Ethmoïd tumors vs normal mucosa samples
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Sylvia Quéméner
PROVIDER: E-GEOD-17433 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Transcriptional profiling of ethmoïd tumors samples comparing normal samples from the controlateral sinus. RNA were extracted from biopsies. Sinonasal adenocarcinomas are uncommon tumors developping in ethmoid sinus after wood dust exposure. Although the etiology of these tumors is well defined very little is known regarding the molecular basis of these tumors. In an attempt to identify genes involved in this disease we proceed to a gene expression profiling using cancer-dedicated microarrays, on matched samples of nine sinonasal adenocarcinomas and non-tumoral sinusal tissue. Among the genes with significant differential expression we selected: LGALS4, ACS5, CLU, BAX, PDGFRa, SRI and CCT5 for further exploration by quantitative real-time reverse-transcription-PCR on a larger set of tumors and confirmed the microarray data. Protein expression alterations were shown for LGALS4, ACS5, and CLU by immunohistochemistry. Our results suggest that two genes might be involved in the pathogenesis of these tumors: LGALS4 highly up-regulated, particularly in the most differentiated tumors, and CLU, whose expression was lost. After further evaluation these genes could be used as markers for a better characterization of these tumors and will potentially help to an earlier detection of cancer in woodworkers, who have high risk of developing sinonasal adenocarcinomas.
2009-07-31 | GSE17433 | GEO
Project description:Single cell RNA sequencing analyses of human sinonasal tissue samples of chronic rhinosinusitus patients clustered the sinus cell into 13 types. Two cell types (monocyte/Macrophage and dendritic cells) demonstrated over-lapping expression of MPEG1, BATF3, IRF4, CD86, and HLA-DRA.
2020-08-15 | GSE156285 | GEO
Project description:Identification of cellular functions and signalling pathways of intestinal epithelial cells modulated by enteric glial cells Keywords: Transcriptome regulation Two-condition experiment (intestinal epithelial cells cultured in absence or in presence of enteric glial cells) with 3 time points (t=0, 8 and 24h). 4 Biological replicates/condition. Every replicate was hybridized against a reference pool composed by a mix of the 4 replicates of t=0 condition in equal quantity.
2010-05-16 | E-GEOD-17027 | biostudies-arrayexpress
Project description:The diagnosis of sinonasal tumors is challenging due to a heterogeneous spectrum of various differential diagnoses as well as poorly defined, disputed entities such as sinonasal undifferentiated carcinomas (SNUCs). In this study, we apply machine learning algorithm based on DNA methylation patterns to classify sinonasal tumors with clinical-grade reliability. We further show that sinonasal tumors with SNUC morphology are not as undifferentiated as their current terminology suggests but rather reassigned to four distinct molecular classes defined by epigenetic, mutational and proteomic profiles. This includes two classes with neuroendocrine differentiation, characterized by IDH2 or SMARCA4/ARID1A mutations with an overall favorable clinical course, whereas tumors that are driven by SMARCB1-deficiency and tumors that represent previously misclassified adenoid cystic carcinomas are highly aggressive. Our findings have the potential to dramatically improve the diagnostic classification of sinonasal tumors and will fundamentally change the current perception of SNUCs.
2022-09-25 | GSE196227 | GEO
Project description:Epithelial, non-glandular sinonasal cancers (SNCs) is a rare disease, with a global dismal prognosis. There are no recognized targeted treatments and the knowledge of molecular mechanisms involved in the resistance to available therapies is limited. Dissecting the heterogeneity of paranasal sinus cancersSNCs and providing valuable information on the biology of the malignancy is eagerly needed to improve therapeutic approaches.
2019-12-26 | GSE118386 | GEO
Project description:The histopathological diagnosis of sinonasal tumors is challenging as it encompasses a heterogeneous spectrum of various differential diagnoses as well as poorly defined, disputed entities such as sinonasal undifferentiated carcinomas (SNUCs). In this study, we show that a machine learning algorithm based on DNA methylation is able to classify sinonasal tumors with clinical-grade reliability. We further show that tumors with SNUC morphology are not as undifferentiated as their current terminology suggests, but can be assigned to four molecular classes defined by distinct epigenic, mutational and proteomic profiles. This includes two classes with neuroendocrine differentiation, characterized by IDH2 or SWI/SNF chromatin remodeling complex mutations and overall favorable clinical course, highly aggressive tumors that are driven by SMARCB1-deficiency and tumors that represent previously misclassified adenoid-cystic carcinomas. Our findings have the potential to dramatically improve the diagnostic of challenging sinonasal tumors and could fundamentally change the current perception of SNUCs.
2022-09-25 | GSE189778 | GEO
Project description:Gene expression profiling of 60 lung adenocarcinoma tumors and their matched histologically normal adjacent lung tissue samples were analyzed using Illumina HumanWG-6 v3.0 expression beadchip. We integrated these data with DNA methylation profiles of the same samples to identify potential DNA methylation regulated genes. Lung cancer is the leading cause of cancer death worldwide and adenocarcinoma is its most common histological subtype. Clinical and molecular evidence indicates that lung adenocarcinoma is a heterogeneous disease, which has important implications for treatment. Here we performed genome-scale DNA methylation profiling using the Illumina Infinium HumanMethylation27 platform on 59 matched lung adenocarcinoma/non-tumor lung samples, with genome-scale verification on an independent set of tissues. We identified 766 genes showing altered DNA methylation between tumors and non-tumor lung. By integrating DNA methylation and mRNA expression data, we identified 164 hypermethylated genes showing concurrent downregulation, and 57 hypomethylated genes showing increased expression. Integrated pathways analysis indicates that these genes are involved in cell differentiation, epithelial to mesenchymal transition, RAS and WNT signaling pathways and cell cycle regulation, among others. Comparison of DNA methylation profiles between lung adenocarcinomas of current and never-smokers showed modest differences, identifying only LGALS4 as significantly hypermethylated and downregulated in smokers. LGALS4, encoding a galactoside-binding protein involved in cell-cell and cell-matrix interactions, was recently shown to be a tumor-suppressor in colorectal cancer. Unsupervised analysis of the DNA methylation data identified two tumor subgroups, one of which showed increased DNA methylation and was significantly associated with KRAS mutation and to a lesser extent, with smoking. Our analysis lays the groundwork for further molecular studies of lung adenocarcinoma by providing new candidate DNA methylation biomarkers for early detection, identifying novel molecular alterations potentially involved in lung adenocarcinoma development/progression, and describing an epigenetic subgroup of lung adenocarcinoma associated with KRAS mutation.
2012-03-21 | GSE32863 | GEO
Project description:Background: Oral squamous cell carcinoma (OSCC) is a major world health problem with over 400,000 new cases diagnosed annually. Despite advances in surgery and chemo-radiotherapy, the 5 year survival has remained roughly constant at approximately 50% for several decades. The disease is characterized by both clinical and genetic heterogeneity, so elucidating the molecular basis of this heterogeneity would have significant clinical implications. It is well recognized that OSCCs from Asia that are associated with betel quid chewing are phenotypically distinct from those from the West that are predominantly caused by smoking/drinking, but the genetic basis of these differences are largely unknown. The aim of this study is to examine the most related genetic factors, carcinogenic related pathways, and molecular processes that might be responsible for the phenotypic heterogeneity of OSCC between UK and Sri Lankan population groups. Methods: We have compared the gene expression profiles of OSCCs and normal oral mucosal tissues from both Sri Lankan and UK individuals using Affymetrix gene expression arrays. Results: The gene expression profiles of UK and Sri Lankan OSCC are similar in many respects to other oral cancer expression profiles reported in the literature and were mainly similar to each other. However, genes involved in tumor invasion, metastasis and recurrence were more obviously associated with UK tumors as opposed to those from Sri Lanka. Interestingly, Ingenuity Pathway Analysis (IPA) revealed a highly activated cell-mediated immune response in both Sri Lankan normal and tumor samples relative to UK cohorts, which may, in part, explain the less aggressive behavior of these betel quid-induced OSCCs. Conclusion: The development of OSCCs in both UK and Sri Lankan populations appears largely mediated by similar biological pathways despite the differences related to race, ethnicity, lifestyle, and/or exposure to environmental carcinogens. However, IPA revealed a highly activated M-bM-^@M-^\Cell-mediated Immune ResponseM-bM-^@M-^] in Sri Lankan normal and tumor samples relative to UK cohorts. It seems likely, therefore, that any future attempts to personalize treatment for OSCC patients will need to be different in Western and Asian countries to reflect differences in gene expression and the immune status of the patients. All biopsy specimens of OSCC and normal oral mucosa were harvested with appropriate ethical approval and informed consent of individual patients (LREC 0769). Identical protocols for tissue collection and processing were used in both countries. OSCC samples were obtained from sequential incident cases treated by a single consultant surgeon from 2001 to 2004 at University Hospital of Birmingham, NHS Foundation Trust, Birmingham, UK, and Kandy General Hospital, Kandy, Sri Lanka. A total of 21 UK and 27 Sri Lankan samples yielded RNA of sufficient quality and quantity for microarray analysis. In addition, 8 normal oral mucosa specimens (five samples from UK & three samples from Sri Lankan population) were also profiled. All normal samples were from non-smokers, who did not chew betel quid and did not consume in excess of the national recommended weekly gender allowance of alcohol. Normal samples were taken from individuals with no history of cancer and had no first degree relatives with a history of cancer.
2014-02-02 | E-GEOD-51010 | biostudies-arrayexpress
Project description:Lung cancer is the leading cause of cancer death worldwide and adenocarcinoma is its most common histological subtype. Clinical and molecular evidence indicates that lung adenocarcinoma is a heterogeneous disease, which has important implications for treatment. Here we performed genome-scale DNA methylation profiling using the Illumina Infinium HumanMethylation27 platform on 59 matched lung adenocarcinoma/non-tumor lung samples, with genome-scale verification on an independent set of tissues. We identified 766 genes showing altered DNA methylation between tumors and non-tumor lung. By integrating DNA methylation and mRNA expression data, we identified 164 hypermethylated genes showing concurrent downregulation, and 57 hypomethylated genes showing increased expression. Integrated pathways analysis indicates that these genes are involved in cell differentiation, epithelial to mesenchymal transition, RAS and WNT signaling pathways and cell cycle regulation, among others. Comparison of DNA methylation profiles between lung adenocarcinomas of current and never-smokers showed modest differences, identifying only LGALS4 as significantly hypermethylated and downregulated in smokers. LGALS4, encoding a galactoside-binding protein involved in cell-cell and cell-matrix interactions, was recently shown to be a tumor-suppressor in colorectal cancer. Unsupervised analysis of the DNA methylation data identified two tumor subgroups, one of which showed increased DNA methylation and was significantly associated with KRAS mutation and to a lesser extent, with smoking. Our analysis lays the groundwork for further molecular studies of lung adenocarcinoma by providing new candidate DNA methylation biomarkers for early detection, identifying novel molecular alterations potentially involved in lung adenocarcinoma development/progression, and describing an epigenetic subgroup of lung adenocarcinoma associated with KRAS mutation.
2012-03-21 | GSE32861 | GEO
Project description:Gene expression profiling of 60 lung adenocarcinoma tumors and their matched histologically normal adjacent lung tissue samples were analyzed using Illumina HumanWG-6 v3.0 expression beadchip. We integrated these data with DNA methylation profiles of the same samples to identify potential DNA methylation regulated genes. Lung cancer is the leading cause of cancer death worldwide and adenocarcinoma is its most common histological subtype. Clinical and molecular evidence indicates that lung adenocarcinoma is a heterogeneous disease, which has important implications for treatment. Here we performed genome-scale DNA methylation profiling using the Illumina Infinium HumanMethylation27 platform on 59 matched lung adenocarcinoma/non-tumor lung samples, with genome-scale verification on an independent set of tissues. We identified 766 genes showing altered DNA methylation between tumors and non-tumor lung. By integrating DNA methylation and mRNA expression data, we identified 164 hypermethylated genes showing concurrent downregulation, and 57 hypomethylated genes showing increased expression. Integrated pathways analysis indicates that these genes are involved in cell differentiation, epithelial to mesenchymal transition, RAS and WNT signaling pathways and cell cycle regulation, among others. Comparison of DNA methylation profiles between lung adenocarcinomas of current and never-smokers showed modest differences, identifying only LGALS4 as significantly hypermethylated and downregulated in smokers. LGALS4, encoding a galactoside-binding protein involved in cell-cell and cell-matrix interactions, was recently shown to be a tumor-suppressor in colorectal cancer. Unsupervised analysis of the DNA methylation data identified two tumor subgroups, one of which showed increased DNA methylation and was significantly associated with KRAS mutation and to a lesser extent, with smoking. Our analysis lays the groundwork for further molecular studies of lung adenocarcinoma by providing new candidate DNA methylation biomarkers for early detection, identifying novel molecular alterations potentially involved in lung adenocarcinoma development/progression, and describing an epigenetic subgroup of lung adenocarcinoma associated with KRAS mutation. 58 lung adenocarcinoma and 58 adjacent non-tumor lung fresh frozen tissues were macrodissected, and total RNA was isolated to be analyzed using the Illumina HumanWG-6 v3.0 expression beadchip.
2012-03-21 | E-GEOD-32863 | biostudies-arrayexpress