Evidence map›Paper›PMID 24403051›Full record

ArticleHuman molecular genetics2014

Recurrent genomic alterations in sequential progressive leukoplakia and oral cancer: drivers of oral tumorigenesis?

Nilva K Cervigne, Jerry Machado, Rashmi S Goswami, Bekim Sadikovic, Grace Bradley, Bayardo Perez-Ordonez, Natalie Naranjo Galloni, Ralph Gilbert, Patrick Gullane, Jonathan C Irish and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Human molecular genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

26 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Wnt/β-Catenin Signaling in Oral Carcinogenesis.International journal of molecular sciences · 2020
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Cell death discovery · 2017
    Article
  19. Article
  20. [Precision stomatology: current status and challenges].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2015
    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

13 authors at 8 institutions in 5 countries.

Nilva K CervigneDivision of Applied Molecular Oncology, Ontario Cancer Institute.
Jerry Machado
Rashmi S Goswami
Bekim Sadikovic
Grace Bradley
Bayardo Perez-Ordonez
Natalie Naranjo Galloni
Ralph Gilbert
Patrick Gullane
Jonathan C Irish
Igor Jurisica
Patricia P Reis
Suzanne Kamel-Reid
Cancer Institute (WIA) · INPrincess Margaret Cancer Centre · CAUniversity of Toronto · CAMcMaster University · CAMolecular Oncology (United States) · USOntario Institute for Cancer Research · CAUniversidade Estadual de Campinas (UNICAMP) · BRVancouver General Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A significant proportion (up to 62%) of oral squamous cell carcinomas (OSCCs) may arise from oral potential malignant lesions (OPMLs), such as leukoplakia. Patient outcomes may thus be improved through detection of lesions at a risk for malignant transformation, by identifying and categorizing genetic changes in sequential, progressive OPMLs. We conducted array comparative genomic hybridization analysis of 25 sequential, progressive OPMLs and same-site OSCCs from five patients. Recurrent DNA copy number gains were identified on 1p in 20/25 cases (80%) with minimal, high-level amplification regions on 1p35 and 1p36. Other regions of gains were frequently observed: 11q13.4 (68%), 9q34.13 (64%), 21q22.3 (60%), 6p21 and 6q25 (56%) and 10q24, 19q13.2, 22q12, 5q31.2, 7p13, 10q24 and 14q22 (48%). DNA losses were observed in >20% of samples and mainly detected on 5q31.2 (35%), 16p13.2 (30%), 9q33.1 and 9q33.29 (25%) and 17q11.2, 3p26.2, 18q21.1, 4q34.1 and 8p23.2 (20%). Such copy number alterations (CNAs) were mapped in all grades of dysplasia that progressed, and their corresponding OSCCs, in 70% of patients, indicating that these CNAs may be associated with disease progression. Amplified genes mapping within recurrent CNAs (KHDRBS1, PARP1, RAB1A, HBEGF, PAIP2, BTBD7) were selected for validation, by quantitative real-time PCR, in an independent set of 32 progressive leukoplakia, 32 OSSCs and 21 non-progressive leukoplakia samples. Amplification of BTBD7, KHDRBS1, PARP1 and RAB1A was exclusively detected in progressive leukoplakia and corresponding OSCC. BTBD7, KHDRBS1, PARP1 and RAB1A may be associated with OSCC progression. Protein-protein interaction networks were created to identify possible pathways associated with OSCC progression.

Indexed as

AdultAgedAged, 80 and overBiomarkers, TumorCarcinogenesisCarcinoma, Squamous CellCluster AnalysisComparative Genomic HybridizationDNA Copy Number VariationsFemaleGenome, HumanHumansLeukoplakia, OralMaleMiddle AgedPrognosisBiomarkers, Tumor

Identifiers

PMID24403051
PMCPMC3990162
OpenAlexW2160237511

What OpenQuestion holds

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LicenceCC BY
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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.