Evidence map›Paper›PMID 16203770›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2005

Molecular alterations in primary prostate cancer after androgen ablation therapy.

Carolyn J M Best, John W Gillespie, Yajun Yi, Gadisetti V R Chandramouli, Mark A Perlmutter, Yvonne Gathright, Heidi S Erickson, Lauren Georgevich, Michael A Tangrea, Paul H Duray and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed, 1 pooled it
5.7field-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

92 citing papers in PubMed, 1 synthesis or guideline pooled it, 186 citations in OpenAlex.

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  20. Protein tyrosine kinase 6 signaling in prostate cancer.American journal of clinical and experimental urology · 2020
    Review

32 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

18 authors at 3 institutions in 2 countries.

Carolyn J M BestPathogenetics Unit, Laboratory of Pathology, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA. bestcar@mail.nih.gov
John W Gillespie
Yajun Yi
Gadisetti V R Chandramouli
Mark A Perlmutter
Yvonne Gathright
Heidi S Erickson
Lauren Georgevich
Michael A Tangrea
Paul H Duray
Sergio González
Alfredo Velasco
W Marston Linehan
Robert J Matusik
Douglas K Price
William D Figg
Michael R Emmert-Buck
Rodrigo F Chuaqui
National Cancer Institute · USPontificia Universidad Católica de Chile · CLVanderbilt University · US

Funding

TRANSGENIC MOUSE MODEL FOR PROSTATE CANCERR01CA076142 · NCI · VANDERBILT UNIVERSITY · PI MATUSIK, ROBERT J. · 1998 to 2012
$4.8M
Molecular Pathology of CancerZ01SC010437 · SC · DIVISION OF CLINICAL SCIENCES - NCI · PI EMMERT-BUCK, MICHAEL R · 2002 to 2008
$1.4M
SNPs /Polymorphisms in Development of Prostate CancerZ01BC010453 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI FIGG, WILLIAM DOUGLAS · 2002 to 2008
$938k
Intramural NIH HHSNCI NIH HHS R01 CA076142NCI NIH HHS R01 CA76142-06NCI NIH HHS Z01 SC010437-05
6 · The paper itself

Abstract

purposeAfter an initial response to androgen ablation, most prostate tumors recur, ultimately progressing to highly aggressive androgen-independent cancer. The molecular mechanisms underlying progression are not well known in part due to the rarity of androgen-independent samples from primary and metastatic sites. EXPERIMENTAL

designWe compared the gene expression profiles of 10 androgen-independent primary prostate tumor biopsies with 10 primary, untreated androgen-dependent tumors. Samples were laser capture microdissected, the RNA was amplified, and gene expression was assessed using Affymetrix Human Genome U133A GeneChip. Differential expression was examined with principal component analysis, hierarchical clustering, and Student's t testing. Analysis of gene ontology was done with Expression Analysis Systematic Explorer and gene expression data were integrated with genomic alterations with Differential Gene Locus Mapping.

resultsUnsupervised principal component analysis showed that the androgen-dependent and androgen-independent tumors segregated from one another. After filtering the data, 239 differentially expressed genes were identified. Two main gene ontologies were found discordant between androgen-independent and androgen-dependent tumors: macromolecule biosynthesis was down-regulated and cell adhesion was up-regulated in androgen-independent tumors. Other differentially expressed genes were related to interleukin-6 signaling as well as angiogenesis, cell adhesion, apoptosis, oxidative stress, and hormone response. The Differential Gene Locus Mapping analysis identified nine regions of potential chromosomal deletion in the androgen-independent tumors, including 1p36, 3p21, 6p21, 8p21, 11p15, 11q12, 12q23, 16q12, and 16q21.

conclusionsTaken together, these data identify several unique characteristics of androgen-independent prostate cancer that may hold potential for the development of targeted therapeutic intervention.

Indexed as

Gene Expression RegulationGene Expression Regulation, NeoplasticAgedAndrogen AntagonistsAndrogensAntineoplastic Agents, HormonalBiopsyCell AdhesionChromosome DeletionChromosome MappingChromosomesCluster AnalysisDisease ProgressionDown-RegulationGene DeletionGenomeAndrogen AntagonistsAndrogensAntineoplastic Agents, HormonalInterleukin-6RNA

Identifiers

PMID16203770
PMCPMC1432092
OpenAlexW2168850532

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.