Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA106675 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Oral dysplasias and oral squamous cell carcinoma
| PRJNA102765 | ENA
Project description:Primary tumor recurrence occurs commonly after surgical resection of lung squamous cell carcinoma (SCC). The aim of this study was to identify genes involved in recurrence in lung squamous cell carcinoma patients. Array comparative genomic hybridization (aCGH) was performed on DNA extracted from tumour tissue from 62 patients with primary lung squamous cell carcinomas. aCGH data was analysed to identify genes affected by copy number alterations that may be involved in SCC recurrence. Candidate genes were then selected for technical validation based on differential copy number between recurrence and non-recurrence SCC tumour samples. Genes technically validated advanced to tests of biological replication by qPCR using an independent test set of 72 primary lung SCC tumour samples. 18q22.3 loss was identified by aCGH as significantly associated with recurrence (p=0.038). Although aCGH copy number loss associated with recurrence was found for seven genes within 18q22.3, only SOCS6 copy number loss was both technically replicated by qPCR and biologically validated in the test set. DNA copy number profiling using 44K element array comparative genomic hybridization microarrays of 62 primary lung squamous cell carcinomas.
2011-12-25 | E-GEOD-32058 | biostudies-arrayexpress
Project description:Primary tumor recurrence occurs commonly after surgical resection of lung squamous cell carcinoma (SCC). The aim of this study was to identify genes involved in recurrence in lung squamous cell carcinoma patients. Array comparative genomic hybridization (aCGH) was performed on DNA extracted from tumour tissue from 62 patients with primary lung squamous cell carcinomas. aCGH data was analysed to identify genes affected by copy number alterations that may be involved in SCC recurrence. Candidate genes were then selected for technical validation based on differential copy number between recurrence and non-recurrence SCC tumour samples. Genes technically validated advanced to tests of biological replication by qPCR using an independent test set of 72 primary lung SCC tumour samples. 18q22.3 loss was identified by aCGH as significantly associated with recurrence (p=0.038). Although aCGH copy number loss associated with recurrence was found for seven genes within 18q22.3, only SOCS6 copy number loss was both technically replicated by qPCR and biologically validated in the test set.
2011-12-25 | GSE32058 | GEO
Project description:Analysis of DNA from 89 oral lesions by whole genome tiling-path array comparative genomic hybridization. Keywords: array comparative genomic hybridization Genomic DNA isolated from 89 formalin-fixed paraffin-embedded oral dysplasias and tumors, then profiled by whole genome tiling-path array CGH to identify DNA copy alterations for each case.
2009-07-01 | E-GEOD-11275 | biostudies-arrayexpress
Project description:Clinically evident oral lesions, oral epithelial dysplasia, precede development of oral squamous cell carcinomas (SCC) and are considered to transform to cancer by acquisition of genetic or epigenetic alterations. Here, we show that, +3q24-qter, -8pter-p23.1, +8q12-q24.2 and +20 are early events identifying two pathways to oral cancers that differ in clinical behavior. One or more of these copy number aberrations is present in the major subgroup (3q8pq20 subtype, 75-80% of lesions) that develops with chromosomal instability and risk for metastasis, while they are absent from the smaller and chromosomally stable non-3q8pq20 subgroup (20-25% of lesions) associated with low risk for metastasis. Thus, +3q, -8p, +8q and +20 is a biomarker for oral SCC metastasis. On the other hand, while increased numbers of genomic alterations can be harbingers of progression to cancer, dysplastic lesions lacking copy number changes cannot be considered benign as they are potential precursors to non-3q8pq20 oral SCC. 63 oral SCCs and adjacent regions of normal tissue, 44 oral dysplasias
2011-11-18 | E-GEOD-28407 | biostudies-arrayexpress
Project description:An investigation of canine oral squamous cell carcinomas
2024-06-30 | PRJEB77007 | EVA
Project description:RNA-Seq of oral squamous cell carcinomas and matched normal tissues
| PRJNA124251 | ENA
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. Oral squamous cell carcinomas (OSCC) and matched normal tissue from 3 patients.
2010-02-25 | E-GEOD-20116 | biostudies-arrayexpress
Project description:The 5-year survival rate for patients with oral squamous cell carcinomas (SCC), including tongue SCC, has not significantly improved over the last several decades. Oral potentially malignant disorders (OPMD), including oral dysplasias, are oral epithelial disorders that can develop into oral SCCs. To identify molecular characteristics that might predict conversion of OPMDs to SCCs and guide treatment plans, we performed global transcriptomic analysis of human tongue OPMD (n=9) and tongue SCC (n=11) samples with paired normal margin tissue from patients treated at Weill Cornell Medicine. Compared to margin tissue, SCCs showed more transcript changes than OPMDs. OPMDs and SCCs shared some altered transcripts, but these changes were generally greater in SCCs than OPMDs. Both OPMDs and SCCs showed altered signaling pathways related to cell migration, basement membrane disruption, and metastasis. We suggest that OPMDs were on the path towards malignant transformation. Based in patterns of gene expression, both OPMD samples and SCC samples can be categorized into subclasses (mesenchymal, classical, basal, and atypical) similar to those seen in human head and neck SCC (HNSCC). These subclasses of OPMDs the potential to be used to stratify patient prognosis and therapeutic options for tongue OPMDs. Lastly, we developed Firth logistic regression models to classify OPMDs and SCCs using a signature gene set ELF5, RPTN, IGSF10, HTR3A, and CRMP1, and this predictive model is amenable to testing as data sets become available. We suggest that changes in these five transcripts relative to paired normal tissue could be used to predict of the likelihood of an OPMD developing into a SCC.
2023-10-08 | GSE202048 | GEO