Ontology highlight
ABSTRACT:
PROVIDER: PRJNA939428 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Over the last 10 years, technological advances in molecular biology enabled a more accurate genomic characterization of tumors. For each tumor location, this led to the identification of subgroups with similar molecular characteristics. This identification allowed the development of targeted therapies and thus to improve the patient prognosis. This molecular characterization has also revealed the tumor heterogeneity. It may be the cause of treatment resistance and therefore of relapses. Additionally, tumor cells are in constant dialogue with their microenvironment composed of different immune or non immune cells. This microenvironment is now targeted in cancer treatment.
To date, there are few studies that combine a deep genomic characterization of both tumor and tumor microenvironment of the patient. Combining the two types of studies on the same tumor should help to define new therapeutic targets and should allow a combination of targeted and immunomodulatory therapies. To this end, our project is to conduct an exhaustive integrated exploratory analysis at genomic, transcriptomic and immunological levels of 3 tumor types (in colon, kidney and liver cancer).
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Project description:This SuperSeries is composed of the following subset Series: GSE11929: Identification of a subgroup of head and neck cancers lacking numerical chromosomal aberrations GSE11931: Copy Number Alterations in HNSCC with or without Oncogene Expressing Human Papillomavirus Refer to individual Series
2009-03-11 | E-GEOD-12020 | biostudies-arrayexpress
Project description:Oral squamous cell carcinoma (OSCC) is the most common malignancy of the oral cavity and despite therapeutic advances, late-stage diagnoses continue to negatively affect survival, presenting a continuing challenge for clinicians. Detailed molecular characterization by recent bulk and single-cell RNA-sequencing datasets from OSCC suggest that identification of prognostic biomarkers may lead to more targeted therapies, improving patient outcomes. Development of OSCC is associated with exposure to tobacco, alcohol consumption, and infection with human papillomavirus. The mouse model of 4-Nitroquinoline 1-oxide (4NQO) carcinogenesis produces a spectrum of neoplastic lesions that are a robust model of tobacco-induced OSCC. Specifically, studies have shown that similar to human OSCC, mouse OSCC shows upregulation of the oncogenic master transcription factor p63. We performed complementary loss- and gain-of-function experiments of p63 in mouse 4NQO-transformed OSCC cell lines and utilized RNA-sequencing and ChIP-sequencing to uncover the p63 oncogenic network. By combining our signature with publicly available bulk and scRNA-seq data, we generated a murine p63 signature that we have utilized to better understand the role of p63 in mOSCC. Our analyses have identified several potential biomarkers and conserved pathways that are relevant to hOSCC, as well as highlighted the dynamic role of p63 in migration and invasion.
2023-01-10 | GSE217668 | GEO
Project description:Identification of genetic/cytogenetic alterations and differentially expressed cellular genes in HPV16 E6, E7 and E6/E7 positive human foreskin keratinocytes Keywords: ordered We used microarrays to identify differentially expressed genes in human foreskin keratinocytes (HFK) transfected with retroviral vectors harboring the human papillomavirus type 16 oncogenes E6, E7, or E6/E7 in comparison to HFK containing the empty vector control pLXSN.
2013-11-27 | E-GEOD-14051 | biostudies-arrayexpress
Project description:Chromatin alterations mediate mutations and gene expression changes in cancer. Chromatin immunoprecipitation followed by sequencing (ChIP-Seq) has been utilized to study genome-wide chromatin structure in human cancer cell lines, yet numerous technical challenges limit comparable analyses in primary tumors. Here we have developed a new whole-genome analytic pipeline to optimize ChIP-Seq protocols on patient-derived xenografts from human papillomavirus-related (HPV+) head and neck squamous cell carcinoma (HNSCC) samples. We further associated chromatin aberrations with gene expression changes from a larger cohort of the tumor and normal samples with RNA-Seq data. We detect differential histone enrichment associated with tumor-specific gene expression variation, sites of HPV integration in the human genome, and HPV-associated histone enrichment sites upstream of cancer driver genes, which play central roles in cancer-associated pathways. These comprehensive analyses enable unprecedented characterization of the complex network of molecular changes resulting from chromatin alterations that drive HPV-related tumorigenesis.
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