Evidence map›Paper›PMID 29455663›Full record

ReviewMolecular cancer2018

Targeting tumour microenvironment by tyrosine kinase inhibitor.

Hor-Yue Tan, Ning Wang, Wing Lam, Wei Guo, Yibin Feng, Yung-Chi Cheng

Open access · goldAbstract readReview
In one paragraph

Review in Molecular cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 2 pooled it
5.5field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 2 syntheses or guidelines pooled it, 106 citations in OpenAlex.

  1. Pooled it
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  11. Sorafenib with or without co-interventions for hepatocellular carcinoma.The Cochrane database of systematic reviews · 2025
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7 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

6 authors at 2 institutions in 3 countries.

Hor-Yue TanSchool of Chinese Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, People's Republic of China.
Ning WangSchool of Chinese Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, People's Republic of China.
Wing LamDepartment of Pharmacology, Yale University School of Medicine, New Haven, CT, USA.
Wei GuoSchool of Chinese Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, People's Republic of China.
Yibin FengSchool of Chinese Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, People's Republic of China. yfeng@hku.hk.
Yung-Chi ChengDepartment of Pharmacology, Yale University School of Medicine, New Haven, CT, USA. yccheng@yale.edu.
Chinese University of Hong Kong · CNYale University · US

Funding

Clinical Study of PHY906, a Novel Chinese Herbal Medicine, as a Modulator of IrinP01CA154295 · NCI · YALE UNIVERSITY · PI CHENG, YUNG-CHI · 2011 to 2016
$6.4M
NCI NIH HHS P01 CA154295NCI NIH HHS PO1CA154295-01A1
6 · The paper itself

Abstract

Tumour microenvironment (TME) is a key determinant of tumour growth and metastasis. TME could be very different for each type and location of tumour and TME may change constantly during tumour growth. Multiple counterparts in surrounding microenvironment including mesenchymal-, hematopoietic-originated cells as well as non-cellular components affect TME. Thus, therapeutics that can disrupt the tumour-favouring microenvironment should be further explored for cancer therapy. Previous efforts in unravelling the dysregulated mechanisms of TME components has identified numerous protein tyrosine kinases, while its corresponding inhibitors have demonstrated potent modulatory effect on TME. Recent works have demonstrated that beyond the direct action on cancer cells, tyrosine kinase inhibitors (TKIs) have been implicated in inactivation or normalization of dysregulated TME components leading to cancer regression. Either through re-sensitizing the tumour cells or reversing the immunological tolerance microenvironment, the emergence of these TME modulatory mechanism of TKIs supports the combinatory use of TKIs with current chemotherapy or immunotherapy for cancer therapy. Therefore, an appropriate understanding on TME modulation by TKIs may offer another mode of action of TKIs for cancer treatment. This review highlights mode of kinase activation or paracrine ligand production from TME components and summarises the findings on the potential use of various TKIs on regulating TME components. At last, the combination use of current TKIs with immunotherapy in the perspectives of efficacy and safety are discussed.

Indexed as

AnimalsHumansImmunotherapyNeoplasmsProtein Kinase InhibitorsTumor MicroenvironmentProtein Kinase InhibitorsImmunotherapyTumour microenvironmentTyrosine kinase inhibitors

Identifiers

PMID29455663
PMCPMC5817793
OpenAlexW2794836336

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.