Evidence map›Paper›PMID 31427592›Full record

ArticleScientific reports2019

Analysis of head and neck carcinoma progression reveals novel and relevant stage-specific changes associated with immortalisation and malignancy.

Ratna Veeramachaneni, Thomas Walker, Timothée Revil, Antoine De Weck, Dunarel Badescu, James O'Sullivan, Catherine Higgins, Louise Elliott, Triantafillos Liloglou, Janet M Risk and 10 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

30 citing papers in PubMed, 47 citations in OpenAlex.

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  19. The role of KMT2 gene in human tumors.Histology and histopathology · 2022
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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

20 authors at 9 institutions in 3 countries.

Ratna VeeramachaneniFaculty of Biology, Medicine and Health, University of Manchester, Manchester, M13 9PL, UK.
Thomas WalkerFaculty of Biology, Medicine and Health, University of Manchester, Manchester, M13 9PL, UK.ORCID http://orcid.org/0000-0003-4607-7321
Timothée RevilMcGill University and Genome Quebec Innovation Centre, McGill University, Montreal, Quebec, H3A 0G1, Canada.ORCID http://orcid.org/0000-0003-1210-7748
Antoine De WeckWellcome Trust Centre for Human Genetics, University of Oxford, Oxford, OX3 7BN, UK.
Dunarel BadescuMcGill University and Genome Quebec Innovation Centre, McGill University, Montreal, Quebec, H3A 0G1, Canada.
James O'SullivanFaculty of Biology, Medicine and Health, University of Manchester, Manchester, M13 9PL, UK.
Catherine HigginsDepartment of Cellular Pathology, Manchester University NHS Foundation Trust, Manchester, M13 9WL, UK.
Louise ElliottDepartment of Cellular Pathology, Manchester University NHS Foundation Trust, Manchester, M13 9WL, UK.
Triantafillos LiloglouDepartment of Molecular and Clinical Cancer Medicine, Institute of Translational Medicine, University of Liverpool, Liverpool, L69 3BX, UK.ORCID http://orcid.org/0000-0003-0460-1404
Janet M RiskDepartment of Molecular and Clinical Cancer Medicine, Institute of Translational Medicine, University of Liverpool, Liverpool, L69 3BX, UK.ORCID http://orcid.org/0000-0002-8770-7783
Richard ShawDepartment of Molecular and Clinical Cancer Medicine, Institute of Translational Medicine, University of Liverpool, Liverpool, L69 3BX, UK.
Lynne HampsonFaculty of Biology, Medicine and Health, University of Manchester, Manchester, M13 9PL, UK.
Ian HampsonFaculty of Biology, Medicine and Health, University of Manchester, Manchester, M13 9PL, UK.
Simon DeardenPrecision Medicine and Genomics, IMED Biotech Unit, Astra Zeneca, Cambridge, CB4 OFZ, UK.
Robert WoodwardsDepartment of Oral and Maxillofacial Surgery, Pennine Acute NHS Trust, Manchester, M8 5RB, UK.
Stephen PrimeCentre for Immunology and Regenerative Medicine, Institute of Dentistry, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, E1 4NS, UK.
Keith HunterSchool of Clinical Dentistry, University of Sheffield, Sheffield, S10 2TA, UK.
Eric Kenneth ParkinsonCentre for Immunology and Regenerative Medicine, Institute of Dentistry, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, E1 4NS, UK.
Jiannis RagoussisMcGill University and Genome Quebec Innovation Centre, McGill University, Montreal, Quebec, H3A 0G1, Canada.
Nalin ThakkerFaculty of Biology, Medicine and Health, University of Manchester, Manchester, M13 9PL, UK. nthakker@manchester.ac.uk.ORCID http://orcid.org/0000-0002-8664-1508
University of Manchester · GBMcGill University and Génome Québec Innovation Centre · CAUniversity of Liverpool · GBManchester University NHS Foundation Trust · GBQueen Mary University of London · GBAstraZeneca (United Kingdom) · GBNovartis (Switzerland) · CHPennine Acute Hospitals NHS Trust · GBUniversity of Sheffield · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We report changes in the genomic landscape in the development of head and neck squamous cell carcinomas HNSCC from potentially premalignant lesions (PPOLS) to malignancy and lymph node metastases. Likely pathological mutations predominantly involved a relatively small set of genes reported previously (TP53, KMT2D, CDKN2A, PIK3CA, NOTCH1 and FAT1) but also other predicted cancer drivers (MGA, PABPC3, NR4A2, NCOR1 and MACF1). Notably, all these mutations arise early and are present in PPOLs. The most frequent genetic changes, which follow acquisition of immortality and loss of senescence, are of consistent somatic copy number alterations (SCNAs) involving chromosomal regions enriched for genes in known and previously unreported cancer-related pathways. We mapped the evolution of SCNAs in HNSCC progression. One of the earliest SCNAs involved deletions of CSMD1 (8p23.2). CSMD1 deletions or promoter hypermethylation were present in all of the immortal PPOLs and occurred at high frequency in the immortal HNSCC cell lines. Modulation of CSMD1 in cell lines revealed significant suppression of proliferation and invasion by forced expression, and significant stimulation of invasion by knockdown of expression. Known cancer drivers NOTCH1, PPP6C, RAC1, EIF4G1, PIK3CA showed significant increase in frequency of SCNA in transition from PPOLs to HNSCC that correlated with their expression. In the later stages of progression, HNSCC with and without nodal metastases showed some clear differences including high copy number gains of CCND1, hsa-miR-548k and TP63 in the metastases group.

Indexed as

Cell Transformation, NeoplasticBiomarkersCellular SenescenceChromosome MappingComputational BiologyDisease ProgressionDisease SusceptibilityDNA Copy Number VariationsGene Expression ProfilingGenomic InstabilityHead and Neck NeoplasmsHumansKeratinocytesMutationNeoplasm StagingSquamous Cell Carcinoma of Head and NeckBiomarkers

Identifiers

PMID31427592
PMCPMC6700135
OpenAlexW2968646153

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.