Immortalization of epithelial cells in oral carcinogenesis as revealed by genome‐wide array comparative genomic hybridization: A meta‐analysis

Vincent‐Chong, Vui King; Salahshourifar, Iman; Razali, Rozaimi Mohamad; Anwar, Arif; Zain, Rosnah Binti

doi:10.1002/hed.24102

Cited by 6 publications

(19 citation statements)

References 78 publications

(101 reference statements)

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“…A customized array CGH platform was designed for OSCC based on our previous research [11, 23] and previously reported candidate regions/genes for OSCC. This customized oligonucleotide array CGH (8x60k) was manufactured by Agilent Technologies, CA, USA.…”

Section: Methodsmentioning

confidence: 99%

Genome wide profiling in oral squamous cell carcinoma identifies a four genetic marker signature of prognostic significance

et al. 2017

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BackgroundCancers of the oral cavity are primarily oral squamous cell carcinomas (OSCCs). Many of the OSCCs present at late stages with an exceptionally poor prognosis. A probable limitation in management of patients with OSCC lies in the insufficient knowledge pertaining to the linkage between copy number alterations in OSCC and oral tumourigenesis thereby resulting in an inability to deliver targeted therapy.ObjectivesThe current study aimed to identify copy number alterations (CNAs) in OSCC using array comparative genomic hybridization (array CGH) and to correlate the CNAs with clinico-pathologic parameters and clinical outcomes.Materials and methodsUsing array CGH, genome-wide profiling was performed on 75 OSCCs. Selected genes that were harboured in the frequently amplified and deleted regions were validated using quantitative polymerase chain reaction (qPCR). Thereafter, pathway and network functional analysis were carried out using Ingenuity Pathway Analysis (IPA) software.ResultsMultiple chromosomal regions including 3q, 5p, 7p, 8q, 9p, 10p, 11q were frequently amplified, while 3p and 8p chromosomal regions were frequently deleted. These findings were in confirmation with our previous study using ultra-dense array CGH. In addition, amplification of 8q, 11q, 7p and 9p and deletion of 8p chromosomal regions showed a significant correlation with clinico-pathologic parameters such as the size of the tumour, metastatic lymph nodes and pathological staging. Co-amplification of 7p, 8q, 9p and 11q regions that harbored amplified genes namely CCND1, EGFR, TPM2 and LRP12 respectively, when combined, continues to be an independent prognostic factor in OSCC.ConclusionAmplification of 3q, 5p, 7p, 8q, 9p, 10p, 11q and deletion of 3p and 8p chromosomal regions were recurrent among OSCC patients. Co-alteration of 7p, 8q, 9p and 11q was found to be associated with clinico-pathologic parameters and poor survival. These regions contain genes that play critical roles in tumourigenesis pathways.

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Section: Methodsmentioning

confidence: 99%

Genome wide profiling in oral squamous cell carcinoma identifies a four genetic marker signature of prognostic significance

et al. 2017

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“…PGG family 1149 had significant terms related to neurogeneration (Figure 7A). Pseudogene AL356458.1 is contained in PGG family 1149 and has copy number variations in oral carcinogenesis 39 . Pseudogene TNPO1P2 is also in PGG family 1149 and has implications in neurodegeneration in the frontotemporal lobe 40 .…”

Section: Resultsmentioning

confidence: 99%

Network analysis of pseudogene-gene relationships: from pseudogene evolution to their functional potentials

Johnson¹,

Kho

et al. 2017

Biocomputing 2018

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Pseudogenes are fossil relatives of genes. Pseudogenes have long been thought of as "junk DNAs", since they do not code proteins in normal tissues. Although most of the human pseudogenes do not have noticeable functions, ~20% of them exhibit transcriptional activity. There has been evidence showing that some pseudogenes adopted functions as lncRNAs and work as regulators of gene expression. Furthermore, pseudogenes can even be "reactivated" in some conditions, such as cancer initiation. Some pseudogenes are transcribed in specific cancer types, and some are even translated into proteins as observed in several cancer cell lines. All the above have shown that pseudogenes could have functional roles or potentials in the genome. Evaluating the relationships between pseudogenes and their gene counterparts could help us reveal the evolutionary path of pseudogenes and associate pseudogenes with functional potentials. It also provides an insight into the regulatory networks involving pseudogenes with transcriptional and even translational activities.In this study, we develop a novel approach integrating graph analysis, sequence alignment and functional analysis to evaluate pseudogene-gene relationships, and apply it to human gene homologs and pseudogenes. We generated a comprehensive set of 445 pseudogene-gene (PGG) families from the original 3,281 gene families (13.56%). Of these 438 (98.4% PGG, 13.3% total) were non-trivial (containing more than one pseudogene). Each PGG family contains multiple genes and pseudogenes with high sequence similarity. For each family, we generate a sequence alignment network and phylogenetic trees recapitulating the evolutionary paths. We find evidence supporting the evolution history of olfactory family (both genes and pseudogenes) in human, which also supports the validity of our analysis method. Next, we evaluate these networks in respect to the gene ontology from which we identify functions enriched in these pseudogene-gene families and infer functional impact of pseudogenes involved in the networks. This demonstrates the application of our PGG network database in the study of pseudogene function in disease context.

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“…), oral squamous cell carcinoma, epilepsy (?) 31 , 74 , 75 , 85 , 96 EEF1A1P13 70 , 97 , 98 EEF1A1 pseudogene 13 5 5p15.2 1747 – EEF1A1P14 70 , 99 EEF1A1 pseudogene 14 1 1q31.3 1666 Liver cancer (? ), rectum cancer (?…”

Section: Methodsmentioning

confidence: 99%

“…), oral squamous cell carcinoma, breast cancer (?) 74 , 100 EEF1A1P15 70 EEF1A1 pseudogene 15 X Xq21.33 1689 – EEF1A1P16 EEF1A1 pseudogene 16 12 12p12.3 1635 Gastric cancer, Glioma (?) 101 , 102 EEF1A1P17 EEF1A1 pseudogene 17 12 12q12 1413 – EEF1A1P18 EEF1A1 pseudogene 18 11 11q13.1 467 – EEF1A1P19 103 EEF1A1 pseudogene 19 5 5p12 1645 Hepatocellular carcinoma (?)…”

Section: Methodsmentioning

confidence: 99%

“…31 EEF1A1P20 EEF1A1 pseudogene 20 5 5q21.1 1644 Nonalcoholic fatty liver disease (?) 104 EEF1A1P21 EEF1A1 pseudogene 21 4 4p15.1 1339 Oral squamous cell carcinoma 74 EEF1A1P22 99 EEF1A1 pseudogene 22 15 15q21.3 1639 Multiple myeloma (?) 85 EEF1A1P23 EEF1A1 pseudogene 23 Transcribed processed pseudogene 3 3q29 658 – EEF1A1P24 EEF1A1 pseudogene 24 Processed pseudogene 3 3p22.1 1638 Acute lymphoblastic leukemia (?)…”

Section: Methodsmentioning

confidence: 99%

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The pseudogenes of eukaryotic translation elongation factors (EEFs): Role in cancer and other human diseases

Cristiano¹

2022

Genes & Diseases

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Immortalization of epithelial cells in oral carcinogenesis as revealed by genome‐wide array comparative genomic hybridization: A meta‐analysis

Abstract: This study has identified multiple recurrent CNAs that are involved in various biological annotations associated with oral carcinogenesis. © 2015 Wiley Periodicals, Inc. Head Neck 38: E783-E797, 2016.

Cited by 6 publications

References 78 publications

Genome wide profiling in oral squamous cell carcinoma identifies a four genetic marker signature of prognostic significance

Genome wide profiling in oral squamous cell carcinoma identifies a four genetic marker signature of prognostic significance

Network analysis of pseudogene-gene relationships: from pseudogene evolution to their functional potentials

The pseudogenes of eukaryotic translation elongation factors (EEFs): Role in cancer and other human diseases

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