RNA-Seq of oral squamous cell carcinomas and matched normal tissues
ABSTRACT: RNA-Seq was applied to oral squamous cell carcinomas and matched normal oral tissue to measure gene expression patterns and identify examples of allelic imbalance. Oral squamous cell carcinomas (OSCC) and matched normal tissue from 3 patients.
Due to growing throughput and shrinking cost, massively parallel sequencing is rapidly becoming an attractive alternative to microarrays for the genome-wide study of gene expression and copy number alterations in primary tumors. The sequencing of transcripts (RNA-Seq) should offer several advantages over microarray-based methods, including the ability to detect somatic mutations and accurately measure allele-specific expression. To investigate these advantages we have applied a novel, strand-spe ...[more]
Project description:RNA-Seq was applied to oral squamous cell carcinomas and matched normal oral tissue to measure gene expression patterns and identify examples of allelic imbalance. Overall design: Oral squamous cell carcinomas (OSCC) and matched normal tissue from 3 patients.
Project description:Genome-wide expression array measurements for 9 head and neck squamous cell carcinomas (HNSCC) stratified by worst pattern of invasion (WPOI) Jayakar et al. (2016). Apolipoprotein E promotes invasion in oral squamous cell carcinoma. Li et al. (2013). Validation of the risk model: high-risk classification and tumor pattern of invasion predict outcome for patients with low-stage oral cavity squamous cell carcinoma. Comparison of transcription profiles between OSCC tumors with a more invasive (WPOI 5) versus a less invasive (WPOI 3) pattern of invasion using two independent Illumina platforms.
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:Array Comparative Genomic Hybridization (CGH) profiling of Oral Leukoplakia (OPL) and early stage Oral Squamous Cell Carcinoma (OSCC) was performed to delineate candidate non-random chromosomal loci associated with disease progression and clinico-pathological parameters. The array CGH hybridizations were performed for 24 OPL and 38 OSCC samples with pooled gender matched controls. All tissue samples were collected after obtaining written informed consent. Overall design: Agilent two-color CGH experiment,Organism: Agilent-21764 Human Genome CGH Microarray 105A (G4412A), Labeling kit: Agilent Sure tag DNA labeling kit (Agilent Technologies, 5190-3400).
Project description:Using Affymetrix Mapping 250K array, we studied copy number aberrations in oral squamous cell carcinoma (OSCC) to identified biomarkers associated with occult lymph node metastasis. We used frozen specimens from 60 OSCC patients. Copy number analysis was performed using homogenized samples of 60 oral squamous cell carcinoma patients by GeneChip Human Mapping 250k Sty arrays. As a reference, SNP array data set of 50 normal Asians (Japanese & Chinese) from HapMap database was used.
Project description:Using Affymetrix Mapping 250K array, we studied copy number aberrations in oral squamous cell carcinoma (OSCC) to identified biomarkers associated with occult lymph node metastasis. We used frozen specimens from 60 OSCC patients. Overall design: Copy number analysis was performed using homogenized samples of 60 oral squamous cell carcinoma patients by GeneChip Human Mapping 250k Sty arrays. As a reference, SNP array data set of 50 normal Asians (Japanese & Chinese) from HapMap database was used.
Project description:In our previous study, we identified global genetic and epigenetic aberrations in the tumors of oral squamous cell carcinoma (OSCC) patients who were habitual smokers. We hypothesized that cigarette smoke might play a role in oral malignant transformation. DOK cell line is a dysplasitc oral keratinocyte derived from a heavy smoker with OSCC. The differentially expressed genes between DOK and normal human oral keratinocytes (HOK) may provide important information about OSCC carcinogenesis mediated by cigarette smoking. Total RNA was collected from DOK and HOK cells followed by gene expression microarray analysis.
Project description:The aim of this study is to identify and validate clinically implementable gene signatures for outcome prediction of patients with oral squamous cell carcinoma. Overall design: Tumor gene expression profiles of surgical specimen of patients with oral squamous cell carcinoma (OSCC)
Project description:MicroRNAs (miRNAs) participate in many biological processes and have emerged as key players in carcinogenesis. In order to identify changes in miRNAs specific for betelquid-associated oral squamous cell carcinoma (OSCC), we investigated the expression profiles of 858 miRNAs in a panel of 40 pairs of OSCC specimens and their matched non-tumorous epithelial counterparts. Eighty-four miRNAs were differentially expressed in the OSCC specimens compared to the matched tissue. Among these miRNAs, 19 downregulated miRNAs located in the chromosome 14q32.2 miRNA cluster region were analyzed. This miRNA cluster resides within a parentally imprinted region known to be important in development and growth. The re-expression of miR-329 and miR-410from this cluster significantly reduced OSCC cell proliferation and invasion and downregulated Wnt-7b, an activator of the Wnt/b-catenin pathway. Furthermore, the expression of those 2 miRNAs was restored by 5-aza-2′-deoxycytidine treatment and the expression levels of the 2 miRNAs were inversely correlated with the hypermethylation of the Meg-3 promoter in OSCC cells. Specifically, arecoline, a major betel nut alkaloid, reduces miR-329 and miR-410 expression. Our results thus provide a novel molecular insight into how betel quid may contribute to oral carcinogenesis through the epigenetic silencing of tumor suppressor miRNAs targeting the Wnt/b-catenin signaling pathway. Total RNA was obtained from 40 pairs of OSCC patients with tumor specimens and their adjacent non-tumorous epithelia.