Evidence map›Paper›PMID 29651130›Full record

ReviewNature reviews. Clinical oncology2018

Targeting the tumour stroma to improve cancer therapy.

Kenneth C Valkenburg, Amber E de Groot, Kenneth J Pienta

Abstract readReview
In one paragraph

Review in Nature reviews. Clinical oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 637 papers.

0numbers the graph read from it
0cells of the map it votes in
637citing 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

637 citing papers in PubMed.

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  9. Epithelial-mesenchymal transition and cancer-associated fibroblasts in tumor progression and therapy resistance: mechanistic convergence and therapeutic opportunities.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
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577 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.

Kenneth C ValkenburgThe James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA. kvalken1@jhmi.edu.
Amber E de GrootThe James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Kenneth J PientaThe James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0002-4138-2186

Funding

Tumor microvesicle-mediated modulation of the bone microenvironmentP01CA093900 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KELLER, EVAN T · 2004 to 2024
$29.6M
TRANS_NETWORK PROJECTSU54CA143803 · NCI · PRINCETON UNIVERSITY · PI GETZENBERG, ROBERT H. · 2009 to 2013
$14.2M
Multidiciplinary Integrative Genomic Approach to Distinguish Lethal from Indolent Prostate Cancer in Men of Europena and African AncestryU01CA196390 · NCI · JOHNS HOPKINS UNIVERSITY · PI DE MARZO, ANGELO MICHAEL, PIENTA, KENNETH J. · 2015 to 2020
$5.8M
Mechanisms That Regulate Dormancy of Disseminated Tumor Cells in the Bone MarrowU54CA163124 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SHIOZAWA, YUSUKE · 2011 to 2015
$3.0M
Reactive Stroma and Tumor Associated Macrophages in Prostate Cancer ProgressionU01CA143055 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PIENTA, KENNETH J., ROWLEY, DAVID R · 2010 to 2014
$2.7M
Targeting SDF1/CXCR4 signaling to mobilize and kill circulating and disseminated prostate tumor cellsF32CA206394 · NCI · JOHNS HOPKINS UNIVERSITY · PI VALKENBURG, KENNETH C · 2016 to 2017
$112k
NCI NIH HHS F32 CA206394NCI NIH HHS P01 CA093900NCI NIH HHS U01 CA143055NCI NIH HHS U01 CA196390NCI NIH HHS U54 CA143803NCI NIH HHS U54 CA163124
6 · The paper itself

Abstract

Cancers are not composed merely of cancer cells alone; instead, they are complex 'ecosystems' comprising many different cell types and noncellular factors. The tumour stroma is a critical component of the tumour microenvironment, where it has crucial roles in tumour initiation, progression, and metastasis. Most anticancer therapies target cancer cells specifically, but the tumour stroma can promote the resistance of cancer cells to such therapies, eventually resulting in fatal disease. Therefore, novel treatment strategies should combine anticancer and antistromal agents. Herein, we provide an overview of the advances in understanding the complex cancer cell-tumour stroma interactions and discuss how this knowledge can result in more effective therapeutic strategies, which might ultimately improve patient outcomes.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsCell LineageHumansNeoplasmsStromal CellsTumor Microenvironment

Identifiers

PMID29651130
PMCPMC5960434

What OpenQuestion holds

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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.