Evidence map›Paper›PMID 16175182›Full record

ArticleBritish journal of cancer2005

Interaction between the bone morphogenetic proteins and Ras/MAP-kinase signalling pathways in lung cancer.

K S Kraunz, H H Nelson, M Liu, J K Wiencke, K T Kelsey

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

29 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
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  8. 1,25-Dihydroxyvitamin DOncoTargets and therapy · 2019
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  11. DNA methylation in lung tissues of mouse offspring exposed in utero to polycyclic aromatic hydrocarbons.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2017
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  15. Review
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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 2 institutions in 1 country.

K S KraunzDepartment of Genetics and Complex Diseases, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, USA.
H H Nelson
M Liu
J K Wiencke
K T Kelsey
Harvard University · USNeurological Surgery · US

Funding

Translational Research Support CoreP30ES000002 · NIEHS · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI SUSAN A KORRICK · 1985 to 2026
$44.6M
The Boston Collaborative Oral Cancer StudyR01CA078609 · NCI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI KELSEY, KARL TIMOTHY · 1999 to 2010
$5.3M
Patterns of Somatic Gene Alterations in Oral CancerR01CA100679 · NCI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI KELSEY, KARL TIMOTHY · 2004 to 2012
$2.6M
NCI NIH HHS CA078609NCI NIH HHS CA100679NCI NIH HHS R01 CA078609NCI NIH HHS R01 CA100679NIEHS NIH HHS ES00002NIEHS NIH HHS P30 ES000002
6 · The paper itself

Abstract

Bone morphogenetic proteins (BMPs) are an integral component of the TGFbeta superfamily, responsible for regulation of cell proliferation, differentiation, migration and programmed cell death in a variety of cell types. The BMPs transduce their signals directly through the SMAD family of proteins but they also have been reported to interact with the MAPK and Erk pathways. Inactivation of the BMP pathway genes has been implicated as important in several cancers. Recent work has shown that BMP3b is epigenetically inactivated in cancer and suggests that BMP6 can be epigenetically inactivated. We investigated whether BMP6 is epigenetically inactivated in cell lines and whether BMP3b and BMP6 are epigenetically inactivated in non-small-cell lung cancer (NSCLC). We also studied the relationship between BMP methylation and k-ras mutation. Here, we demonstrate that the BMP3b and BMP6 genes are common targets of epigenetic inactivation in NSCLC, and that they are significantly more likely to be concurrently inactivated (P=0.009). Furthermore, this coinactivation of BMP3b and BMP6 is significantly associated with mutation of k-ras codon 12 in lung cancer (P=0.003); those with a k-ras mutation were six times more likely to have concurrent methylation of these BMP loci. Hence, these data suggest that concurrent inactivation of the BMP and activation of the Ras signalling pathways are important in lung carcinogenesis.

Indexed as

Bone Morphogenetic Protein 3Bone Morphogenetic Protein 6Bone Morphogenetic ProteinsCarcinoma, Non-Small-Cell LungCell Transformation, NeoplasticEpigenesis, GeneticGene Expression RegulationGenes, rasGrowth Differentiation Factor 10HumansLung NeoplasmsMethylationMutationPolymerase Chain Reactionras ProteinsSignal TransductionBMP3 protein, humanBMP6 protein, humanBone Morphogenetic Protein 3Bone Morphogenetic Protein 6Bone Morphogenetic ProteinsGDF10 protein, humanGrowth Differentiation Factor 10ras Proteins

Identifiers

PMID16175182
PMCPMC2361658
OpenAlexW2069871250

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.