Affymetrix SNP array data for oral squamous cell carcinoma
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ABSTRACT: In order to identify biomarkers that contribute to genetic causes of OSCC, we attempt to identify copy number variation regions (CNV) in patients with OSCC. We identified and confirmed the clinical significance of amplification regions scattered from 8q22.2 to 8q24.3.
Project description:In order to identify biomarkers that contribute to genetic causes of OSCC, we attempt to identify copy number variation regions (CNV) in patients with OSCC. We identified and confirmed the clinical significance of amplification regions scattered from 8q22.2 to 8q24.3. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from normal oral tissues and OSCC specimens. Copy number analysis of Affymetrix SNP 6.0 arrays was performed for 112 OSCC specimens and 10 non-cancerous samples.
Project description:The development of oral squamous cell carcinoma (OSCC) is a multistep process requiring the accumulation of genetic alterations. Oral carcinogenesis is a multifactorial process involving numerous genetic changes that affect the activity of oncogenes, tumor suppressor genes and other classes of disease-related genes.Therefore, to identify the responsive genes for progression of oral dysplasia or OSCC, we here performed CGH analysis to DNA from oral dysplasia and OSCC by microdissection
Project description:The development of oral squamous cell carcinoma (OSCC) is a multistep process requiring the accumulation of genetic alterations. To identify genes responsible for OSCC development, we performed high-density single-nucleotide polymorphism array analysis and genome-wide gene expression profiling on OSCC tumors. These analyses identified "absent in melanoma (AIM2)" and "interferon-inducible gene 16 (IFI16)," mapped to the hematopoietic IFN-inducible nuclear proteins with 200-amino acid repeat (HIN-200) gene cluster in the amplified region of chromosome 1q23, with overexpression in OSCCs. AIM2 and IFI16 are cytoplasmic double-stranded DNA sensors for innate immunity and act as tumor suppressors in several human cancers. Knockdown of AIM2 or IFI16 in OSCC cells resulted in the suppression of cell growth and the induction of apoptosis, accompanied by the downregulation of NF-κB activation. Because all of the OSCC cell lines had impairment of p53 activity, wild-type p53 was introduced in p53-deficient OSCC cells, and as a result, the expression of wild-type p53 suppressed cell growth and induced apoptosis via suppression of NF-κB activity. Finally, the coexpression of AIM2 and IFI16 significantly enhanced cell growth in p53-deficient cells; in contrast, the expression of AIM2 and/or IFI16 in cells bearing wild-type p53 suppressed cell growth. Moreover, AIM2 and IFI16 synergistically enhanced NF-κB signaling in p53-deficient cells. Thus, expression of AIM2 and IFI16 may have oncogenic functions in OSCC cells inactivating p53 system.
Project description:The development of oral squamous cell carcinoma (OSCC) is a multistep process requiring the accumulation of genetic alterations. To identify genes responsible for OSCC development, we performed high-density single-nucleotide polymorphism array analysis and genome-wide gene expression profiling on OSCC tumors. These analyses identified "absent in melanoma (AIM2)" and "interferon-inducible gene 16 (IFI16)," mapped to the hematopoietic IFN-inducible nuclear proteins with 200-amino acid repeat (HIN-200) gene cluster in the amplified region of chromosome 1q23, with overexpression in OSCCs. AIM2 and IFI16 are cytoplasmic double-stranded DNA sensors for innate immunity and act as tumor suppressors in several human cancers. Knockdown of AIM2 or IFI16 in OSCC cells resulted in the suppression of cell growth and the induction of apoptosis, accompanied by the downregulation of NF-κB activation. Because all of the OSCC cell lines had impairment of p53 activity, wild-type p53 was introduced in p53-deficient OSCC cells, and as a result, the expression of wild-type p53 suppressed cell growth and induced apoptosis via suppression of NF-κB activity. Finally, the coexpression of AIM2 and IFI16 significantly enhanced cell growth in p53-deficient cells; in contrast, the expression of AIM2 and/or IFI16 in cells bearing wild-type p53 suppressed cell growth. Moreover, AIM2 and IFI16 synergistically enhanced NF-κB signaling in p53-deficient cells. Thus, expression of AIM2 and IFI16 may have oncogenic functions in OSCC cells inactivating p53 system. Copy number analysis of Affymetrix 250K SNP arrays was performed for 5 oral leukoplakia samples, 20 oral squamous cell carcinoma samples, and 8 oral squamous cell carcinoma cell lines.
Project description:The development of oral squamous cell carcinoma (OSCC) is a multistep process requiring the accumulation of genetic alterations. Oral carcinogenesis is a multifactorial process involving numerous genetic changes that affect the activity of oncogenes, tumor suppressor genes and other classes of disease-related genes.Therefore, to identify the responsive genes for progression of oral dysplasia or OSCC, we here performed CGH analysis to DNA from oral dysplasia and OSCC by microdissection Copy number analysis of Affymetrix 250K SNP arrays was performed for 8 oral dysplasia samples, 8 oral squamous cell carcinoma samples, using microdissection
Project description:In an attempt to further elucidate the pathomechanisms in oral squamous cell carcinoma (OSCC), gene expression profiling to a set of 35 primary OSCCs compared to 6 oral mucosa from healthy non-tumor patients was performed. Keywords: expression profiling
Project description:Over last decade several studies on oral cancer patients from eastern India have identified alterations in copy numbers in many regions of the chromosome such as 3p21.3, 8q24.21, 9p21, 9p22, 11q13, 11q21-24. However, all these studies employed microsatellite markers to map these CNV regions. This resulted in large map intervals (10-12 megabases) between the adjacent markers studied. As these regions contain a large number of genes, a high resolution CNV map of these regions was necessary to precisely identify novel genes affected by the amplifications and deletions. We thus used custom made Agilent 4X44K oligonucleotide array CGH platform to map the identified CNV regions in a resolution of 3 Kb in oral cancer patients from eastern India.
Project description:Over last decade several studies on oral cancer patients from eastern India have identified alterations in copy numbers in many regions of the chromosome such as 3p21.3, 8q24.21, 9p21, 9p22, 11q13, 11q21-24. However, all these studies employed microsatellite markers to map these CNV regions. This resulted in large map intervals (10-12 megabases) between the adjacent markers studied. As these regions contain a large number of genes, a high resolution CNV map of these regions was necessary to precisely identify novel genes affected by the amplifications and deletions. We thus used custom made Agilent 4X44K oligonucleotide array CGH platform to map the identified CNV regions in a resolution of 3 Kb in oral cancer patients from eastern India. Twenty-nine defined genomic intervals of ten male and two female oral cancer patients were compared with a normal male and normal female sample, respectively, by Agilent's custom oligo CGH array of 4X44K format.
Project description:In an attempt to further elucidate the pathomechanisms in oral squamous cell carcinoma (OSCC), gene expression profiling to a set of 35 primary OSCCs compared to 6 oral mucosa from healthy non-tumor patients was performed. Keywords: expression profiling Gene expression profiling using a whole-transcriptome chip that contains 35,035 gene-specific 70mere oligonucleotides (Human Oligoset 4.0; Operon) to a set of 35 primary OSCCs and 6 mucosa of healthy non-tumor patients.
Project description:In order to aid the development of patient-tailored diagnostics and therapeutics, we attempted to identify a genetic signature associated with disease prognosis in OSCC. A genome-wide analysis of transcription with the Affymetrix GeneChip Human Gene 1.0 ST Array was conducted. In this dataset, we include the expression data obtained from 57 specimens from patients with OSCC and 22 oral tissues from normal persons. 79 samples were analyzed. We compared gene expression levels between patients with and without OSCC. In addition, among 57 patients with OSCC, we also compared the expression levels between patients with and without amplicons scattered in chromosome 8q22.2~24.3.