Evidence map›Paper›PMID 29100335›Full record

ArticleOncotarget2017

Breast cancer induced nociceptor aberrant growth and collateral sensory axonal branching.

Matt Austin, Laura Elliott, Niovi Nicolaou, Anna Grabowska, Richard P Hulse

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

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  15. Coordinated NADPH oxidase/hydrogen peroxide functions regulate cutaneous sensory axon de- and regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  16. Sympathetic and parasympathetic innervation in cancer: therapeutic implications.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2021
    Review
  17. Review
  18. Article
  19. Transient receptor potential cation channel subfamily V and breast cancer.Laboratory investigation; a journal of technical methods and pathology · 2020
    Review
  20. Article
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

5 authors at 1 institution in 1 country.

Matt AustinCancer Biology, School of Cancer and Stem Sciences, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
Laura ElliottCancer Biology, School of Cancer and Stem Sciences, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
Niovi NicolaouCancer Biology, School of Cancer and Stem Sciences, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
Anna GrabowskaCancer Biology, School of Cancer and Stem Sciences, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
Richard P HulseCancer Biology, School of Cancer and Stem Sciences, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
University of Nottingham · GB

Funding

National Centre for the Replacement, Refinement and Reduction of Animals in Research NC/L001861/1
6 · The paper itself

Abstract

The tumour and neuron interaction has a significant impact upon disease progression and the patients quality of life. In breast cancer patients, it is known that there is an interaction between the tumour microenvironment and the sensory neurons to influence the progression of cancer as well as pain, though these mechanisms still need to be clearly defined. Here it is demonstrated that in a rodent orthotopic model of breast cancer (MDA MB 231) there was an increase in nerve fibre innervation into the tumour microenvironment (protein gene product 9.5), which were calcitonin gene related peptide positive C fibre nociceptors. In contrast, there was a reduction in myelinated nerve fibres (NF200). A sensory neuronal cell line was cultured in response to conditioned media from MDA MB231 and MCF7 as well as vascular endothelial growth factor-A (VEGF-A). All these experimental conditions induced sensory neuronal growth, with increased formation of collateral axonal branches. Furthermore, it was demonstrated that MDA MB231 and VEGF-A induced sensory neuronal sensitisation in response to capsaicin a TRPV1 agonist. MDA MB231 induced neuronal growth was suppressed by VEGFR2 inhibition (ZM323881 and neutralising antibody DC101), in addition both MDA MB231 and VEGF-A induced neurite growth was attenuated by the inhibition of ARP2/3 complex through co-treatment with CK666. This demonstrates that breast cancer can interact with the sensory nervous system to drive neuritogenesis through a VEGF-A/VEGFR2/ARP2/3 mediated pathway.

Indexed as

breastcancerMDA MB231painVEGF-A

Identifiers

PMID29100335
PMCPMC5652729
OpenAlexW2752703457

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.