Evidence map›Paper›PMID 23275340›Full record

Trial reportThe Journal of biological chemistry2013

Deletion of leucine zipper tumor suppressor 2 (Lzts2) increases susceptibility to tumor development.

Daniel T Johnson, Richard Luong, Suk Hyung Lee, Yue Peng, Atossa Shaltouki, Jane T Lee, Dong Lin, Yuzhuo Wang, Zijie Sun

Open access · hybridAbstract readClinical Trial
In one paragraph

Trial report in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 32% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Heterogeneity in readouts of canonical wnt pathway activity within intestinal crypts.Developmental dynamics : an official publication of the American Association of Anatomists · 2016
    Article
  17. Article
  18. 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 2 institutions in 2 countries.

Daniel T JohnsonDepartment of Urology, Stanford University School of Medicine, Stanford, California 94305-5328, USA.
Richard Luong
Suk Hyung Lee
Yue Peng
Atossa Shaltouki
Jane T Lee
Dong Lin
Yuzhuo Wang
Zijie Sun
Stanford University · USBC Cancer Agency · CA

Funding

Roles of the androgen receptor and its co-regulators in prostate tumorigenesisR01CA070297 · NCI · STANFORD UNIVERSITY · PI SUN, ZIJIE · 2003 to 2025
$5.0M
A new regulator for Wnt/beta-catenin signaling and prostate tumorigenesisR01CA151623 · NCI · STANFORD UNIVERSITY · PI SUN, ZIJIE · 2011 to 2015
$1.7M
ANDROGEN RECEPTOR ASSOCIATED PROTEINS IN PROSTATE CANCERR29CA070297 · NCI · STANFORD UNIVERSITY · PI SUN, ZIJIE · 1997 to 2002
$329k
NCI NIH HHS CA-070297NCI NIH HHS CA-151623NCI NIH HHS R01 CA070297NCI NIH HHS R01 CA151623NCI NIH HHS R29 CA070297
6 · The paper itself

Abstract

Using an Lzts2 knock-out mouse model, we characterized the biological role of Lzts2 in tumorigenesis. Both heterozygous and homozygous deletion of the Lzts2-targeted allele in mice shows an increased incidence in spontaneous tumor development, although Lzts2 homozygous knock-out mice show significantly higher incidences than heterozygous mice. Treatment of Lzts2-deficient mice with a carcinogen, N-butyl-N-(4-hydroxybutyl) nitrosamine, increases the susceptibility to N-butyl-N-(4-hydroxybutyl) nitrosamine-induced bladder carcinoma development. Examination of human prostate cancer tissue specimens shows a reduction of LZTS2 protein expression in prostate cancer cells. Further analyses of mouse embryonic fibroblasts isolated from Lzts2 knock-out embryos show that loss of Lzts2 enhances cell growth. These data provide the first line of evidence demonstrating that deletion of Lzts2 increases susceptibility to spontaneous and carcinogen-induced tumor development.

Indexed as

Gene DeletionGenetic Predisposition to DiseaseAnimalsButylhydroxybutylnitrosamineCarcinogensCell Cycle ProteinsDNA-Binding ProteinsFemaleGene Expression Regulation, NeoplasticHEK293 CellsHeterozygoteHumansMaleMiceMice, KnockoutProstatic NeoplasmsButylhydroxybutylnitrosamineCarcinogensCell Cycle ProteinsDNA-Binding ProteinsLZTS2 protein, humanLZTS2 protein, mouseTumor Suppressor Proteins

Identifiers

PMID23275340
PMCPMC3567628
OpenAlexW1986181778

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.