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Pan KRAS inhibitor selectively inactivates oncogenic signaling and tumor growth
- Authors
- Lito, PiroKim, Dongsung
- Description
Summary from GEO: "To investigate the effect of KRASi treatment on transcriptional output, we sequenced RNAs from 22 cell lines with different KRAS genotypes. We then performed gene expression profiling analysis using data obtained from RNA-seq comparing untreated and 2hr treated samples." Overall design from GEO: "Comparative gene expression profiling analysis of RNA-seq data for cells with...
- Subject
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Gene Expression ProfilingGenes, rasGenes, Tumor SuppressorRNA-Seq
- Access Rights
- Free to All
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An epigenetic program established by gene – environment interactions initiates pancreatic carcinogenesis [Set2]
- Authors
- Alonso-Curbelo, DirenaLowe, Scott W.
- Description
Summary from GEO: "Damaged tissues have increased risk of cancer development through poorly understood mechanisms. In the pancreas, tissue damage collaborates with activating mutations in the Kras oncogene to dramatically accelerate the formation of early neoplastic lesions and ultimately pancreatic cancer. By integrating genomics, single-cell chromatin assays and spatiotemporally-controlled functional...
- Subject
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CarcinogenesisChromatin Immunoprecipitation SequencingDoxycyclineEpithelial CellsGenes, rasGenomicsInterleukin-33Pancreatic Neoplasms
- Access Rights
- Free to All
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An epigenetic program established by gene – environment interactions initiates pancreatic carcinogenesis [Set1]
- Authors
- Alonso-Curbelo, DirenaLowe, Scott W.
- Description
Summary from GEO: "Damaged tissues have increased risk of cancer development through poorly understood mechanisms. In the pancreas, tissue damage collaborates with activating mutations in the Kras oncogene to dramatically accelerate the formation of early neoplastic lesions and ultimately pancreatic cancer. By integrating genomics, single-cell chromatin assays and spatiotemporally-controlled functional...
- Subject
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Chromatin Immunoprecipitation SequencingEpithelial CellsGenes, rasGenomicsInterleukin-33Pancreatic Neoplasms
- Access Rights
- Free to All
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An epigenetic program established by gene – environment interactions initiates pancreatic carcinogenesis [ATAC-seq]
- Authors
- Alonso-Curbelo, DirenaLowe, Scott W.
- Description
Summary from GEO: "Damaged tissues have increased risk of cancer development through poorly understood mechanisms. For example, in the pancreas, tissue damage collaborates with activating mutations in the Kras oncogene to dramatically accelerate the formation of early neoplastic lesions and, ultimately, pancreatic cancer. By integrating genomics, single-cell chromatin assays and spatiotemporally-controlled...
- Subject
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CarcinogenesisChromatin Immunoprecipitation SequencingEpithelial CellsGenes, rasGenomicsInterleukin-33Pancreatic Neoplasms
- Access Rights
- Free to All
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An epigenetic program established by gene – environment interactions initiates pancreatic carcinogenesis [scATAC-Seq]
- Authors
- Alonso-Curbelo, DirenaLowe, Scott W.
- Description
Summary from GEO: "Damaged tissues have increased risk of cancer development through poorly understood mechanisms. For example, in the pancreas, tissue damage collaborates with activating mutations in the Kras oncogene to dramatically accelerate the formation of early neoplastic lesions and, ultimately, pancreatic cancer. By integrating genomics, single-cell chromatin assays and spatiotemporally-controlled...
- Subject
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CarcinogenesisChromatin Immunoprecipitation SequencingEpithelial CellsGenes, rasGenomicsInterleukin-33Pancreatic Neoplasms
- Access Rights
- Free to All
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An epigenetic program established by gene – environment interactions initiates pancreatic carcinogenesis [ATACSeq_shBrd4]
- Authors
- Alonso-Curbelo, DirenaKoche, Richard PatrickLowe, Scott W.
- Description
Summary from GEO: "Damaged tissues have increased risk of cancer development through poorly understood mechanisms. In the pancreas, tissue damage collaborates with activating mutations in the Kras oncogene to dramatically accelerate the formation of early neoplastic lesions and ultimately pancreatic cancer. By integrating genomics, single-cell chromatin assays and spatiotemporally-controlled functional...
- Subject
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CarcinogenesisChromatin Immunoprecipitation SequencingEpithelial CellsGenes, rasGenomicsInterleukin-33Pancreatic Neoplasms
- Access Rights
- Free to All
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An epigenetic program established by gene – environment interactions initiates pancreatic carcinogenesis [ATACSeq_rIL33]
- Authors
- Alonso-Curbelo, DirenaKoche, Richard PatrickLowe, Scott W.
- Description
Summary from GEO: "Damaged tissues have increased risk of cancer development through poorly understood mechanisms. In the pancreas, tissue damage collaborates with activating mutations in the Kras oncogene to dramatically accelerate the formation of early neoplastic lesions and ultimately pancreatic cancer. By integrating genomics, single-cell chromatin assays and spatiotemporally-controlled functional...
- Subject
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CarcinogenesisChromatin Immunoprecipitation SequencingEpithelial CellsGenes, rasGenomicsInterleukin-33Pancreatic Neoplasms
- Access Rights
- Free to All
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An epigenetic program established by gene – environment interactions initiates pancreatic carcinogenesis [Set3]
- Authors
- Alonso-Curbelo, DirenaLowe, Scott W.
- Description
Summary from GEO: "Damaged tissues have increased risk of cancer development through poorly understood mechanisms. In the pancreas, tissue damage collaborates with activating mutations in the Kras oncogene to dramatically accelerate the formation of early neoplastic lesions and ultimately pancreatic cancer. By integrating genomics, single-cell chromatin assays and spatiotemporally-controlled functional...
- Subject
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CarcinogenesisEpithelial CellsGenes, rasGenomicsInterleukin-33Pancreatic NeoplasmsRNA-Seq
- Access Rights
- Free to All
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Cell type-dependent differential activation of ERK by oncogenic KRAS in human colon cancer and mouse intestinal epithelium
- Authors
- Brandt, RaphaelSell, ThomasLüthen, MareenUhlitz, Florian13 more author(s)...
- Description
Summary from GEO: "Mutations activating the KRAS GTPase or the BRAF kinase are frequent in colorectal cancer and are thought to constitutively activate the terminal mitogen-activated protein kinase, ERK. Using mass cytometry, we found graded phosphorylation of ERK anti-correlated with cell differentiation in patient-derived colorectal cancer organoids, and unexpectedly this gradient was observed...
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Cell DifferentiationColonic NeoplasmsGenes, rasMitogen-Activated Protein KinasesPhosphorylationProto-Oncogene Proteins B-rafRNA-SeqSingle-Cell Analysis
- Access Rights
- Free to All
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Oncogenic KRAS(G12V) and BRAF(V600E) in intestinal organoids
- Authors
- Riemer, PamelaMorkel, Marcus
- Description
Summary from GEO: "Goals of the study was to compare transcripional and phenotypic response of mouse intestinal organoid cultures to the KRAS(G12V) or BRAF(V600E)oncogenes." Overall design from GEO: "Two biological replicates of organoids with transgenic luc-tdTomato, KRAS(G12V)-tdTomato, BRAF(V600E)-tdTomato were analysed by RNA-Seq. By comparing 7-10 x 10E7 50bp paired end reads per library...
- Subject
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Epithelial CellsGenes, rasOncogenesProto-Oncogene Proteins B-rafRNA-Seq
- Access Rights
- Free to All