Evidence map›Paper›PMID 26579471›Full record

ReviewActa pharmaceutica Sinica. B2015

Cancer metastases: challenges and opportunities.

Xiangming Guan

Open access · diamondAbstract readReview
In one paragraph

Review in Acta pharmaceutica Sinica. B, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 487 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
487citing papers in PubMed, 2 pooled it
23.6field-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

487 citing papers in PubMed, 2 syntheses or guidelines pooled it, 959 citations in OpenAlex.

  1. Pooled it
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  7. Review
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  11. Organoid technology in cancer research.Molecular biomedicine · 2026
    Review
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427 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

1 author at 1 institution in 1 country.

Xiangming GuanDepartment of Pharmaceutical Sciences, College of Pharmacy, South Dakota State University, Brookings, SD 57007, USA.
South Dakota State University · US

Funding

Thiol Specific Fluorogenic Agents for Laser Scanning Confocal MicroscopyR15GM093678 · NIGMS · SOUTH DAKOTA STATE UNIVERSITY · PI GUAN, XIANGMING · 2010 to 2010
$430k
Benzofurazan sulfide fluorogenic agents for live cell subcellular thiol imagingR15GM107197 · NIGMS · SOUTH DAKOTA STATE UNIVERSITY · PI GUAN, XIANGMING · 2014 to 2014
$328k
NIGMS NIH HHS R15 GM093678NIGMS NIH HHS R15 GM107197
6 · The paper itself

Abstract

Cancer metastasis is the major cause of cancer morbidity and mortality, and accounts for about 90% of cancer deaths. Although cancer survival rate has been significantly improved over the years, the improvement is primarily due to early diagnosis and cancer growth inhibition. Limited progress has been made in the treatment of cancer metastasis due to various factors. Current treatments for cancer metastasis are mainly chemotherapy and radiotherapy, though the new generation anti-cancer drugs (predominantly neutralizing antibodies for growth factors and small molecule kinase inhibitors) do have the effects on cancer metastasis in addition to their effects on cancer growth. Cancer metastasis begins with detachment of metastatic cells from the primary tumor, travel of the cells to different sites through blood/lymphatic vessels, settlement and growth of the cells at a distal site. During the process, metastatic cells go through detachment, migration, invasion and adhesion. These four essential, metastatic steps are inter-related and affected by multi-biochemical events and parameters. Additionally, it is known that tumor microenvironment (such as extracellular matrix structure, growth factors, chemokines, matrix metalloproteinases) plays a significant role in cancer metastasis. The biochemical events and parameters involved in the metastatic process and tumor microenvironment have been targeted or can be potential targets for metastasis prevention and inhibition. This review provides an overview of these metastasis essential steps, related biochemical factors, and targets for intervention.

Indexed as

AdhesionBM, basement membraneCAFs, cancer-associated fibroblastsCAMs, cell adhesion moleculesCancerCAT, collective amoeboid transitionCCL2, chemokine (C–C motif) ligand 2CCR3, chemokine receptor 3Col, collagenCOX2, cyclooxygenase 2CSF-1, chemokine colonystimulating factor–1CTGF, connective tissue growth factorCXCR2, chemokine receptor type 2DetachmentDISC, death-inducing signaling complexECM, extracellular matrixEGF, epidermal growth factorEGFR, EGF receptorEMT, epithelial–mesenchymal transitionFAK, focal adhesion kinaseFAs, focal adhesionsFGF, fibroblast growth factorFN, fibronectinHA, hyaluronanHGF, hepatocyte growth factorHIFs, hypoxia-inducible factorsIKK, IκB kinaseInvasionJAK, the Janus kinasesLN, lamininMAPK, mitogen-activated protein kinaseMAT, mesenchymal to amoeboid transitionMetastasisMET, mesenchymal–epithelial transitionMigrationMMPs, matrix metalloproteinasesPDGF, platelet-derived growth factorPI3K, phosphatidylinositol 3-kinaseSTATs, signal transducers and activators of transcriptionTAMs, tumor-associated macrophagesTGF-β, transforming growth factor βTME, tumor microenvironmentVCAMs, vascular cell adhesion moleculesVEGF, vascular endothelial growth factorVN, vitronectin

Identifiers

PMID26579471
PMCPMC4629446
OpenAlexW2209093312

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.