Evidence map›Paper›PMID 20112052›Full record

ReviewCancer metastasis reviews2010

Natural history of bronchial preinvasive lesions.

Taichiro Ishizumi, Annette McWilliams, Calum MacAulay, Adi Gazdar, Stephen Lam

Abstract readReview
In one paragraph

Review in Cancer metastasis reviews, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 99 citations in OpenAlex.

  1. A Randomized Phase IIb Trial of myo-Inositol in Smokers with Bronchial Dysplasia.Cancer prevention research (Philadelphia, Pa.) · 2016
    Trial
  2. Review
  3. Article
  4. Signaling pathways and targeted interventions for precancers.Signal transduction and targeted therapy · 2026
    Review
  5. Article
  6. Review
  7. Automatic lesion detection for narrow-band imaging bronchoscopy.Journal of medical imaging (Bellingham, Wash.) · 2024
    Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. In situ growth in early lung adenocarcinoma may represent precursor growth or invasive clone outgrowth-a clinically relevant distinction.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2019
    Article
  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 3 countries.

Taichiro IshizumiDepartment of Thoracic Surgery, Tokyo Medical University, Tokyo, Japan. tishizumi@hotmail.co.jp
Annette McWilliams
Calum MacAulay
Adi Gazdar
Stephen Lam
BC Cancer Agency · CASouthwestern Medical CenterTokyo Medical University · JP

Funding

UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI GIBBONS, DON LYNN · 1996 to 2024
$57.4M
NCI NIH HHS P50 CA070907
6 · The paper itself

Abstract

Preinvasive bronchial lesions defined as dysplasia and carcinoma in situ (CIS) have been considered as precursors of squamous cell carcinoma of the lung. The risk and rate of progression of preinvasive lesions to invasive squamous cell carcinoma as well as the mechanism of progression or regression are incompletely understood. While the evidence for the multistage, stepwise progression model is weak with relatively few documented lesions that progress through various grades of dysplasia to CIS and then to invasive carcinoma, the concept of field carcinogenesis is strongly supported. The presence of high-grade dysplasia or CIS is a risk marker for lung cancer both in the central airways and peripheral lung. Genetic alterations such as loss of heterozygosity in chromosome 3p or chromosomal aneusomy as well as host factors such as the inflammatory load and levels of anti-inflammatory proteins in the lung influence the progression or regression of preinvasive lesions. CIS is different than severe dysplasia at the molecular level and has different clinical outcome. Molecular analysis of dysplastic lesions that progress to CIS or invasive cancer and rare lesions that progress rapidly from hyperplasia or metaplasia to CIS or invasive cancer will shed light on the key molecular determinants driving development to an invasive phenotype versus those associated with tobacco smoke damage.

Indexed as

British ColumbiaBronchiCarcinoma, Squamous CellCell Transformation, NeoplasticDisease ProgressionHumansLongitudinal StudiesLung NeoplasmsNeoplasm InvasivenessPrecancerous Conditions

Identifiers

PMID20112052
PMCPMC3417071
OpenAlexW1973315596

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.