Evidence map›Paper›PMID 36452176›Full record

ArticleMatrix biology plus2022

Modelling stromal compartments to recapitulate the ameloblastoma tumour microenvironment.

Deniz Bakkalci, Amir Zaki Abdullah Zubir, Syed Ali Khurram, Judith Pape, Kristiina Heikinheimo, Stefano Fedele, Umber Cheema

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Matrix biology plus, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. 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

7 authors.

Deniz BakkalciUCL Centre for 3D Models of Health and Disease, Division of Surgery and Interventional Science, University College London, Charles Bell House, 43-45 Foley Street, W1W 7TS London, UK.
Amir Zaki Abdullah ZubirUnit of Oral and Maxillofacial Pathology, School of Clinical Dentistry, University of Sheffield, 19 Claremont Crescent, S10 2TA Sheffield, UK.
Syed Ali KhurramUnit of Oral and Maxillofacial Pathology, School of Clinical Dentistry, University of Sheffield, 19 Claremont Crescent, S10 2TA Sheffield, UK.
Judith PapeUCL Centre for 3D Models of Health and Disease, Division of Surgery and Interventional Science, University College London, Charles Bell House, 43-45 Foley Street, W1W 7TS London, UK.
Kristiina HeikinheimoDepartment of Oral and Maxillofacial Surgery, Institute of Dentistry, University of Turku and Turku University Hospital, Turku, Finland.
Stefano FedeleEastman Dental Institute, University College London, London, UK.
Umber CheemaUCL Centre for 3D Models of Health and Disease, Division of Surgery and Interventional Science, University College London, Charles Bell House, 43-45 Foley Street, W1W 7TS London, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumour development and progression is dependent upon tumour cell interaction with the tissue stroma. Bioengineering the tumour-stroma microenvironment (TME) into 3D biomimetic models is crucial to gain insight into tumour cell development and progression pathways and identify therapeutic targets. Ameloblastoma is a benign but locally aggressive epithelial odontogenic neoplasm that mainly occurs in the jawbone and can cause significant morbidity and sometimes death. The molecular mechanisms for ameloblastoma progression are poorly understood. A spatial model recapitulating the tumour and stroma was engineered to show that without a relevant stromal population, tumour invasion is quantitatively decreased. Where a relevant stroma was engineered in dense collagen populated by gingival fibroblasts, enhanced receptor activator of nuclear factor kappa-B ligand (RANKL) expression was observed and histopathological properties, including ameloblastoma tumour islands, developed and were quantified. Using human osteoblasts (bone stroma) further enhanced the biomimicry of ameloblastoma histopathological phenotypes. This work demonstrates the importance of the two key stromal populations, osteoblasts, and gingival fibroblasts, for accurate 3D biomimetic ameloblastoma modelling.

Indexed as

3D modelsAM, AmeloblastomaBPE, Bovine pituitary extractBSA, Bovine serum albuminCCN, Cellular communication network factor 2dl-CGH, Double-layered collagen gel hemisphereDMEM, Dulbecco’s modified Eagle mediumECM, Extracellular matrixFBS, Foetal bovine serumFibroblastsH&E, Haematoxylin and eosinHFF-2, Human fibroblasts (HFF-2)HGF, Primary gingival fibroblastshOB, Human osteoblastsIF, ImmunofluorescenceIHCIHC, ImmunohistochemistryMEM, Minimal Essential MediumMin, MinutesMIQE, Minimum Information for Publication of Quantitative Real-Time PCR ExperimentsM, MolarMMPs, Matrix metalloproteinasesMRC5, Human lung fibroblastsN.A, Neutralising agentPTHLH, Parathyroid Hormone Like HormoneRANKLRANKL, The tumour necrosis factor (TNF) superfamily members receptor activator of nuclear factor kappa-B ligand (TNFSF11)RANK, The tumour necrosis factor (TNF) superfamily members receptor activator of nuclear factor kappa-B receptorRT, Room temperatureSD, Standard deviationSEM, Standard error meanSPARC, anti-osteonectinTGF-β, Transforming growth factorTME, Tumour microenvironmentTNF, Tumour necrosis factorTumour microenvironmentα-SMA, alpha-smooth muscle actin

Identifiers

PMID36452176
PMCPMC9703037

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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.