING THE PROSTACYCLIN/PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR GAMMA AXIS IN LUNG CANCER CHEMOPREVENTION.

Mark W Geraci

Abstract read
In one paragraph

Article in Transactions of the American Clinical and Climatological Association, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. 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

1 author.

Mark W GeraciINDIANAPOLIS, INDIANA.

Funding

Tissue Bank and Biomarkers CoreP50CA058187 · NCI · UNIVERSITY OF COLORADO DENVER · PI MILLER, YORK E · 1992 to 2018
$43.8M
Common targeting of the prostacyclin-PPARy axis in COPD and lung cancerR01CA164780 · NCI · UNIVERSITY OF COLORADO DENVER · PI TUDER, RUBIN M. · 2011 to 2014
$2.3M
NCI NIH HHS P50 CA058187NCI NIH HHS R01 CA164780
6 · The paper itself

Abstract

Lung cancer remains an important target of cancer research, and accounts for most deaths of any cancer type in the United States. Chemoprevention refers to the use of agents to prevent the development of cancer in high-risk populations, often in patients with predisposing lesions. In the following, we describe our ongoing work examining the role of the eicosanoid prostacyclin in lung cancer chemoprevention. Our findings include the fact that most adenocarcinomas lose the expression of prostacyclin synthase through methylation silencing. In addition, transgenic mice with overexpression of prostacyclin synthase are protected from tumorigenesis in multiple preclinical lung cancer models. Our phase IIb clinical trial using iloprost, a prostacyclin analogue, showed the reversal of airway dysplasia in high-risk individuals. This trial represents the first to show regression of airway dysplasia from the administration of a chemoprevention agent and forms the basis for future trials in lung cancer chemoprevention.

Indexed as

Adenocarcinoma of LungAnimalsAnticarcinogenic AgentsCell Line, TumorCell Transformation, NeoplasticClinical Trials, Phase II as TopicCytochrome P-450 Enzyme SystemHumansIloprostIntramolecular OxidoreductasesLung NeoplasmsMiceMolecular Targeted TherapyMutationPPAR gammaSignal TransductionAnticarcinogenic AgentsCytochrome P-450 Enzyme SystemIloprostIntramolecular OxidoreductasesPPAR gammaprostacyclin synthetase

Identifiers

PMID30166698
PMCPMC6116597

What OpenQuestion holds

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Registered trials

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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.