Evidence map›Paper›PMID 19653896›Full record

ArticleBMC medical genomics2009

Candidate pathways and genes for prostate cancer: a meta-analysis of gene expression data.

Ivan P Gorlov, Jinyoung Byun, Olga Y Gorlova, Ana M Aparicio, Eleni Efstathiou, Christopher J Logothetis

Open access · goldAbstract read
In one paragraph

Article in BMC medical genomics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 3 pooled it
4.1field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 3 syntheses or guidelines pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Type XX Collagen Is Elevated in Circulation of Patients with Solid Tumors.International journal of molecular sciences · 2022
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  11. Prognostic Utility of a New mRNA Expression Signature of Gleason Score.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
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  13. Imputation of TruncatedThe annals of applied statistics · 2014
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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 1 institution in 1 country.

Ivan P GorlovDepartment of Genitourinary Medical Oncology, The University of Texas M, D, Anderson Cancer Center, Houston, TX, USA. ipgorlov@mdanderson.org
Jinyoung Byun
Olga Y Gorlova
Ana M Aparicio
Eleni Efstathiou
Christopher J Logothetis
The University of Texas MD Anderson Cancer Center · US

Funding

Targeting Tumor Microenvironment-Induced Therapy Resistance in Prostate Cancer Bone MetastasisP50CA140388 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LOGOTHETIS, CHRISTOPHER J., THOMPSON, TIMOTHY CHARLES · 2009 to 2022
$23.4M
Modeling Lung Cancer: Risks, Progression, and ScreeningU01CA097431 · NCI · RICE UNIVERSITY · PI KIMMEL, MAREK · 2002 to 2009
$1.8M
NCI NIH HHS P50 CA140388NCI NIH HHS U01 CA097431
6 · The paper itself

Abstract

backgroundThe genetic mechanisms of prostate tumorigenesis remain poorly understood, but with the advent of gene expression array capabilities, we can now produce a large amount of data that can be used to explore the molecular and genetic mechanisms of prostate tumorigenesis.

methodsWe conducted a meta-analysis of gene expression data from 18 gene array datasets targeting transition from normal to localized prostate cancer and from localized to metastatic prostate cancer. We functionally annotated the top 500 differentially expressed genes and identified several candidate pathways associated with prostate tumorigeneses.

resultsWe found the top differentially expressed genes to be clustered in pathways involving integrin-based cell adhesion: integrin signaling, the actin cytoskeleton, cell death, and cell motility pathways. We also found integrins themselves to be downregulated in the transition from normal prostate tissue to primary localized prostate cancer. Based on the results of this study, we developed a collagen hypothesis of prostate tumorigenesis. According to this hypothesis, the initiating event in prostate tumorigenesis is the age-related decrease in the expression of collagen genes and other genes encoding integrin ligands. This concomitant depletion of integrin ligands leads to the accumulation of ligandless integrin and activation of integrin-associated cell death. To escape integrin-associated death, cells suppress the expression of integrins, which in turn alters the actin cytoskeleton, elevates cell motility and proliferation, and disorganizes prostate histology, contributing to the histologic progression of prostate cancer and its increased metastasizing potential.

conclusionThe results of this study suggest that prostate tumor progression is associated with the suppression of integrin-based cell adhesion. Suppression of integrin expression driven by integrin-mediated cell death leads to increased cell proliferation and motility and increased tumor malignancy.

Identifiers

PMID19653896
PMCPMC2731785
OpenAlexW2133986912

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.