Bulk RNA-Seq of colorectal cancer patient samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAS00001006666 | EGA |
REPOSITORIES: EGA
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Project description:Primitive neuroectodermal tumours of the central nervous system (CNS PNETs) are highly aggressive, poorly differentiated embryonal tumours occurring predominantly in young children. Using DNA methylation and gene expression profiling we have demonstrated that a significant proportion of institutionally diagnosed CNS PNETs display molecular profiles indistinguishable from those of various other well defined CNS tumour entities, facilitating diagnosis and appropiate therapy for children with these tumours. From the remaining fraction of CNS PNETs, we have identified four distinct new CNS tumour entities extending to other neuroepithelial tumours, each associated with a recurrent genetic alteration and particular histopathological and clinical features. These molecular entities, designated “CNS Neuroblastoma with FOXR2 activation (CNS NB FOXR2)”, “CNS Ewing sarcoma family tumour with CIC alteration (CNS EFT CIC)”, “CNS high grade neuroepithelial tumour with MN1 alteration (CNS HGNET MN1)”, and “CNS high grade neuroepithelial tumour with BCOR alteration (CNS HGNET BCOR)”, will enable meaningful clinical trials and the development of therapeutic strategies for patients affected by these poorly differentiated CNS tumours.
2016-02-25 | GSE73801 | GEO
Project description:In this study, we performed a comparative analysis of gut microbiota composition and gut microbiome-derived bacterial extracellular vesicles (bEVs) isolated from patients with solid tumours and healthy controls. After isolating bEVs from the faeces of solid tumour patients and healthy controls, we performed spectrometry analysis of their proteomes and next-generation sequencing (NGS) of the 16S gene. We also investigated the gut microbiomes of faeces from patientsand controls using 16S rRNA sequencing. Machine learning was used to classify the samples into patients and controls based on their bEVs and faecal microbiomes.
2024-08-08 | PXD047510 | Pride
Project description:Head and neck squamous cell carcinoma (HNSCC) often present with locoregional or distant disease, despite multimodal therapeutic approaches, which include surgical resection, chemoradiotherapy, and more recently immunotherapy for metastatic, or recurrent HNSCC. Therapies often target the primary and nodal regional HNSCC sites, and efficacy at controlling occult distant sites remains poor. Whilst our understanding of the tumour microenvironment, conducive for effective therapies is increasing, the biology underpinning locoregional sites remains unclear. Here, we applied targeted spatial proteomic approaches to primary and lymph node metastasis from an oropharyngeal SCC (OPSCC) cohort, to understand the expression of proteins within tumour, and stromal compartments of the respective sites in both matched and unmatched patients’ samples. In unmatched analyses of n=43 primary and 11 nodal metastasis, our data indicated that tumour cells in nodal metastases had higher levels of Ki-67, PARP, BAD and cleaved caspase 9, suggesting a role for increased proliferation, DNA repair and apoptosis within these metastatic cells. Conversely, in matched analyses (n=7), pro-apoptotic markers BIM and BAD were enriched in the stroma of primary tumours. Univariate, overall survival (OS) analysis indicated CD25 in tumour regions of primary tumours to be associated with reduced survival (HR=3.3, p=0.003), while partial response (PR) was associated with an improved OS (HR=0.33, p=0.015). This study highlights the utility of spatial proteomics for delineating tumour and stroma compartment composition, and the utility towards understanding these properties in locoregional metastasis. These findings indicate the unique biological properties of lymph node metastases that may elucidate further understanding of the subsequent distant metastatic potential of OPSCC. In this dataset, we applied GeoMx DSP protein profiling to tumour and tumour microenvironment regions of primary and lymphnode metastasis FFPE samples. The files here represent the Ncounter readout from this assay.
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Project description:Multiple tumours from the same patient were analysed for copy number alterations to assess tumour clonality. Seventy-four tumours corresponding to 37 patients were stratified into four groups based on the anatomic location of the multiple breast cancers (ipsilateral or bilateral) and time interval between the diagnoses (synchronous or metachronous). Ipsilateral was defined as tumours occurring in the same breast while bilateral was defined as the occurrence of tumours in both breasts. Metachronicity was defined as a time interval greater than six months between the diagnoses of the first and second tumours, while synchronicity specified that the two tumours occurred concurrently (BM: bilateral-metachronous; BS: bilateral-synchronous; IM: ipsilateral-metachronous; IS: ipsilateral-synchronous).
2019-01-03 | GSE108984 | GEO
Project description:A "Cartes d'Identite des Tumeurs" (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net). 37 samples hybridized on Affymetrix HG-U133A arrays. Analysis of advanced breast cancers treated with a dose-intense epirubicin /cyclophosphamide regimen followed by mastectomy; Validation of TP53-related genes in breast and bladder cancers. We found that a complete response to chemotherapy was only observed in TP53 mutant tumours. We further show that, among TP53 mutant tumours, high basalcytokeratin and low ESR1 expression levels were associated with complete responses. These observations pave the way to molecular tailoring of chemotherapy in breast cancer.
2007-03-26 | E-TABM-43 | biostudies-arrayexpress
Project description:Primitive neuroectodermal tumours of the central nervous system (CNS PNETs) are highly aggressive, poorly differentiated embryonal tumours occurring predominantly in young children. Using DNA methylation and gene expression profiling we have demonstrated that a significant proportion of institutionally diagnosed CNS PNETs display molecular profiles indistinguishable from those of various other well defined CNS tumour entities, facilitating diagnosis and appropiate therapy for children with these tumours. From the remaining fraction of CNS PNETs, we have identified four distinct new CNS tumour entities extending to other neuroepithelial tumours, each associated with a recurrent genetic alteration and particular histopathological and clinical features. These molecular entities, designated â??CNS Neuroblastoma with FOXR2 activation (CNS NB FOXR2)â??, â??CNS Ewing sarcoma family tumour with CIC alteration (CNS EFT CIC)â??, â??CNS high grade neuroepithelial tumour with MN1 alteration (CNS HGNET MN1)â??, and â??CNS high grade neuroepithelial tumour with BCOR alteration (CNS HGNET BCOR)â??, will enable meaningful clinical trials and the development of therapeutic strategies for patients affected by these poorly differentiated CNS tumours. 586 brain tumor samples were profiled using the Illumina HumanMethylation450 BeadChip (450k) array.
2016-02-25 | E-GEOD-73801 | biostudies-arrayexpress
Project description:Breast cancer is the most frequent cancer in women and consists of heterogeneous types of tumours that are classified into different histological and molecular subtypes1-3. Pik3ca and p53 are the two most frequently mutated genes and are associated with different types of human breast cancers4. The cellular origin and the mechanisms leading to Pik3ca-induced tumour heterogeneity remain unknown. Here, we used a genetic approach in mice to define the cellular origin of Pik3ca-derived tumours and its impact on tumour heterogeneity. Surprisingly, oncogenic Pik3ca-H1047R expression at physiological levels5 in basal cells (BCs) using K5CREERT2 induced the formation of luminal ER+PR+ tumours, while its expression in luminal cells (LCs) using K8CREERT2 gave rise to luminal ER+PR+ tumours or basal-like ER-PR- tumours. Concomitant deletion of p53 and expression of Pik3ca-H1047R accelerated tumour development and induced more aggressive mammary tumours. Interestingly, expression of Pik3ca-H1047R in unipotent BCs gave rise to luminal-like cells, while its expression in unipotent LCs gave rise to basal-like cells before progressing into invasive tumours. Transcriptional profiling of cells that have undergone cell fate transition upon Pik3ca-H1047R expression in unipotent progenitors demonstrate a profound oncogene-induced reprogramming of these newly formed cells and identified gene signatures, characteristic of the different cell fate switches that occur upon Pik3ca-H1047R expression in BC and LCs, which correlated with the cell of origin, tumour type and different clinical outcomes. Altogether our study identifies the cellular origin of Pik3ca-induced tumours and reveals that oncogenic Pik3ca-H1047R activates a multipotent genetic program in normally lineage-restricted populations at the early stage of tumour initiation, setting the stage for future intratumoural heterogeneity. These results have important implications for our understanding of the mechanisms controlling tumour heterogeneity and the development of new strategies to block PIK3CA breast cancer initiation.
2015-08-13 | GSE69290 | GEO
Project description:BRCA-1 Associated Protein (BAP1) is a deubiquitinating enzyme that acts as a tumour suppressor. Inactivating mutations in the BAP1 gene have been identified in many cancers including cholangiocarcinoma, hepatocellular carcinoma, mesothelioma, uveal melanoma and renal cell carcinoma. Current standard therapeutic approaches for BAP1-deficient tumours are not particularly promising, contributing to poor overall survival and disease-free survival rates. Here, we found BAP1 to mediate the turnover of the key proteins in the DNA nucleotide excision repair (NER) pathway, and therefore promotes DNA repair. Importantly, we demonstrate that the loss of functional BAP1 sensitise tumour cells to LSD1 inhibitor, SP2509, in vitro and in vivo, through further impairment of NER efficiency. When used in combination with PARP1 inhibitor, Olaparib, we show that a synergistic drug combination response is achieved. Overall, our study identifies a drug combination approach that has the potential to be exploited clinically to target BAP1 deficient tumours.
2022-09-15 | PXD028470 | JPOST Repository
Project description:Breast cancer is the most frequent cancer in women and consists of heterogeneous types of tumours that are classified into different histological and molecular subtypes1-3. Pik3ca and p53 are the two most frequently mutated genes and are associated with different types of human breast cancers4. The cellular origin and the mechanisms leading to Pik3ca-induced tumour heterogeneity remain unknown. Here, we used a genetic approach in mice to define the cellular origin of Pik3ca-derived tumours and its impact on tumour heterogeneity. Surprisingly, oncogenic Pik3ca-H1047R expression at physiological levels5 in basal cells (BCs) using K5CREERT2 induced the formation of luminal ER+PR+ tumours, while its expression in luminal cells (LCs) using K8CREERT2 gave rise to luminal ER+PR+ tumours or basal-like ER-PR- tumours. Concomitant deletion of p53 and expression of Pik3ca-H1047R accelerated tumour development and induced more aggressive mammary tumours. Interestingly, expression of Pik3ca-H1047R in unipotent BCs gave rise to luminal-like cells, while its expression in unipotent LCs gave rise to basal-like cells before progressing into invasive tumours. Transcriptional profiling of cells that have undergone cell fate transition upon Pik3ca-H1047R expression in unipotent progenitors demonstrate a profound oncogene-induced reprogramming of these newly formed cells and identified gene signatures, characteristic of the different cell fate switches that occur upon Pik3ca-H1047R expression in BC and LCs, which correlated with the cell of origin, tumour type and different clinical outcomes. Altogether our study identifies the cellular origin of Pik3ca-induced tumours and reveals that oncogenic Pik3ca-H1047R activates a multipotent genetic program in normally lineage-restricted populations at the early stage of tumour initiation, setting the stage for future intratumoural heterogeneity. These results have important implications for our understanding of the mechanisms controlling tumour heterogeneity and the development of new strategies to block PIK3CA breast cancer initiation. Luminal and basal cells, or tumour cells, from mice in which expression of PIK3CA-H1047R and YFP (and in some conditions loss of p53) was targeted in basal cells using K5CREERT2 or in luminal cells using K8CREERT2 were FACS isolated and RNA was extracted before being hybridized Affymetrix microarrays.
2015-08-13 | E-GEOD-69290 | biostudies-arrayexpress
Project description:Kidney tumours are among the most common solid tumours in children, comprising several distinct subtypes differing in many aspects, including cell-of-origin, genetics, and pathology. Pre-clinical cell models capturing the disease heterogeneity are currently lacking. Here, we describe the first paediatric cancer organoid biobank. It contains tumour and matching normal kidney organoids from over 50 children with different subtypes of kidney cancer, including Wilms tumours, malignant rhabdoid tumours, renal cell carcinomas, and congenital mesoblastic nephromas. The malignant rhabdoid tumour organoids represent the first organoid model for tumours of non-epithelial origin. The tumour organoids retain key properties of native tumours, useful for revealing patient-specific drug vulnerabilities. We further demonstrate that organoid cultures derived from Wilms tumours consist of multiple different cell types, including epithelial, stromal and blastemal-like. Our organoid biobank captures the cellular heterogeneity of paediatric kidney tumours, providing a representative collection of well-characterized models for basic cancer research, drug-screening, and personalized medicine.
2019-09-18 | GSE137544 | GEO