Evidence map›Paper›PMID 12651626›Full record

ArticleThe American journal of pathology2003

Deletion, mutation, and loss of expression of KLF6 in human prostate cancer.

Ceshi Chen, Eija-Riitta Hyytinen, Xiaodong Sun, Heikki J Helin, Pasi A Koivisto, Henry F Frierson, Robert L Vessella, Jin-Tang Dong

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

60 citing papers in PubMed, 138 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Targeting Splicing in Prostate Cancer.International journal of molecular sciences · 2018
    Review
  8. Review
  9. Article
  10. Article
  11. Mutations and Krüppel-like factor 6 (KLF6) expression levels in breast cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  12. Molecular pathways in prostate cancer.Nephro-urology monthly · 2013
    Review
  13. Effects of Kruppel-like factor 6 on osteosarcoma cell biological behavior.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Article
  14. Article
  15. Review
  16. MicroRNA-181a promotes gastric cancer by negatively regulating tumor suppressor KLF6.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2012
    Article
  17. Article
  18. Review
  19. Article
  20. A small interfering RNA targeting the KLF6 splice variant, KLF6-SV1, as gene therapy for gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2011
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 2 countries.

Ceshi ChenWinship Cancer Institute, Emory University School of Medicine, Atlanta, Georgia, USA.
Eija-Riitta Hyytinen
Xiaodong Sun
Heikki J Helin
Pasi A Koivisto
Henry F Frierson
Robert L Vessella
Jin-Tang Dong
Emory University · USTampere University · FITampere University Hospital · FIUniversity of Virginia · USUniversity of Washington · US

Funding

MOLECULAR DISSECTION OF 13Q14 IN PROSTATE CANCERR01CA085560 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI DONG, JIN-TANG · 2000 to 2010
$2.5M
TUMOR SUPPRESSOR GENE AT 13Q21 IN PROSTATE CANCERR01CA087921 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI DONG, JIN-TANG · 2000 to 2010
$2.4M
NCI NIH HHS CA85560NCI NIH HHS CA87921NCI NIH HHS R01 CA085560NCI NIH HHS R01 CA087921
6 · The paper itself

Abstract

Kruppel-like factors (KLFs) are a group of transcription factors that appear to be involved in different biological processes including carcinogenesis. In a recent study, KLF6 was reported as a tumor suppressor gene in prostate cancer because of its frequent loss of heterozygosity (LOH) and mutation as well as functional suppression of cell proliferation. Loss of chromosomal locus spanning KLF6 is relatively infrequent in other published studies of prostate cancer, however. To clarify the role of KLF6 in prostate cancers, particularly those that are high grade, we examined KLF6 for deletion, mutation, and loss of expression in 96 prostate cancer samples including 21 xenografts/cell lines. Loss of heterozygosity occurred in 4 (19%) of 21 xenografts/cell lines and 8 (28%) of 29 informative tumors. Fourteen of the 96 (15%) samples showed 15 somatic sequence changes in the KLF6 gene, including 7 that changed KLF6 peptide sequences, 4 that did not, and 4 that were located in untranslated regions. Expression levels of KLF6 were significantly lost in 4 of 20 (20%) xenografts/cell lines of prostate cancer, as detected by RT-PCR and Northern blot analysis. These findings indicate that significant genetic alterations of KLF6 occur in a minority of high-grade prostate cancers.

Indexed as

Gene DeletionGene Expression Regulation, NeoplasticLoss of HeterozygosityMutationProto-Oncogene Proteins5' Untranslated RegionsAnimalsBase SequenceDNA PrimersExonsHumansKruppel-Like Factor 6Kruppel-Like Transcription FactorsMaleMiceProstatic Neoplasms5' Untranslated RegionsDNA PrimersKLF6 protein, humanKlf6 protein, mouseKruppel-Like Factor 6Kruppel-Like Transcription FactorsProto-Oncogene ProteinsTrans-Activators

Identifiers

PMID12651626
PMCPMC1851229
OpenAlexW2038243825

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.