Evidence map›Paper›PMID 22179824›Full record

ArticleOncogene2012

Recurrent deletion of CHD1 in prostate cancer with relevance to cell invasiveness.

S Huang, Z G Gulzar, K Salari, J Lapointe, J D Brooks, J R Pollack

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 4% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. CHD2-Related CNS Pathologies.International journal of molecular sciences · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Molecular Subtypes of Prostate Cancer.Current oncology reports · 2018
    Review
  20. Article

2 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 2 countries.

S HuangDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305-5176, USA.
Z G Gulzar
K Salari
J Lapointe
J D Brooks
J R Pollack
Stanford University · USMcGill University · CA

Funding

Translational Oncology Research Program (Project-005)P30CA124435 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI · 2007 to 2026
$71.4M
Translating Prostate Cancer Gene Expression SubtypesR01CA111782 · NCI · STANFORD UNIVERSITY · PI BROOKS, JAMES D. · 2005 to 2008
$1.1M
Pathogenetics of a Clinically-favorable Prostate Cancer SubtypeR01CA122246 · NCI · STANFORD UNIVERSITY · PI POLLACK, JONATHAN R · 2008 to 2010
$619k
Identifying the tumor suppressor gene at 6q15 indolent prostate cancerF32CA130472 · NCI · STANFORD UNIVERSITY · PI HUANG, STEPHANIE · 2008 to 2011
$157k
NCI NIH HHS CA111782NCI NIH HHS CA122246NCI NIH HHS CA130472NCI NIH HHS F32 CA130472NCI NIH HHS P30 CA124435NCI NIH HHS R01 CA111782NCI NIH HHS R01 CA122246
6 · The paper itself

Abstract

Though prostate cancer is often indolent, it is nonetheless a leading cause of cancer death. Defining the underlying molecular genetic alterations may lead to new strategies for prevention or treatment. Towards this goal, we performed array-based comparative genomic hybridization (CGH) on 86 primary prostate tumors. Among the most frequent alterations not associated with a known cancer gene, we identified focal deletions within 5q21 in 15 out of 86 (17%) cases. By high-resolution tiling array CGH, the smallest common deletion targeted just one gene, the chromatin remodeler chromodomain helicase DNA-binding protein 1 (CHD1). Expression of CHD1 was significantly reduced in tumors with deletion (P=0.03), and compared with normal prostate (P=0.04). Exon sequencing analysis also uncovered nonsynonymous mutations in 1 out of 7 (14%) cell lines (LAPC4) and in 1 out of 24 (4%) prostate tumors surveyed. RNA interference-mediated knockdown of CHD1 in two nontumorigenic prostate epithelial cell lines, OPCN2 and RWPE-1, did not alter cell growth, but promoted cell invasiveness, and in OPCN2-enhanced cell clonogenicity. Taken together, our findings suggest that CHD1 deletion may underlie cell invasiveness in a subset of prostate cancers, and indicate a possible novel role of altered chromatin remodeling in prostate tumorigenesis.

Indexed as

Sequence DeletionCell Line, TumorCell ProliferationCell Transformation, NeoplasticChromatin Assembly and DisassemblyComparative Genomic HybridizationDNA-Binding ProteinsDNA HelicasesGene Expression ProfilingHumansMaleNeoplasm InvasivenessProstatic NeoplasmsRNA InterferenceRNA, Small InterferingCHD1 protein, humanDNA-Binding ProteinsDNA HelicasesRNA, Small Interfering

Identifiers

PMID22179824
PMCPMC5512870
OpenAlexW2085019446

What OpenQuestion holds

Textmetadata
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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.