Evidence map›Paper›PMID 14711377›Full record

ReviewReproductive biology and endocrinology : RB&E2004

Changes in extracellular matrix (ECM) and ECM-associated proteins in the metastatic progression of prostate cancer.

Delisha A Stewart, Carlton R Cooper, Robert A Sikes

Abstract readReview
In one paragraph

Review in Reproductive biology and endocrinology : RB&E, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
–field-weighted citation impact
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

64 citing papers in PubMed.

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4 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

3 authors.

Delisha A StewartLaboratory for Cancer Ontogeny and Therapeutics, Department of Biological Sciences, University of Delaware, Newark, DE 19716, USA. dstewart@udel.edu
Carlton R Cooper
Robert A Sikes

Funding

EIHC and Prostate Cancer Adhesion to Bone EndotheliumK22CA097117 · NCI · UNIVERSITY OF DELAWARE · PI COOPER, CARLTON R. · 2002 to 2004
$471k
NCI NIH HHS 1K22CA97117-01NCI NIH HHS K22 CA097117NIDDK NIH HHS DK/ES59146
6 · The paper itself

Abstract

Prostate cancer (PCa) is no exception to the multi-step process of metastasis. As PCa progresses, changes occur within the microenvironments of both the malignant cells and their targeted site of metastasis, enabling the necessary responses that result in successful translocation. The majority of patients with progressing prostate cancers develop skeletal metastases. Despite advancing efforts in early detection and management, there remains no effective, long-term cure for metastatic PCa. Therefore, the elucidation of the mechanism of PCa metastasis and preferential establishment of lesions in bone is an intensive area of investigation that promises to generate new targets for therapeutic intervention. This review will survey what is currently know concerning PCa interaction with the extracellular matrix (ECM) and the roles of factors within the tumor and ECM microenvironments that contribute to metastasis. These will be discussed within the context of changes in expression and functional heterodimerization patterns of integrins, changes in ECM expression and reorganization by proteases facilitating invasion. In this context we also provide a brief summary of how growth factors (GFs), cytokines and regulatory signaling pathways favor PCa metastasis to bone.

Indexed as

AnimalsExtracellular MatrixExtracellular Matrix ProteinsHumansMaleNeoplasm ProteinsProstatic NeoplasmsExtracellular Matrix ProteinsNeoplasm Proteins

Identifiers

PMID14711377
PMCPMC320496

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.