Evidence map›Paper›PMID 37499655›Full record

ArticleCell reports2023

FOXC2 promotes vasculogenic mimicry and resistance to anti-angiogenic therapy.

Ian G Cannell, Kirsty Sawicka, Isabella Pearsall, Sophia A Wild, Lauren Deighton, Sarah M Pearsall, Giulia Lerda, Fadwa Joud, Showkhin Khan, Alejandra Bruna and 9 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 50 citations in OpenAlex.

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  11. Unravelling theTheranostics · 2026
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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

19 authors at 5 institutions in 2 countries.

Ian G CannellCancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK; New York Genome Center, 101 Avenue of the Americas, New York, NY 10013, USA. Electronic address: Ian.Cannell@cruk.cam.ac.uk.
Kirsty SawickaCancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK; New York Genome Center, 101 Avenue of the Americas, New York, NY 10013, USA.
Isabella PearsallCancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK; New York Genome Center, 101 Avenue of the Americas, New York, NY 10013, USA.
Sophia A WildCancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK.
Lauren DeightonCancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK.
Sarah M PearsallCancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK; Cancer Research UK Cancer Biomarker Centre, Manchester M20 4BX, UK; CRUK Manchester Institute, Manchester M20 4BX, UK.
Giulia LerdaCancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK.
Fadwa JoudCancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK.
Showkhin KhanNew York Genome Center, 101 Avenue of the Americas, New York, NY 10013, USA.
Alejandra BrunaCancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK; Preclinical Modelling of Paediatric Cancer Evolution Team, The Institute of Cancer Research, Cotswold Road, Sutton, Surrey SM2 5N, UK.
Kathryn L SimpsonCancer Research UK Cancer Biomarker Centre, Manchester M20 4BX, UK; CRUK Manchester Institute, Manchester M20 4BX, UK.
Claire M MulveyCancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK.
Fiona NugentCancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK.
Fatime QosajCancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK.
Dario BressanCancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK.
CRUK IMAXT Grand Challenge TeamCRUK IMAXT Grand Challenge Team, Cambridge, UK.
Caroline DiveCancer Research UK Cancer Biomarker Centre, Manchester M20 4BX, UK; CRUK Manchester Institute, Manchester M20 4BX, UK.
Carlos CaldasCancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK; Department of Oncology and Breast Cancer Programme, CRUK Cambridge Centre, Cambridge University Hospitals NHS and University of Cambridge, Cambridge CB2 2QQ, UK.
Gregory J HannonCancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK; New York Genome Center, 101 Avenue of the Americas, New York, NY 10013, USA. Electronic address: Greg.Hannon@cruk.cam.ac.uk.
Cancer Research UK · GBUniversity of Cambridge · GBCancer Research UK Manchester Institute · GBCancer Research UK Cambridge Center · GBNew York Genome Center · US

Funding

Cancer Research UK 22582Cancer Research UK 29569Cancer Research UK A21143Cancer Research UK C9545/A24042Cancer Research UK CRI_CORE_LIMIC_2324Cancer Research UK CTRNBC-2022/100001Wellcome Trust 110161Wellcome Trust 110161/Z/15/Z
6 · The paper itself

Abstract

Vasculogenic mimicry (VM) describes the formation of pseudo blood vessels constructed of tumor cells that have acquired endothelial-like properties. VM channels endow the tumor with a tumor-derived vascular system that directly connects to host blood vessels, and their presence is generally associated with poor patient prognosis. Here we show that the transcription factor, Foxc2, promotes VM in diverse solid tumor types by driving ectopic expression of endothelial genes in tumor cells, a process that is stimulated by hypoxia. VM-proficient tumors are resistant to anti-angiogenic therapy, and suppression of Foxc2 augments response. This work establishes co-option of an embryonic endothelial transcription factor by tumor cells as a key mechanism driving VM proclivity and motivates the search for VM-inhibitory agents that could form the basis of combination therapies with anti-angiogenics.

Indexed as

ImmunotherapyNeovascularization, PathologicCell Line, TumorHumansanti-angiogenic therapyCP: Cancerepithelial-to-endothelial transistiontranscriptional reprogrammingtransdifferentiationtumor vasculature

Identifiers

PMID37499655
PMCPMC7617767
OpenAlexW4385281701

What OpenQuestion holds

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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.