Evidence map›Paper›PMID 19004026›Full record

ArticleInternational journal of cancer2009

Genetic and epigenetic inactivation of LPL gene in human prostate cancer.

Jin Woo Kim, Yu Cheng, Wennuan Liu, Tao Li, Srinivasan Yegnasubramanian, Siqun L Zheng, Jianfeng Xu, William B Isaacs, Bao-Li Chang

Open access · bronzeAbstract read
In one paragraph

Article in International journal of cancer, 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
2.3field-weighted citation impact, top 12% 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, 34 citations in OpenAlex.

  1. Article
  2. Deletions ofBiomolecules · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Associations of the ABCA1 and LPL Gene Polymorphisms With Lipid Levels in a Hyperlipidemic Population.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis · 2018
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Identification of collaboration patterns of dysfunctional pathways in breast cancer.International journal of clinical and experimental pathology · 2014
    Article
  16. Article
  17. Article
  18. TGF-β mediated DNA methylation in prostate cancer.Translational andrology and urology · 2012
    Article
  19. 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

9 authors at 3 institutions in 1 country.

Jin Woo KimCenter for Cancer Genomics, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
Yu Cheng
Wennuan Liu
Tao Li
Srinivasan Yegnasubramanian
Siqun L Zheng
Jianfeng Xu
William B Isaacs
Bao-Li Chang
Wake Forest University · USJohns Hopkins Hospital · USSidney Kimmel Comprehensive Cancer Center · US

Funding

Interaction of PTEN and CDKN1B in Pca susceptibilityR01CA106523 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI XU, JIANFENG · 2004 to 2008
$1.6M
Mapping Prostate Cancer Susceptibility Genes at 8p22-23R01CA095052 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI XU, JIANFENG · 2003 to 2007
$1.4M
QTL mapping for genes regulating apoptosis capacityR01CA119069 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI XU, JIANFENG · 2006 to 2010
$1.2M
NCI NIH HHS CA106523NCI NIH HHS CA119069NCI NIH HHS CA95052NCI NIH HHS R01 CA095052NCI NIH HHS R01 CA106523NCI NIH HHS R01 CA119069
6 · The paper itself

Abstract

Lipoprotein lipase (LPL) is in chromosome 8p22, site of one of the most common somatic deletions in prostate tumors. Additionally, a CpG island (CGI) was identified in the LPL promoter region. To test the hypothesis that LPL is a tumor suppressor gene, which is inactivated by somatic deletion and hypermethylation in prostate cancer, we evaluated somatic DNA deletion and methylation status at LPL in 56 pairs of DNA samples isolated from prostate cancer tissues and matching normal controls and 11 prostate cell lines. We found that the DNA in 21 of 56 primary cancers (38%) was methylated in the LPL promoter CGI, whereas no methylation was detected in any normal samples. In addition, we found a hemizygous deletion at LPL in 38 of the 56 tumors (68%). When the results of deletion and methylation were considered together, we found LPL promoter CGI methylation occurred in 45% of LPL deleted tumors and in 22% of LPL retained tumors. Within several clinical characteristics tested, the preoperative PSA levels were found to be significantly higher in subjects with LPL promoter CGI methylation compared with subjects without LPL promoter methylation (p=0.0012). Additionally, demethylation of the LPL promoter CGI was accompanied by transcriptional reactivation of LPL in the prostate cancer cell lines DU145 and PC3. In summary, we report a novel finding that the LPL gene is commonly methylated in prostate tumors, and our results suggest that biallelic inactivation of LPL by chromosomal deletion and promoter hypermethylation may play a role in human prostate cancer.

Indexed as

Chromosome DeletionEpigenesis, GeneticGenes, Tumor SuppressorCpG IslandsDNA MethylationHumansLipoprotein LipaseMalePromoter Regions, GeneticProstatic NeoplasmsReverse Transcriptase Polymerase Chain ReactionRNA, MessengerLipoprotein LipaseRNA, Messenger

Identifiers

PMID19004026
PMCPMC3667349
OpenAlexW2007433014

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.