Affymetrix SNP array data for Ovarian Cancer Samples
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE71522 | GEO | 2016/08/11
SECONDARY ACCESSION(S): PRJNA291448
REPOSITORIES: GEO
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Project description:This study aimed to generate a new panel of comprehensively, genomically characterized high-grade serous ovarian carcinoma (HGSOC) cell line and xenograft models. Multidimensional genomic data were generated and compared between cell lines/xenografts and the tumours they were derived from, indicating the cell lines/xenografts are highly similar to their patient-matched tumours. Cell line/xenograft data were also compared to TCGA ovarian tumours to show the cell lines are good models of clinical HGSOC. Illumina HT-12 v4 arrays were performed according to the manufacturer's directions on total RNA extracted from i) tumour cells purified from ovarian tumour ascites, and ii) established cell lines. Evaluation of the similarity in copy number/methylation/gene expression/mutational profiles of cell lines/tumours/xenografts was performed.
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Project description:This study aimed to generate a new panel of comprehensively, genomically characterized high-grade serous ovarian carcinoma (HGSOC) cell line and xenograft models. Multidimensional genomic data were generated and compared between cell lines/xenografts and the tumours they were derived from, indicating the cell lines/xenografts are highly similar to their patient-matched tumours. Cell line/xenograft data were also compared to TCGA ovarian tumours to show the cell lines are good models of clinical HGSOC. Illumina HumanMethylation450 arrays were performed according to the manufacturer's directions on DNA extracted from i) tumour cells purified from ovarian tumour ascites, and ii) established cell lines. Evaluation of the similarity in copy number/methylation/gene expression/mutational profiles of cell lines/tumours/xenografts was performed.
2016-08-11 | E-GEOD-71523 | biostudies-arrayexpress
Project description:This study aimed to generate a new panel of comprehensively, genomically characterized high-grade serous ovarian carcinoma (HGSOC) cell line and xenograft models. Multidimensional genomic data were generated and compared between cell lines/xenografts and the tumours they were derived from, indicating the cell lines/xenografts are highly similar to their patient-matched tumours. Cell line/xenograft data were also compared to TCGA ovarian tumours to show the cell lines are good models of clinical HGSOC.
2016-08-11 | GSE71524 | GEO
Project description:This study aimed to generate a new panel of comprehensively, genomically characterized high-grade serous ovarian carcinoma (HGSOC) cell line and xenograft models. Multidimensional genomic data were generated and compared between cell lines/xenografts and the tumours they were derived from, indicating the cell lines/xenografts are highly similar to their patient-matched tumours. Cell line/xenograft data were also compared to TCGA ovarian tumours to show the cell lines are good models of clinical HGSOC.
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Project description:This study aimed to generate a new panel of comprehensively, genomically characterized high-grade serous ovarian carcinoma (HGSOC) cell line and xenograft models. Multidimensional genomic data were generated and compared between cell lines/xenografts and the tumours they were derived from, indicating the cell lines/xenografts are highly similar to their patient-matched tumours. Cell line/xenograft data were also compared to TCGA ovarian tumours to show the cell lines are good models of clinical HGSOC. Affymetrix SNP 6 arrays were performed according to the manufacturer's instructions on genomic DNA extracted from i) tumour cells purified from ovarian tumour ascites, ii) established cell lines, iii) patient derived xenografts, and iv) lymphoblast lines. Evaluation of the similarity in copy number/methylation/gene expression/mutational profiles of cell lines/tumours/xenografts was performed.
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Project description:High-grade serous ovarian carcinoma (HGSOC) is the most lethal gynecological cancer with few effective targeted therapies. HGSOC tumors exhibit genomic instability with frequent alterations in the protein kinome; however, only a small fraction of the kinome has been therapeutically targeted in HGSOC. Using multiplexed inhibitor beads and mass spectrometry (MIB-MS), we mapped the kinome landscape of HGSOC patient tumors and tumors isolated from HGSOC patient-derived xenograft (PDX) models. Kinome profiling of HGSOC tumors uncovered a prevalent MIB-MS kinome signature consisting of established HGSOC driver kinases, as well as several kinases previously unexplored in HGSOC. Loss-of-function analysis targeting the tumor kinome signature in HGSOC cells nominated CDC42BPA (also known as MRCKA) as a putative therapeutic target. Characterization of MRCKA knockdown in established HGSOC cell lines demonstrated MRCKA was integral to signaling that regulated the cell cycle checkpoint and focal adhesion/ actin remodeling, and depletion of MRCKA impaired cell migration, proliferation and survival. Moreover, small molecule inhibition of MRCKA using BDP9066 inhibited cell growth and induced apoptosis in HGSOC cells, as well as blocked spheroid formation, supporting MRCKA as a novel therapeutic target for the treatment of HGSOC.
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Project description:High-grade serous ovarian carcinoma (HGSOC) is the most lethal gynecological cancer with few effective targeted therapies. HGSOC tumors exhibit genomic instability with frequent alterations in the protein kinome; however, only a small fraction of the kinome has been therapeutically targeted in HGSOC. Using multiplexed inhibitor beads and mass spectrometry (MIB-MS), we mapped the kinome landscape of HGSOC patient tumors and tumors isolated from HGSOC patient-derived xenograft (PDX) models. Kinome profiling of HGSOC tumors uncovered a prevalent MIB-MS kinome signature consisting of established HGSOC driver kinases, as well as several kinases previously unexplored in HGSOC. Loss-of-function analysis targeting the tumor kinome signature in HGSOC cells nominated CDC42BPA (also known as MRCKA) as a putative therapeutic target. Characterization of MRCKA knockdown in established HGSOC cell lines demonstrated MRCKA was integral to signaling that regulated the cell cycle checkpoint and focal adhesion/ actin remodeling, and depletion of MRCKA impaired cell migration, proliferation and survival. Moreover, small molecule inhibition of MRCKA using BDP9066 inhibited cell growth and induced apoptosis in HGSOC cells, as well as blocked spheroid formation, supporting MRCKA as a novel therapeutic target for the treatment of HGSOC.
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Project description:High-grade serous ovarian carcinoma (HGSOC) is the most lethal gynecological cancer with few effective targeted therapies. HGSOC tumors exhibit genomic instability with frequent alterations in the protein kinome; however, only a small fraction of the kinome has been therapeutically targeted in HGSOC. Using multiplexed inhibitor beads and mass spectrometry (MIB-MS), we mapped the kinome landscape of HGSOC patient tumors and tumors isolated from HGSOC patient-derived xenograft (PDX) models. Kinome profiling of HGSOC tumors uncovered a prevalent MIB-MS kinome signature consisting of established HGSOC driver kinases, as well as several kinases previously unexplored in HGSOC. Loss-of-function analysis targeting the tumor kinome signature in HGSOC cells nominated CDC42BPA (also known as MRCKA) as a putative therapeutic target. Characterization of MRCKA knockdown in established HGSOC cell lines demonstrated MRCKA was integral to signaling that regulated the cell cycle checkpoint and focal adhesion/ actin remodeling, and depletion of MRCKA impaired cell migration, proliferation and survival. Moreover, small molecule inhibition of MRCKA using BDP9066 inhibited cell growth and induced apoptosis in HGSOC cells, as well as blocked spheroid formation, supporting MRCKA as a novel therapeutic target for the treatment of HGSOC.
2020-02-19 | PXD015782 | Pride
Project description:High-grade serous ovarian carcinoma (HGSOC) is the most lethal gynecological cancer with few effective targeted therapies. HGSOC tumors exhibit genomic instability with frequent alterations in the protein kinome; however, only a small fraction of the kinome has been therapeutically targeted in HGSOC. Using multiplexed inhibitor beads and mass spectrometry (MIB-MS), we mapped the kinome landscape of HGSOC patient tumors and tumors isolated from HGSOC patient-derived xenograft (PDX) models. Kinome profiling of HGSOC tumors uncovered a prevalent MIB-MS kinome signature consisting of established HGSOC driver kinases, as well as several kinases previously unexplored in HGSOC. Loss-of-function analysis targeting the tumor kinome signature in HGSOC cells nominated CDC42BPA (also known as MRCKA) as a putative therapeutic target. Characterization of MRCKA knockdown in established HGSOC cell lines demonstrated MRCKA was integral to signaling that regulated the cell cycle checkpoint and focal adhesion/ actin remodeling, and depletion of MRCKA impaired cell migration, proliferation and survival. Moreover, small molecule inhibition of MRCKA using BDP9066 inhibited cell growth and induced apoptosis in HGSOC cells, as well as blocked spheroid formation, supporting MRCKA as a novel therapeutic target for the treatment of HGSOC.
2020-02-19 | PXD015783 | Pride
Project description:High-grade serous ovarian carcinoma (HGSOC) is the most genomically complex cancer, characterised by ubiquitous TP53 mutation, profound structural variation and heterogeneity. Multiple mutational processes driving chromosomal instability can be distinguished by specific copy number signatures. To develop clinically relevant models of these mutational processes we derived 15 continuous HGSOC patient-derived organoids (PDOs) and provide detailed transcriptomic and genomic profiles using shallow whole genome sequencing single cell and bulk analysis. We show that PDOs comprise communities of different clonal populations and represent models of CCNE1 amplification, chromothripsis, tandem-duplicator phenotype and whole genome duplication. PDOs can also be used as exploratory tools to study transcriptional effects of copy number alterations as well as compound-sensitivity tests. In summary, HGSOC PDO cultures provide a genomic tool for studies of specific mutational processes and precision therapeutics.
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