Evidence map›Paper›PMID 27275004›Full record

ArticleNew horizons in translational medicine2016

Translational aspects in targeting the stromal tumour microenvironment: from bench to bedside.

R Bhome, H A Al Saihati, R W Goh, M D Bullock, J N Primrose, G J Thomas, A E Sayan, A H Mirnezami

Open access · hybridAbstract read
In one paragraph

Article in New horizons in translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

R BhomeCancer Sciences, Faculty of Medicine, University of Southampton, Somers Building, Southampton General Hospital, Tremona Road, Southampton, SO16 6YD UK.; University Surgery, South Academic Block, Southampton General Hospital, Tremona Road, Southampton, SO16 6YD UK.
H A Al SaihatiCancer Sciences, Faculty of Medicine, University of Southampton, Somers Building, Southampton General Hospital, Tremona Road, Southampton, SO16 6YD UK.
R W GohCancer Sciences, Faculty of Medicine, University of Southampton, Somers Building, Southampton General Hospital, Tremona Road, Southampton, SO16 6YD UK.; School of Medicine, University of Southampton, University Road, Southampton, SO17 1BJ UK.
M D BullockCancer Sciences, Faculty of Medicine, University of Southampton, Somers Building, Southampton General Hospital, Tremona Road, Southampton, SO16 6YD UK.; University Surgery, South Academic Block, Southampton General Hospital, Tremona Road, Southampton, SO16 6YD UK.
J N PrimroseUniversity Surgery, South Academic Block, Southampton General Hospital, Tremona Road, Southampton, SO16 6YD UK.
G J ThomasCancer Sciences, Faculty of Medicine, University of Southampton, Somers Building, Southampton General Hospital, Tremona Road, Southampton, SO16 6YD UK.
A E SayanCancer Sciences, Faculty of Medicine, University of Southampton, Somers Building, Southampton General Hospital, Tremona Road, Southampton, SO16 6YD UK.
A H MirnezamiCancer Sciences, Faculty of Medicine, University of Southampton, Somers Building, Southampton General Hospital, Tremona Road, Southampton, SO16 6YD UK.; University Surgery, South Academic Block, Southampton General Hospital, Tremona Road, Southampton, SO16 6YD UK.
Southampton General Hospital · GBUniversity of Southampton · GB

Funding

Cancer Research UK 20526Cancer Research UK A20526Medical Research Council MR/K000799/1
6 · The paper itself

Abstract

Solid tumours comprise, not only malignant cells but also a variety of stromal cells and extracellular matrix proteins. These components interact via an array of signalling pathways to create an adaptable network that may act to promote or suppress cancer progression. To date, the majority of anti-tumour chemotherapeutic agents have principally sought to target the cancer cell. Consequently, resistance develops because of clonal evolution, as a result of selection pressure during tumour expansion. The concept of activating or inhibiting other cell types within the tumour microenvironment is relatively novel and has the advantage of targeting cells which are genetically stable and less likely to develop resistance. This review outlines key players in the stromal tumour microenvironment and discusses potential targeting strategies that may offer therapeutic benefit.

Indexed as

cancerfibroblastmicroenvironmentmicroRNAprognosticstromaT celltherapeutictumour

Identifiers

PMID27275004
PMCPMC4888939
OpenAlexW2330831661

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.