Evidence map›Paper›PMID 19336734›Full record

ArticleCancer prevention research (Philadelphia, Pa.)2009

The chemopreventive agent myoinositol inhibits Akt and extracellular signal-regulated kinase in bronchial lesions from heavy smokers.

Wei Han, Joell J Gills, Regan M Memmott, Stephen Lam, Phillip A Dennis

Open access · bronzeAbstract readClinical Trial, Phase I
In one paragraph

Article in Cancer prevention research (Philadelphia, Pa.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

26 citing papers in PubMed, 52 citations in OpenAlex.

  1. Myo-inositol reduces β-catenin activation in colitis.World journal of gastroenterology · 2017
    Trial
  2. A Randomized Phase IIb Trial of myo-Inositol in Smokers with Bronchial Dysplasia.Cancer prevention research (Philadelphia, Pa.) · 2016
    Trial
  3. Review
  4. Article
  5. Article
  6. Inositol depletion regulates phospholipid metabolism and activates stress signaling in HEK293T cells.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2022
    Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. SOX2 Drives Bronchial Dysplasia in a Novel Organotypic Model of Early Human Squamous Lung Cancer.American journal of respiratory and critical care medicine · 2017
    Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  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

5 authors at 3 institutions in 2 countries.

Wei HanMedical Oncology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20889, USA.
Joell J Gills
Regan M Memmott
Stephen Lam
Phillip A Dennis
BC Cancer Agency · CACenter for Cancer Research · USNational Cancer Institute · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
Development of Akt InhibitorsZIABC010450 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI DENNIS, PHILLIP A. · 2009 to 2012
$4.0M
Clinical Investigation of Signal Transduction InhibitorsZIABC010748 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI DENNIS, PHILLIP A. · 2009 to 2012
$2.0M
Intramural NIH HHSNCI NIH HHS N01-CN85188NCI NIH HHS N01 CO012400NCI NIH HHS N01-CO-12400NCI NIH HHS P30 CA006973
6 · The paper itself

Abstract

Myoinositol is an isomer of glucose that has chemopreventive activity in animal models of cancer. In a recent phase I clinical trial, myoinositol administration correlated with a statistically significant regression of preexisting bronchial dysplastic lesions in heavy smokers. To shed light on the potential mechanisms involved, activation of Akt and extracellular signal-regulated kinase (ERK), two kinases that control cellular proliferation and survival, was assessed in 206 paired bronchial biopsies from 21 patients who participated in this clinical trial. Before myoinositol treatment, strongly positive staining for activation of Akt was detected in 27% of hyperplastic/metaplastic lesions and 58% of dysplastic lesions (P = 0.05, chi(2) test). There was also a trend toward increased activation of ERK (28% in regions of hyperplasia/metaplasia to 42% of dysplastic lesions). Following myoinositol treatment, significant decreases in Akt and ERK phosphorylation were observed in dysplastic (P < 0.01 and 0.05, respectively) but not hyperplastic/metaplastic lesions (P > 0.05). In vitro, myoinositol decreased endogenous and tobacco carcinogen-induced activation of Akt and ERK in immortalized human bronchial epithelial cells, which decreased cell proliferation and induced a G(1)-S cell cycle arrest. These results show that the phenotypic progression of premalignant bronchial lesions from smokers correlates with increased activation of Akt and ERK and that these kinases are targets of myoinositol. Moreover, they suggest that myoinositol might cause regression of bronchial dysplastic lesions through inhibition of active Akt and ERK.

Indexed as

AdultAgedAntineoplastic AgentsBronchial DiseasesCell LineCell ProliferationExtracellular Signal-Regulated MAP KinasesFemaleHumansImmunohistochemistryInositolLung NeoplasmsMaleMiddle AgedPhosphorylationPrecancerous ConditionsAntineoplastic AgentsExtracellular Signal-Regulated MAP KinasesInositolProto-Oncogene Proteins c-akt

Identifiers

PMID19336734
PMCPMC3715041
OpenAlexW2170627452

What OpenQuestion holds

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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.