Evidence map›Paper›PMID 18834524›Full record

ArticleBMC cancer2008

Methylation screening of the TGFBI promoter in human lung and prostate cancer by methylation-specific PCR.

Jinesh N Shah, Genze Shao, Tom K Hei, Yongliang Zhao

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

28 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
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  8. Molecules and cells · 2019
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  14. Review
  15. Article
  16. Article
  17. Hypermethylation of TGF-β1 gene promoter in gastric cancer.World journal of gastroenterology · 2013
    Article
  18. TGF-β mediated DNA methylation in prostate cancer.Translational andrology and urology · 2012
    Article
  19. Article
  20. TGFBI promoter hypermethylation correlating with paclitaxel chemoresistance in ovarian cancer.Journal of experimental & clinical cancer research : CR · 2012
    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

4 authors at 1 institution in 1 country.

Jinesh N ShahCenter for Radiological Research, Columbia University, New York, NY 10032, USA. Jinesh.Shah@nyumc.org
Genze Shao
Tom K Hei
Yongliang Zhao
Columbia University · US

Funding

MECHANISMS OF ARSENIC CARCINOGENESISR01ES011804 · NIEHS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI HEI, TOM K. · 2002 to 2005
$1.5M
Role of TGFBI gene in cell proliferation and tumor progressionR01CA127120 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ZHAO, YONGLIANG · 2008 to 2011
$1.3M
NCI NIH HHS CA127120NCI NIH HHS R01 CA127120NIEHS NIH HHS ES 11804NIEHS NIH HHS R01 ES011804
6 · The paper itself

Abstract

backgroundHypermethylation of the TGFBI promoter has been shown to correlate with decreased expression of this gene in human tumor cell lines. In this study, we optimized a methylation-specific polymerase chain reaction (MSP) method and investigated the methylation status of the TGFBI promoter in human lung and prostate cancer specimens.

methodsMethylation-specific primers were designed based on the methylation profiles of the TGFBI promoter in human tumor cell lines, and MSP conditions were optimized for accurate and efficient amplification. Genomic DNA was isolated from lung tumors and prostatectomy tissues of prostate cancer patients, bisulfite-converted, and analyzed by MSP.

resultsAmong 50 lung cancer samples, 44.0% (22/50) harbored methylated CpG sites in the TGFBI promoter. An analysis correlating gene methylation status with clinicopathological cancer features revealed that dense methylation of the TGFBI promoter was associated with a metastatic phenotype, with 42.9% (6/14) of metastatic lung cancer samples demonstrating dense methylation vs. only 5.6% (2/36) of primary lung cancer samples (p < 0.05). Similar to these lung cancer results, 82.0% (41/50) of prostate cancer samples harbored methylated CpG sites in the TGFBI promoter, and dense methylation of the promoter was present in 38.9% (7/18) of prostate cancer samples with the feature of locoregional invasiveness vs. only 19.4% (6/31) of prostate cancer samples without locoregional invasiveness (p < 0.05). Furthermore, promoter hypermethylation correlated with highly reduced expression of the TGFBI gene in human lung and prostate tumor cell lines.

conclusionWe successfully optimized a MSP method for the precise and efficient screening of TGFBI promoter methylation status. Dense methylation of the TGFBI promoter correlated with the extent of TGFBI gene silencing in tumor cell lines and was related to invasiveness of prostate tumors and metastatic status of lung cancer tumors. Thus, TGFBI promoter methylation can be used as a potential prognostic marker for invasiveness and metastasis in prostate and lung cancer patients, respectively.

Indexed as

DNA MethylationCarcinoma, Non-Small-Cell LungDNA, NeoplasmHumansLung NeoplasmsMaleNeoplasm InvasivenessNeoplasm MetastasisPolymerase Chain ReactionPromoter Regions, GeneticProstatic NeoplasmsTransforming Growth Factor beta1DNA, NeoplasmTGFB1 protein, humanTransforming Growth Factor beta1

Identifiers

PMID18834524
PMCPMC2572632
OpenAlexW2011510627

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LicenceCC BY
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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.