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Microarray analysis of xenograft models in use at the Developmental Therapeutics Program of the National Cancer Institute (DTP-NCI)

ABSTRACT: Xenograft models remain a cornerstone technology in the development of anti-cancer agents. The ability of immunocompromised rodents to support the growth of human tumors provides an invaluable transition between in vitro testing and clinical trials. Therefore, approaches to improve model selection are required. In this study, cDNA microarray data was generated for a collection of xenograft models at in vivo passages 1, 4 and 10 (P1, P4 and P10) along with originating cell lines (P0). These data can be mined to determine transcript expression 1) relative to other models 2) with successive in vivo passage and 3) during the in vitro (P0) to in vivo (P1) transition.

ORGANISM(S): Homo sapiens

PROVIDER: GSE48433 | GEO | 2013/07/01

SECONDARY ACCESSION(S): PRJNA210119

REPOSITORIES: GEO

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Microarray analysis of xenograft models in use at the Developmental Therapeutics Program of the National Cancer Institute (DTP-NCI)

Project description:Xenograft models remain a cornerstone technology in the development of anti-cancer agents. The ability of immunocompromised rodents to support the growth of human tumors provides an invaluable transition between in vitro testing and clinical trials. Therefore, approaches to improve model selection are required. In this study, cDNA microarray data was generated for a collection of xenograft models at in vivo passages 1, 4 and 10 (P1, P4 and P10) along with originating cell lines (P0). These data can be mined to determine transcript expression 1) relative to other models 2) with successive in vivo passage and 3) during the in vitro (P0) to in vivo (P1) transition. For originating cell lines (P0) and xenograft fragments at P1, P4 and P10, RNA was isolated, cDNA transcribed and hybridized to Affymetrix HG-U133 Plus 2.0 arrays. P0 samples have 2-3 replicates, whereas P1, P4 and P10 samples have 5 replicates. This dataset comprises a total of 823 array files.

2013-07-01 | E-GEOD-48433 | biostudies-arrayexpress

Phenotypic and genotypic stability in a preclinical model of renal cell carcinoma

Project description:Renal cell carcinomas are often resistant to conventional cytotoxic agents. Xenograft models are used for in vivo preclinical studies and drug development. The validity of these studies is highly dependent on the phenotypic and genotypic stability of the models. We evaluated the stability of six kidney tumors xenografted in nude/NMRI mice. We compared the initial sample (P0), 1st (P1) and 5th (P5) passages for the following criteria: histopathological analysis, immunohistochemistry for CK7, CD10, vimentin and p53, and DNA analysis with 10 microsatellites. We also performed CGH-array and we compared the sensitivity to sunitinib with tumor response in patients. The six xenografted tumors showed no difference between the morphology of the primary tumor and that of the xenografted tumor at P1 and P5 but we observed differences for CK7 expression in one case and for p53 expression in another. Out of 44 P0-P1-P5 groups with fully available microsatellite data, 29 (66%) showed no significant difference from P0 to P5 while 15 (34%) showed new or lost alleles. In CGH-array, genomic alterations at P5 were close to those already present in the initial tumor. We also observed similarity between the models and the patients for response to antiangiogenic treatment. We showed that the six xenograft models were phenotypically and genotypically stable across passages and showed similarity with response to treatment in patients.

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Microarray analysis of xenograft models in use at the Developmental Therapeutics Program of the National Cancer Institute (DTP-NCI)

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Using next generation sequencing to study the genetic diversity of candidate live attenuated Zika vaccines

Project description:Zika virus (ZIKV) is a mosquito-transmitted positive-sense RNA virus in the family Flaviviridae. Candidate live-attenuated vaccine (LAV) viruses with engineered deletions in the 3’UTR provide immunity and protection in animal models of ZIKV infection, and phenotypic studies show that LAVs retain protective abilities following in vitro passage. The present study investigates the genetic diversity of wild-type (WT) parent ZIKV and its candidate LAVs using next generation sequencing analysis of five sequential in vitro passages. ZIKV RNA from was transfected into Vero cells, incubated for nine days, harvested, and clarified by centrifugation to generate passage 0 (P0) ZIKV infectious clones. Subsequently, P0 ZIKVs were blind-passaged into fresh cultures to generate P1, then serially through P5. P1-P5 stocks were harvested from cell media at 4-5 days post-infection. ZIKV RNA from 3’UTR deletion mutants were transfected into Vero cells, incubated for nine days, harvested, and clarified by centrifugation to generate passage 0 (P0) ZIKV infectious clones. Subsequently, P0 ZIKVs were blind-passaged into fresh cultures to generate P1, then serially through P5. P1-P5 stocks were harvested from cell media at 4-5 days post-infection. Genetic diversity of the viruses were assessed by evaluating both the variability (or uncertainty) at each nucleotide position was determined using Shannon entropy calculations and identified single nucleotide variants (SNVs). The results showed both the parental WT and LAV derivatives increase in genetic diversity with evidence of adaptation following passage.

2020-04-13 | E-MTAB-8905 | biostudies-arrayexpress

Epithelial-to-Mesenchymal Transition of Murine PTEN-/- Liver Tumor Cells Promotes Tumor Growth and Invasion

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2010-05-28 | E-GEOD-18255 | biostudies-arrayexpress

Campylobacter jejuni murine adaptation: unadapted v. adapted

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Epithelial-to-Mesenchymal Transition of Murine PTEN-/- Liver Tumor Cells Promotes Tumor Growth and Invasion

Project description:Background: Epithelial-to-Mesenchymal Transition (EMT) is predicted to play a critical role in tumor progression and metastasis in Hepatocellular Carcinoma. Our goal was to elucidate a mechanism of tumor proliferation and metastasis using a novel murine model of EMT. Methods: 2×106 liver cells isolated from Ptenloxp/loxp;Alb-Cre+ mice, expanded from a single CD133+CD45- cell clone, Passage 0 (P0), were sequentially transplanted to obtain two passages of tumor cells, Passage 1 and 2 (P1 & P2) . Cells were analyzed for gene expression using microarray and real-time PCR. Functional analysis included cell proliferation, migration, and invasion in-vitro and orthotopic tumor growth and metastasis assays in-vivo. Results: Although P0, P1, and P2 each formed tumors consistent with mixed liver epithelium, within the P2 cells, two distinct cell types were clearly visible: cells with epithelial morphology similar to the P0 cells, and cells with fibroblastoid morphology. The P2 mesenchymal cells demonstrated increased locomotion on wound healing, increased cell invasion on Matrigel basement membrane, increased EMT associated gene Snail1, Zeb1, and Zeb2 expression, and down-regulated E-cadherin. P2 mesenchymal cells demonstrated significantly faster tumor growth compared to P2 Epithelial counterparts, with peritoneal seeding and invasion of intestine, pancreas, spleen, and lymph nodes. Furthermore, P2 mesenchymal cells secreted high levels of Hepatocyte Growth Factor (HGF), which acted in paracrine fashion to drive epithelial cells to undergo EMT. Conclusion: EMT is associated with a high rate of liver tumor proliferation, invasion, and metastasis in-vivo, which is driven by HGF in a feed-forward mechanism.

2010-05-12 | GSE18255 | GEO

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Project description:RNA-seq data on primary neurons isolated from P0 or P1 mice pups after stress using MG132 or under control conditions

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RNA sequencing of patient derived xenograft sample AML-388 using prime-seq

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