Evidence map›Paper›PMID 37626054›Full record

ArticleNature communications2023

Driver gene combinations dictate cutaneous squamous cell carcinoma disease continuum progression.

Peter Bailey, Rachel A Ridgway, Patrizia Cammareri, Mairi Treanor-Taylor, Ulla-Maja Bailey, Christina Schoenherr, Max Bone, Daniel Schreyer, Karin Purdie, Jason Thomson and 13 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
8.4field-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

39 citing papers in PubMed, 39 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

23 authors at 10 institutions in 4 countries.

Peter BaileySchool of Cancer Sciences, University of Glasgow, Glasgow, G61 1QH, UK. Peter.Bailey.2@glasgow.ac.uk.ORCID http://orcid.org/0000-0002-0857-2041
Rachel A RidgwayCancer Research UK Beatson Institute, Glasgow, G61 1BD, UK.ORCID http://orcid.org/0000-0003-0198-8244
Patrizia CammareriCancer Research UK Beatson Institute, Glasgow, G61 1BD, UK.
Mairi Treanor-TaylorCancer Research UK Beatson Institute, Glasgow, G61 1BD, UK.ORCID http://orcid.org/0000-0002-8908-3900
Ulla-Maja BaileyCancer Research UK Beatson Institute, Glasgow, G61 1BD, UK.ORCID http://orcid.org/0000-0003-3641-9252
Christina SchoenherrCancer Research UK Beatson Institute, Glasgow, G61 1BD, UK.ORCID http://orcid.org/0000-0002-0983-6168
Max BoneSchool of Cancer Sciences, University of Glasgow, Glasgow, G61 1QH, UK.ORCID http://orcid.org/0000-0001-8589-3343
Daniel SchreyerSchool of Cancer Sciences, University of Glasgow, Glasgow, G61 1QH, UK.ORCID http://orcid.org/0000-0002-9788-0168
Karin PurdieFaculty of Medicine and Dentistry, Queen Mary University of London, London, E1 1BB, UK.
Jason ThomsonFaculty of Medicine and Dentistry, Queen Mary University of London, London, E1 1BB, UK.
William RickabySt John's Institute of Dermatology, St Thomas's Hospital, London, SE1 7EP, UK.
Rene JackstadtCancer Research UK Beatson Institute, Glasgow, G61 1BD, UK.
Andrew D CampbellCancer Research UK Beatson Institute, Glasgow, G61 1BD, UK.ORCID http://orcid.org/0000-0003-3930-1276
Emmanouil Dimonitsas1st Department of Dermatology and Venereology, Andreas Sygros Hospital, Medical School, National and Kapodistrian University of Athens, Athens, 16121, Greece.
Alexander J Stratigos1st Department of Dermatology and Venereology, Andreas Sygros Hospital, Medical School, National and Kapodistrian University of Athens, Athens, 16121, Greece.
Sarah T ArronDepartment of Dermatology, University of of California at San Francisco, San Francisco, CA, USA.ORCID http://orcid.org/0000-0001-5669-0627
Jun WangFaculty of Medicine and Dentistry, Queen Mary University of London, London, E1 1BB, UK.ORCID http://orcid.org/0000-0003-2509-9599
Karen BlythSchool of Cancer Sciences, University of Glasgow, Glasgow, G61 1QH, UK.ORCID http://orcid.org/0000-0002-9304-439X
Charlotte M ProbyMolecular and Clinical Medicine, School of Medicine, University of Dundee, Dundee, DD1 4HN, UK.ORCID http://orcid.org/0000-0002-3292-4836
Catherine A HarwoodFaculty of Medicine and Dentistry, Queen Mary University of London, London, E1 1BB, UK.
Owen J SansomSchool of Cancer Sciences, University of Glasgow, Glasgow, G61 1QH, UK.ORCID http://orcid.org/0000-0001-9540-3010
Irene M LeighFaculty of Medicine and Dentistry, Queen Mary University of London, London, E1 1BB, UK. i.m.leigh@qmul.ac.uk.ORCID http://orcid.org/0000-0001-8536-6439
Gareth J InmanSchool of Cancer Sciences, University of Glasgow, Glasgow, G61 1QH, UK. Gareth.Inman@glasgow.ac.uk.ORCID http://orcid.org/0000-0002-6264-4253
Cancer Research UK Scotland Institute · GBQueen Mary University of London · GBNational and Kapodistrian University of Athens · GREdinburgh Cancer Research · GBGerman Cancer Research Center · DEHeidelberg University · DESt Thomas' Hospital · GBUniversity of California, San Francisco · USUniversity of Dundee · GBUniversity of Glasgow · GB

Funding

Cancer Research UK 29799Cancer Research UK 29802Medical Research Council MR/T001720/1
6 · The paper itself

Abstract

The molecular basis of disease progression from UV-induced precancerous actinic keratosis (AK) to malignant invasive cutaneous squamous cell carcinoma (cSCC) and potentially lethal metastatic disease remains unclear. DNA sequencing studies have revealed a massive mutational burden but have yet to illuminate mechanisms of disease progression. Here we perform RNAseq transcriptomic profiling of 110 patient samples representing normal sun-exposed skin, AK, primary and metastatic cSCC and reveal a disease continuum from a differentiated to a progenitor-like state. This is accompanied by the orchestrated suppression of master regulators of epidermal differentiation, dynamic modulation of the epidermal differentiation complex, remodelling of the immune landscape and an increase in the preponderance of tumour specific keratinocytes. Comparative systems analysis of human cSCC coupled with the generation of genetically engineered murine models reveal that combinatorial sequential inactivation of the tumour suppressor genes Tgfbr2, Trp53, and Notch1 coupled with activation of Ras signalling progressively drives cSCC progression along a differentiated to progenitor axis. Taken together we provide a comprehensive map of the cSCC disease continuum and reveal potentially actionable events that promote and accompany disease progression.

Indexed as

Carcinoma, Squamous CellKeratosis, ActinicSkin NeoplasmsAnimalsCell DifferentiationDisease ProgressionGene Expression ProfilingHumansMice

Identifiers

PMID37626054
PMCPMC10457401
OpenAlexW4386156867

What OpenQuestion holds

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Registered trials

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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.