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ABSTRACT: Early genetic drivers in preneoplastic lesions of the Oral Cavity

PROVIDER: PRJNA1272759 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33853428_1.fastq.gz	Fastqsanger.gz
	SRR33853428_2.fastq.gz	Fastqsanger.gz
	SRR33853429_1.fastq.gz	Fastqsanger.gz
	SRR33853429_2.fastq.gz	Fastqsanger.gz
	SRR33853430_1.fastq.gz	Fastqsanger.gz

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Silica-mediated airway chronic inflammation promotes lung carcinogenesis through the activation of preneoplastic lesions in the context of an immunosuppressive microenvirontment

Project description:Basic studies on preneoplastic lesions are important to determine the molecular alterations that take place in early steps of lung carcinogenesis. Little is known about the molecular events preceding the development of lung cancer in the context of an inflammatory environment. In this study we report the generation of a chemical-induced lung carcinogenesis mouse model in the presence of silicotic chronic inflammation. Silica-induced lung inflammation, strongly promoted incidence of lung cancer in mice treated with NDMA, a carcinogen found in tobacco smoke. Histological and molecular analysis revealed that permanent inflammation contributed to lung tumorigenesis through the adquisition of preneoplastic changes in lung epithelial cells. Inflammatory milieu increased the expression of PDCD1, TGFÎ²-1, MCP-1, LAG3, and Foxp3 and the presence of regulatory T cells within preneoplastic lesions. In addition concomitant chronic inflammation changed the K-ras mutational profile of the generated tumors from Q61R to G12D transition. In summary, these data identify early molecular mechanisms underlying lung carcinogenesis in an inflammatory context at different steps, providing a novel approach for the identification of drivers from preneoplastic to neoplastic lesions Gene expression profile was analyzed in 11 individual lesions (8 adenomas and 3 adenocarcinomas) from the NDMA-silica treated mice and 5 lesions (2 adenomas, and 3 adenocarcinomas) from NDMA-only treated mice

2016-07-05 | E-GEOD-43453 | biostudies-arrayexpress

Silica-mediated airway chronic inflammation promotes lung carcinogenesis through the activation of preneoplastic lesions in the context of an immunosuppressive microenvirontment

Project description:Basic studies on preneoplastic lesions are important to determine the molecular alterations that take place in early steps of lung carcinogenesis. Little is known about the molecular events preceding the development of lung cancer in the context of an inflammatory environment. In this study we report the generation of a chemical-induced lung carcinogenesis mouse model in the presence of silicotic chronic inflammation. Silica-induced lung inflammation, strongly promoted incidence of lung cancer in mice treated with NDMA, a carcinogen found in tobacco smoke. Histological and molecular analysis revealed that permanent inflammation contributed to lung tumorigenesis through the adquisition of preneoplastic changes in lung epithelial cells. Inflammatory milieu increased the expression of PDCD1, TGFβ-1, MCP-1, LAG3, and Foxp3 and the presence of regulatory T cells within preneoplastic lesions. In addition concomitant chronic inflammation changed the K-ras mutational profile of the generated tumors from Q61R to G12D transition. In summary, these data identify early molecular mechanisms underlying lung carcinogenesis in an inflammatory context at different steps, providing a novel approach for the identification of drivers from preneoplastic to neoplastic lesions

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Gene expression profiling of oral squamous cell carcinoma (OSCC)

Project description:OSCC is associated with substantial mortality and morbidity. To identify potential biomarkers for the early detection of invasive OSCC, we compared the gene expressions of OSCC, oral dysplasia, and normal oral tissue from patients without oral cancer or preneoplastic oral lesions (controls). Results provided models of gene expression to distinguish OSCC from controls. RNA from 167 OSCC, 17 dysplasia and 45 normal oral tissues were extracted and hybridized to Affymetrix U133 2.0 Plus GeneChip arrays. The differentially expressed genes were identified using GenePlus software and the validation was done using RT-PCR, using independent internal and external datasets.

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Integrative genomic characterization of oral squamous cell carcinoma identifies frequent somatic drivers (methylation)

Project description:Oral cavity squamous cell carcinoma (OSCC) is a disease with extensive morbidity and mortality and few useful molecular targets. Multiplatform integrated genomic analysis was performed in order to identify genomic drivers and molecularly discernible tumor subtypes. mRNA, miRNA and methylation data are all submitted to GEO We measured methylation of 42 OSCC tumors, 2 normal oral epithelial tissues, and 2 normal blood samples with Illumina HumanMethylation450 arrays

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Project description:Gene expression microarray analyses of PIK3CA H1047R and E545K induced preneoplastic lesions and tumors compared to age matched controls. Plasmids expressing oncogenic forms of PIK3CA (H1047R or E545K mutants) were delivered to the mouse liver by tail vein hydrodynamic injection combined with Sleeping Beauty–mediated somatic integration (SBT-HTVI). Resulting preneoplastic and neoplastic lesions were subjected to gene expression microarray analysis. The putative PIK3CA target gene Galectin1 (Gal1) was further characterized by in vitro studies. Transfection of either PIK3CA E545K or H1047R mutants via SBT-HTVI was sufficient to induce hepatocellular carcinomas in mice. A stepwise hepatocarcinogenesis from singular pericentral lipid-rich preneoplastic hepatocytes to clusters, expansive preneoplastic lesions, and HCCs was observed. In PIK3CA H1047R injected mice, HCCs were detected in the 12 months injection group, while PIK3CA E545K injections resulted in tumor occurrence as early as 3 months after SB-HTVI. Histologically, a predominant lipid-rich phenotype characterized all tumorigenesis stages, as confirmed by Sudan III staining and electron microscopy. Immunohistochemically, preneoplastic lesions and tumors displayed high levels of the lipid master regulators Fatty acid synthase and Stearoyl-CoA desaturase-1. Gal1 was commonly overexpressed in PIK3CA-driven preneoplastic and neoplastic liver lesions by gene expression microarray analysis compared with age-matched controls.

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Project description:Head and neck cancers are a complex malignancy comprising multiple anatomical sites, with cancer of the oral cavity ranking among the deadliest and most disfiguring cancers globally. Oral cancer (OC) constitutes a subset of head and neck cancer cases, presenting primarily as tobacco- and alcohol-associated oral squamous cell carcinoma (OSCC), with a 5-year survival rate of ~65%, partly due to the lack of early detection and effective treatments. OSCC arises from premalignant lesions (PMLs) in the oral cavity through a multi-step series of clinical and histopathological stages, including varying degrees of epithelial dysplasia. To gain insights into the molecular mechanisms associated with the progression of PMLs to OSCC, we profiled the whole transcriptome of 66 human PMLs comprising leukoplakia with dysplasia and hyperkeratosis non-reactive (HkNR) pathologies, alongside healthy controls and OSCC. Our data revealed that PMLs were enriched in gene signatures associated with cellular plasticity, such as partial EMT (p-EMT) phenotypes, and with immune response. Integrated analyses of the host transcriptome and microbiome further highlighted a significant association between differential microbial abundance and PML pathway activity, suggesting a contribution of the oral microbiome towards PML evolution to OSCC. Collectively, this study reveals molecular processes associated with PML progression that may help early diagnosis and disease interception at an early stage.

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