Murine models of pancreatic cancer: KPC
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA836890 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We harvested and sequenced the spontaneous pancreatic tumor generated by a 6-month-old KPC mouse (KrasLSL-G12D; Trp53LSL-R172H; Ptf1a-Cre).
2022-10-04 | GSE202651 | GEO
Project description:We established a mouse model of KrasG12D, Trp53-/- and Sf3b1-K700E murine pancreatic cancer to elucidate the impact of the SF3B1 mutation found in human PDAC on the KPC mouse model.
2022-06-07 | GSE203339 | GEO
Project description:Bulk RNA sequencing of sorted peri-pancreatic LN cDC1s from different stages of neoplastic development in the KPC mouse model of pancreatic adenocarcinoma.
2020-04-15 | GSE126361 | GEO
Project description:Recently, Bailey et al (2016, Nature) defined four subtypes of pancreatic cancer that are associated with distinct histopathological characteristics and differential survival, namely, Squamous, Pancreatic Progenitor, Immunogenic, and ADEX (Aberrantly Differentiated Endocrine eXocrine). We set out to assess by RNASeq whether loss of CXCR2 was significantly associated with a specific PDAC subtype. Pancreatic tumors were harvested from KPC or KPC Cxcr2-/- mice at endpoint (n=5 v 5), RNA prepared, and RNASeq analysis carried out. Reads were analysed using the bcbio-nextgen framework (https://bcbio-nextgen.readthedocs.org/en/latest/). After quality control and adaptor trimming, reads were aligned to the mouse genome build (UCSC mouse mm10) using STAR. Counts for known genes were generated using the function featureCounts in the R/Bioconductor package \Rsubread\. The R/Bioconductor package edgeR was used to identify differentially expressed genes.
2018-03-31 | E-MTAB-4659 | biostudies-arrayexpress
Project description:Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy that resists current treatments. To test epigenetic therapy against this cancer we used the DNA demethylating drug 5-aza-2’-deoxycytidine (DAC) in a KrasLSL-G12D; p53LSL-R270H/+; Pdx1-cre; Brca1flex2/flex2 (KPC-Brca1) mouse model of aggressive stroma-rich PDAC. In untreated tumors, we found globally decreased 5-methyl-cytosine (5mC) in malignant epithelial cells and in cancer-associated myofibroblasts (CAFs), and increased amounts of 5-hydroxymethyl-cytosine (5HmC) in CAFs, in progression from pancreatic intraepithelial neoplasia (PanIN) to PDAC. DAC further reduced DNA methylation and slowed PDAC progression, markedly extending survival in an early treatment protocol and significantly though transiently inhibiting tumor growth when initiated later, without adverse side effects. Escaping tumors contained areas of sarcomatoid transformation with disappearance of CAFs. Mixing-allografting experiments and proliferation indices showed that DAC efficacy was due to inhibition of both the malignant epithelial cells and the stromal CAFs. Expression profiling and immunohistochemistry highlighted DAC-induction of STAT1 in the tumors, and DAC plus gamma-interferon produced an additive anti-proliferative effect on PDAC cells. DAC induced strong expression of the testis antigen DAZL in CAFs. These data show that DAC is effective against PDAC in vivo and provide a rationale for future studies combining hypomethylating agents with cytokines and immunotherapy. Treatment of a short-term explant culture of malignant epithelial cells from a KPC-Brca1 mouse pancreatic carcinoma, with 0.5 micromolar 5-aza-dC (decitabine; DAC) for 48 hours. The experiment includes 3 replicate plates untreated and 3 replicates treated.
2013-01-01 | E-GEOD-42365 | biostudies-arrayexpress
Project description:Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy that resists current treatments. To test epigenetic therapy against this cancer we used the DNA demethylating drug 5-aza-2’-deoxycytidine (DAC) in a KrasLSL-G12D; p53LSL-R270H/+; Pdx1-cre; Brca1flex2/flex2 (KPC-Brca1) mouse model of aggressive stroma-rich PDAC. In untreated tumors, we found globally decreased 5-methyl-cytosine (5mC) in malignant epithelial cells and in cancer-associated myofibroblasts (CAFs), and increased amounts of 5-hydroxymethyl-cytosine (5HmC) in CAFs, in progression from pancreatic intraepithelial neoplasia (PanIN) to PDAC. DAC further reduced DNA methylation and slowed PDAC progression, markedly extending survival in an early treatment protocol and significantly though transiently inhibiting tumor growth when initiated later, without adverse side effects. Escaping tumors contained areas of sarcomatoid transformation with disappearance of CAFs. Mixing-allografting experiments and proliferation indices showed that DAC efficacy was due to inhibition of both the malignant epithelial cells and the stromal CAFs. Expression profiling and immunohistochemistry highlighted DAC-induction of STAT1 in the tumors, and DAC plus gamma-interferon produced an additive anti-proliferative effect on PDAC cells. DAC induced strong expression of the testis antigen DAZL in CAFs. These data show that DAC is effective against PDAC in vivo and provide a rationale for future studies combining hypomethylating agents with cytokines and immunotherapy. Treatment of a short-term explant culture of cancer-associated fibroblasts (CAFs) from a KPC-Brca1 mouse pancreatic carcinoma, with 2 micromolar 5-aza-dC (decitabine; DAC) for 48 hours. The experiment includes 3 replicate plates untreated and 3 replicates treated.
2013-01-01 | E-GEOD-42364 | biostudies-arrayexpress
Project description:These experiments aim to determine global gene expression patterns in WT vs KPC isolated pancreatic fibroblasts
2017-02-09 | GSE76498 | GEO
Project description:We identified that Gsdmc gene is important for pancreatic cancer in tumorigenesis and metastasis. Here we used KPC mice (LSL-KrasG12D/+; p53f/f; Pdx1-Cre)-derived cancer cells, KPC cells in short, to check the effects of Gsdmc knockdown on primary tumor growth and metastasis. The results suggested that Gsdmc knockdown inhibited the expression of key genes in multiple pathways, including cell migration, epithelial-mesenchymal transition, immune cell recruitment, and so on. The data deposited here provides the transcriptomic alteration of KPC cells after Gsdmc knockdown with two shRNAs.
2024-09-18 | GSE250062 | GEO
Project description:Single-cell analysis of KPC pancreatic tumor cells
2019-02-15 | GSE126539 | GEO
Project description:To study possible CNVs and genes affected by CNVs in the cancer associated fibroblast populations of pancreatic cancers, we applied single cell sequencing technology (10x Genomics) to identify different subpopulations in murine KPC pancreatic tumors and pancreata of age- and gender-matched non-tumor bearing mice. Single cell RNA sequencing (scRNA-Seq) identified three major CAF subpopulations which were interrogated together with the ductal carcinoma population for CNVs using a previously reported inferCNV algorithm. Fibroblasts and ductal cells identified by scRNA-Seq in normal, uninvolved pancreas were used as reference and inferCNVs in both CAF and ductal carcinoma cells were validated with CNVs previously reported within a large high-resolution array comparative genomic hybridization (aCGH) of KPC tumors. CNVs were exclusively detected in the myelofibroblastic cancer associated fibroblast (myCAF) subpopulation and not in the other CAF phenotypes. In comparison to ductal carcinoma cells, myCAFs were less frequently affected by CNVs. CNVs in the myCAFs which were unique for the myCAFs and not shared with gene loci affected by CNVs in ductal carcinoma cells included known regulators of CAF activation, CAF-mediated cancer cell invasion, or antagonists of TGFβ signaling.
2021-07-29 | GSE180859 | GEO