Evidence map›Paper›PMID 17430594›Full record

ArticleBMC cancer2007

Gene expression profiles of prostate cancer reveal involvement of multiple molecular pathways in the metastatic process.

Uma R Chandran, Changqing Ma, Rajiv Dhir, Michelle Bisceglia, Maureen Lyons-Weiler, Wenjing Liang, George Michalopoulos, Michael Becich, Federico A Monzon

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 298 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
298citing papers in PubMed, 5 pooled it
13.2field-weighted citation impact, top 1% 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

298 citing papers in PubMed, 5 syntheses or guidelines pooled it, 509 citations in OpenAlex.

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238 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

9 authors at 1 institution in 1 country.

Uma R ChandranDepartmental of Biomedical Informatics, University of Pittsburgh, Pittsburgh, PA 15260, USA. chandran@pitt.edu
Changqing Ma
Rajiv Dhir
Michelle Bisceglia
Maureen Lyons-Weiler
Wenjing Liang
George Michalopoulos
Michael Becich
Federico A Monzon
University of Pittsburgh · US

Funding

MOLECULAR RECLASSIFICATION OF PROSTATIC CANCERU01CA088110 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MICHALOPOULOS, GEORGE K · 2000 to 2004
$3.0M
NCI NIH HHS 5 U01 CA88110-02NCI NIH HHS U01 CA088110
6 · The paper itself

Abstract

backgroundProstate cancer is characterized by heterogeneity in the clinical course that often does not correlate with morphologic features of the tumor. Metastasis reflects the most adverse outcome of prostate cancer, and to date there are no reliable morphologic features or serum biomarkers that can reliably predict which patients are at higher risk of developing metastatic disease. Understanding the differences in the biology of metastatic and organ confined primary tumors is essential for developing new prognostic markers and therapeutic targets.

methodsUsing Affymetrix oligonucleotide arrays, we analyzed gene expression profiles of 24 androgen-ablation resistant metastatic samples obtained from 4 patients and a previously published dataset of 64 primary prostate tumor samples. Differential gene expression was analyzed after removing potentially uninformative stromal genes, addressing the differences in cellular content between primary and metastatic tumors.

resultsThe metastatic samples are highly heterogenous in expression; however, differential expression analysis shows that 415 genes are upregulated and 364 genes are downregulated at least 2 fold in every patient with metastasis. The expression profile of metastatic samples reveals changes in expression of a unique set of genes representing both the androgen ablation related pathways and other metastasis related gene networks such as cell adhesion, bone remodelling and cell cycle. The differentially expressed genes include metabolic enzymes, transcription factors such as Forkhead Box M1 (FoxM1) and cell adhesion molecules such as Osteopontin (SPP1).

conclusionWe hypothesize that these genes have a role in the biology of metastatic disease and that they represent potential therapeutic targets for prostate cancer.

Indexed as

Gene ExpressionGenetic HeterogeneityHumansMaleNeoplasm MetastasisProstatic NeoplasmsStromal Cells

Identifiers

PMID17430594
PMCPMC1865555
OpenAlexW1968445925

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.