ArticleInternational journal of cancer2009
Multiple pathways in the FGF signaling network are frequently deregulated by gene amplification in oral dysplasias.
Article in International journal of cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 4 of them syntheses that pooled it.
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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.
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Who cites it
30 citing papers in PubMed, 4 syntheses or guidelines pooled it, 63 citations in OpenAlex.
- The association between the TP53 Arg72Pro polymorphism and colorectal cancer: An updated meta-analysis based on 32 studies.Oncotarget · 2017Pooled it
- Association Between TP53 Gene Codon 72 Polymorphism and Acute Myeloid Leukemia Susceptibility: Evidence Based on a Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2015Pooled it
- The Role of TP53 Gene Codon 72 Polymorphism in Leukemia: A PRISMA-Compliant Systematic Review and Meta-Analysis.Medicine · 2015Pooled it
- Association between the TP53 codon 72 polymorphism and risk of oral squamous cell carcinoma in Asians: a meta-analysis.BMC cancer · 2014Pooled it
- Heterogeneous mechanisms, risk stratification, and translational advances in the malignant transformation of oral potentially malignant disorders to oral squamous cell carcinoma.Frontiers in molecular biosciences · 2026Review
- Escape from Cellular Senescence Is Associated with Chromosomal Instability in Oral Pre-Malignancy.Biology · 2023Review
- Article
- Recurrent copy number alterations involving EGFR, CDKN2A, and CCND1 in oral premalignant lesions.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2022Article
- MiR-148a inhibits oral squamous cell carcinoma progression through ERK/MAPK pathway via targeting IGF-IR.Bioscience reports · 2020Observational
- Functional Precision Medicine Identifies Novel Druggable Targets and Therapeutic Options in Head and Neck Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- Association Between Genetic Variant in the Promoter of Pri-miR-34b/c and Risk of Glioma.Frontiers in oncology · 2018Article
- Genomic characterization of tobacco/nut chewing HPV-negative early stage tongue tumors identify MMP10 asa candidate to predict metastases.Oral oncology · 2017Article
- Association between the rs1042522 polymorphism inChronic diseases and translational medicine · 2017Article
- Prognostic factors, predictive markers and cancer biology: the triad for successful oral cancer chemoprevention.Future oncology (London, England) · 2016Review
- Knocking down of p53 triggers apoptosis and autophagy, concomitantly with inhibition of migration on SSC-4 oral squamous carcinoma cells.Molecular and cellular biochemistry · 2016Article
- Downregulation of CRNN gene and genomic instability at 1q21.3 in oral squamous cell carcinoma.Clinical oral investigations · 2015Article
- Article
- Recurring DNA copy number gain at chromosome 9p13 plays a role in the activation of multiple candidate oncogenes in progressing oral premalignant lesions.Cancer medicine · 2014Article
- Targeting the epidermal growth factor receptor for head and neck cancer chemoprevention.Oral oncology · 2014Article
- Recurrent genomic alterations in sequential progressive leukoplakia and oral cancer: drivers of oral tumorigenesis?Human molecular genetics · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Genetic alteration in oral premalignant lesions (OPLs), the precursors of oral squamous cell carcinomas (OSCCs), may represent key changes in disease initiation and development. We ask if DNA amplification occurs at this early stage of cancer development and which oncogenic pathways are disrupted in OPLs. Here, we evaluated 50 high-grade dysplasias and low-grade dysplasias that later progressed to cancer for gene dosage aberrations using tiling-path DNA microarrays. Early occurrences of DNA amplification and homozygous deletion were frequently detected, with 40% (20/50) of these early lesions exhibiting such features. Expression for 88 genes in 7 recurrent amplicons were evaluated in 5 independent head and neck cancer datasets, with 40 candidates found to be overexpressed relative to normal tissues. These genes were significantly enriched in the canonical ERK/MAPK, FGF, p53, PTEN and PI3K/AKT signaling pathways (p = 8.95 x 10(-3) to 3.18 x 10(-2)). These identified pathways share interactions in one signaling network, and amplification-mediated deregulation of this network was found in 30.0% of these preinvasive lesions. No such alterations were found in 14 low-grade dysplasias that did not progress, whereas 43.5% (10/23) of OSCCs were found to have altered genes within the pathways with DNA amplification. Multitarget FISH showed that amplification of EGFR and CCND1 can coexist in single cells of an oral dysplasia, suggesting the dependence on multiple oncogenes for OPL progression. Taken together, these findings identify a critical biological network that is frequently disrupted in high-risk OPLs, with different specific genes disrupted in different individuals.
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Registered trials
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.