RNA-seq analyses of human ameloblastoma and odontogenic keratocyst
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ABSTRACT:
PROVIDER: PRJNA774061 | ENA |
REPOSITORIES: ENA
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Project description:Ameloblastoma (AM) is a benign but locally invasive tumor with high recurrence rates. Invasive behavior of the odontogenic tumor results in destruction of the adjacent jawbone and formation of daughter cysts, hindering the complete elimination of cancer cells during surgery. To understand the underlying mechanism of AM invasion, we compared the transcriptome of AM with that of an odontogenic keratocyst (OKC), a dental epithelium-originated cyst with non-invasive characteristics.
2022-05-02 | GSE186489 | GEO
Project description:Ameloblastoma of the jaws remains the top difficult to treat odontogenic tumour and has a high recurrence rate. New evidence suggests that non-coding RNAs (ncRNAs) play a critical role in tumour genesis and prognosis of cancer. However, ameloblastoma ncRNA expression data is lacking. Here we present the first report of ameloblastoma ncRNA signatures. A total of 95 ameloblastoma cases and a global array transcriptome technology covering > 285.000 full-length transcripts were used in this two-step analysis. The analysis first identified in a test cohort 31 upregulated ameloblastoma-associated ncRNAs accompanied by signalling pathways of cancer, spliceosome, mRNA surveillance and Wnt. Further validation in an independent cohort points out the long non-coding (lncRNAs) and small nucleolar RNA (snoRNAs): LINC340, LINC342, SNORD116-25, SNORA11, SNORA21, SNORA47 and SNORA65 as a distinct ncRNA signature of ameloblastoma. Importantly, the presence of these ncRNAs was independent of BRAF-V600E and SMO-L412F mutations, histology type or tumour location, but was positively correlated with the tumour size. Taken together, this study shows a systematic investigation of ncRNA expression of ameloblastoma, and illuminates new diagnostic and therapeutic targets for this invasive odontogenic tumour.
2017-03-01 | GSE90518 | GEO
Project description:The aim of the study was to elucidate the cellular origin of ameloblastoma and keratocystic odontogenic tumour, neoplasms believed to arise from dental epithelial cells, by carrying out a genome-wide expression analysis.
2014-12-02 | GSE38494 | GEO
Project description:The aim of this study was to decode the gene expression program characterizing odontogenic keratocyst (OKC) development, by performing a comprehensive transcriptomics analysis applied on whole OKC tissue derived from sporadic and Basal Cell Nevus Syndrome (BCNS)-associated OKCs, and control samples of pericoronal tissues of impacted teeth (dental follicles, DFs) derived from healthy individuals.
2022-06-22 | GSE180706 | GEO
Project description:Odontogenic tumors (OGTs), which originate from cells of odontogenic apparatus and their remnants, are rare entities. Primary intraosseous carcinoma, NOS (PIOC), is one of the OGTs, but it is even rarer and has a worse prognosis. The characteristics of PIOC, especially in immunohistochemical features and its pathogenesis, remain unclear. We characterized a case of PIOC arising from the left mandible, in which histopathological findings showed a transition between the odontogenic keratocyst and the carcinoma. The tumorous lesion of this PIOC exhibited malignant potentials with an invasive growth of carcinoma cells into the bone tissue, an elevated Ki-67 index, and lower signal for CK13 and higher signal for CK17 compared with the non-tumor region, histopathologically and immunohistopathologically. Further immunohistochemical analyses demonstrated increased expression of ADP-ribosylation factor (ARF)-like 4c (ARL4C) (accompanying expression of β-catenin in the nucleus) and yes-associated protein (YAP) in the tumorous lesion. On the other hand, YAP was expressed and the expression of ARL4C was hardly detected in the non-tumor region. In addition, quantitative RT-PCR analysis using RNAs and dot blot analysis using genomic DNA showed the activation of Wnt/β-catenin signaling and epigenetic alterations, such as an increase of 5mC levels and a decrease of 5hmC levels, in the tumorous lesion. A DNA microarray and gene ontology analysis demonstrated that numerous gene expression variations and signal activation, including Notch signaling, were altered in non-tumor and tumor lesions within this PIOC. Experiments with the GSK-3 inhibitor revealed that β-catenin pathway increased not only mRNA levels of ankyrin repeat domain1 (ANKRD1) but also protein levels of YAP and TAZ in oral squamous cell carcinoma cell lines. These results suggested that further activation of YAP signaling by Wnt/β-catenin signaling may be associated with the development of PIOC arising from odontogenic keratocyst in which YAP signaling is activated.
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2020-10-08 | GSE156886 | GEO
Project description:The goal of the study was to characterize the whole genome transcriptome profiles of pure sample population of human ameloblastoma epithelial cells for examination of molecular pathways. Seventeen human ameloblastoma samples were obtained. Both fresh frozen and FFPE samples were used and placed in solution for 1-4 weeks to allow decalcification by EDTA. The tissue was sectioned at -35C at a thickness of 7 microns. These sections were used for laser capture microdissection (LCM) to isolate the neoplastic epithelial portion of the tumors, using static image settings. Total RNA was extracted from each sample and examined using the whole genome microarray against the Stratagene universal human reference RNA.
2016-09-01 | E-GEOD-68531 | biostudies-arrayexpress
Project description:The goal of the study was to characterize the whole genome transcriptome profiles of pure sample population of human ameloblastoma epithelial cells for examination of molecular pathways.
2016-09-01 | GSE68531 | GEO
Project description:We have employed whole genome microarray expression profiling as a discovery platform to identify genes that are associated with pathogenesis of ameloblastoma using ameloblastoma tumor and corresponding normal counterpart from patients.
2019-06-11 | GSE132472 | GEO
Project description:To investigate the minimal genomic alterations in ameloblastoma, we have employed high-resolution CGH as a discovery platform to identify somatic genomic gains and losses in ameloblastoma tumors.
2019-06-11 | GSE132473 | GEO