Evidence map›Paper›PMID 18310086›Full record

ArticleCarcinogenesis2008

Asbestos exposure predicts cell cycle control gene promoter methylation in pleural mesothelioma.

Brock C Christensen, John J Godleski, Carmen J Marsit, E A Houseman, Cristina Y Lopez-Fagundo, Jennifer L Longacker, Raphael Bueno, David J Sugarbaker, Heather H Nelson, Karl T Kelsey

Open access · greenAbstract read
In one paragraph

Article in Carcinogenesis, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
6.1field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 88 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Circulating biomarkers in malignant pleural mesothelioma.Exploration of targeted anti-tumor therapy · 2020
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Targeting the epigenome in malignant pleural mesothelioma.Translational lung cancer research · 2017
    Review
  13. Review
  14. Article
  15. Review
  16. High Incidence of Somatic BAP1 alterations in sporadic malignant mesothelioma.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2015
    Article
  17. Article
  18. Article
  19. Article
  20. Review
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 6 institutions in 2 countries.

Brock C ChristensenDepartment of Environmental Health, Harvard School of Public Health, Boston, MA 02115, USA.
John J Godleski
Carmen J Marsit
E A Houseman
Cristina Y Lopez-Fagundo
Jennifer L Longacker
Raphael Bueno
David J Sugarbaker
Heather H Nelson
Karl T Kelsey
Brigham and Women's Hospital · USBoston University · USBrown University · USUniversity of Massachusetts Lowell · USUniversity of Minnesota · USUniversity of Puerto Rico System · PR

Funding

VANADIUM AND HUMAN HEALTHP42ES005947 · NIEHS · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI KELSEY, KARL TIMOTHY · 1992 to 2006
$19.6M
TRAINING PROGRAM IN ENVIRONMENTAL HEALTH SCIENCEST32ES007155 · NIEHS · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI HOTAMISLIGIL, GOKHAN S · 1985 to 2008
$5.1M
The Epidemiology of Molecular Alterations in MesotheliomaR01CA126939 · NCI · BROWN UNIVERSITY · PI KELSEY, KARL TIMOTHY · 2008 to 2012
$2.4M
NCI NIH HHS CA126939NCI NIH HHS R01 CA126939NIEHS NIH HHS P42 ES005947NIEHS NIH HHS P42ES05947NIEHS NIH HHS T32 ES007155NIEHS NIH HHS T32ES007155
6 · The paper itself

Abstract

Malignant pleural mesothelioma (MPM) is a rapidly fatal tumor with increasing incidence worldwide responsible for many thousands of deaths annually. Although there is a clear link between exposure to asbestos and mesothelioma, and asbestos is known to be both clastogenic and cytotoxic to mesothelial cells, the mechanisms of causation of MPM remain largely unknown. However, there is a rapidly emerging literature that describes inactivation of a diverse array of tumor suppressor genes (TSGs) via promoter DNA CpG methylation in MPM, although the etiology of these alterations remains unclear. We studied the relationships among promoter methylation silencing, asbestos exposure, patient demographics and tumor histology using a directed approach; examining six cell cycle control pathway TSGs in an incident case series of 70 MPMs. Promoter hypermethylation of APC, CCND2, CDKN2A, CDKN2B, HPPBP1 and RASSF1 were assessed. We observed significantly higher lung asbestos body burden if any of these cell cycle genes were methylated (P < 0.02), and there was a significant trend of increasing asbestos body counts as the number of methylated cell cycle pathway genes increased from 0 to 1 to >1 (P < 0.005). This trend of increasing asbestos body count and increasing number of methylated cell cycle pathway genes remained significant (P < 0.05) after controlling for age, gender and tumor histology. These data suggest a novel tumorigenic mechanism of action of asbestos and may contribute to the understanding of precisely how asbestos exposure influences the etiology and clinical course of malignant mesothelioma.

Indexed as

Body BurdenAsbestosCell CycleDNA MethylationDNA, NeoplasmEnvironmental ExposureHumansIncidenceMesotheliomaNeoplasm ProteinsPleural NeoplasmsPromoter Regions, GeneticAsbestosDNA, NeoplasmNeoplasm Proteins

Identifiers

PMID18310086
PMCPMC2516493
OpenAlexW1977849264

What OpenQuestion holds

Textmetadata
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.