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18 PDX of triple-negative breast cancer genotyped with SNP6 Affymetrix arrays

ABSTRACT: To characterize Homologous recombination deficiency (BRCAness) in triple-negative breast cancer PDX models genomic signature was utilized. After normalization using Genotyping Console we obtained absolute copy number profiles using the GAP software (Popova et al, Genome Biol, 2009). The number of Large-scale State Transitions (LSTs) was used to annotate PDX as BRCAness or not (Popova et al, Cancer Res 2012).

ORGANISM(S): Homo sapiens

SUBMITTER: Tatiana Popova

PROVIDER: E-MTAB-8654 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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22 PDX of triple-negative breast cancer genotyped with Affymetrix Cytoscan HD

Project description:To characterize Homologous recombination deficiency (BRCAness) in triple-negative breast cancer PDX models genomic signature was utilized. After normalization using ChAS we obtained absolute copy number profiles using the GAP software (Popova et al, Genome Biol, 2009). The number of Large-scale State Transitions (LSTs) was used to annotate PDX as BRCAness or not (Popova et al, Cancer Res 2012).

2020-01-01 | E-MTAB-8653 | biostudies-arrayexpress

De novo homozygous deletion of segmental KAL1 and entire STS cause Kallmann syndrome and X-linked ichthyosis in a Chinese family

Project description:Kallmann syndrome is a genetically heterogeneous condition and a treatable form of male infertility. Defects in KAL1 gene have been implicated in Kallmann syndrome, which can be associated with X-linked ichthyosis in contiguous gene syndromes. In order to uncover the genetic cause of two brothers with Kallmann syndrome and X-linked ichthyosis, a custom semiconductor targeted resequencing panel to detect seventeen Kallmann syndrome causal genes and STS gene was designed. Next-generation sequencing was performed using this panel in the two affected brothers and their normal parents. To validate the result, we applied CytoScanâ¢ HD array, quantitative real-time PCR and direct PCR electrophoresis analysis with the participants. The patients received clinical assessment, human chorionic gonadotropin treatment and follow-up for 39 months. The results showed that the two affected siblings have the same de novo deletion at Xp22.3 including exons 9-14 of KAL1 gene and entire STS gene but showed different phenotypes in some respects. The secondary sex characteristics of the patients were greatly improved after treatment. We firstly reported that a de novo homozygous deletion contribute to KS with bilateral cryptorchidism and unilateral renal agenesis or normal kidney development and developed a cost-effective and reliable semiconductor targeted resequencing panel for genetic diagnosis of Kallmann syndrome in routinely obtained samples. One of the two brothers with Kallmann syndrome and X-linked ichthyosis was analyzed for validation the results of the deletion detected by next-generation sequencing.

2015-12-05 | E-GEOD-58793 | biostudies-arrayexpress

CNV_Kasumi-1_U-2 OS_Patient

Project description:Arrays were used to determine the copy numbers of genomic regions harboring gene mutations and to identify heterozygous single nucleotide polymorphisms (SNPs) that were located close to these gene mutations. The gene mutations were identified through the COSMIC database and sequencing. The SNPs were used as control in single cell genetic analyses.

2016-10-10 | E-MTAB-4950 | biostudies-arrayexpress

Gene Expression data from Pdx-1CreAPC+/LP53L/L pancreatic ductal adenocarcinoma (PDAC) cells versus Pdx-1CreP53L/L normal pancreatic ductal cells

Project description:Analysis of primary PDAC cells established from Pdx-1CreAPCL/+p53L/L and Pdx-1Crep53L/L mice. APC haploinsufficiency combined with P53 loss in the pancreas drives MCN progression in mice. Results provide insight into molecular mechanisms invloved in the MCN formation of Pdx-1Cre APCL/+P53L/L mice. Pdx-1CreAPC+/LP53L/L PDAC cell lines and 2 Pdx-1CreP53L/L ductal cell lines were analyzed.

2014-10-01 | E-GEOD-61894 | biostudies-arrayexpress

CGH analysis of an extramedullary muletiple myeloma PDX

Project description:A patient derived orthotopic xenograft (PDOX) was generated from a patient with an aggressive EMM to study in-depth genetic and epigenetic events and drug responses related to extramedullary disease. One of these studies was the evaluation of genetic imbalances by Affymetrix Cytoscan 750K array. The PDOX was derived from a fresh punch of an extramedullary cutaneous lesion that was orthotopically implanted in a NSG mouse. The PDOX mimicked histologic and phenotypic features of patient’s tumor. Cytogenetic studies revealed a hyperploid genome with multiple genetic poor-prognosis alterations. Copy number alterations were detected in all chromosomes.

2021-06-18 | E-MTAB-10630 | biostudies-arrayexpress

Expression profiling of DLBCL subtypes PDX model

Project description:Identify the PDX model of DLBCL subtypes by the microarray expression profiling Four samples without relplicates

2016-02-29 | E-GEOD-65988 | biostudies-arrayexpress

Pdx-1 activates islet M-NM-1- and M-NM-2-cell proliferation via a TRPC3/6- and ERK 1/2-regulated mechanism

Project description:The homeodomain transcription factor, Pdx-1, has important roles in pancreatic development and M-NM-2-cell function and survival. In the present study, we demonstrate that adenovirus-mediated overexpression of Pdx-1 in rat or human islets also stimulates cell replication. Moreover, co-overexpression of Pdx-1 with another homeodomain transcription factor, Nkx6.1, has an additive effect on proliferation compared to either factor alone, implying discrete activating mechanisms. Consistent with this, Nkx6.1 stimulates mainly M-NM-2-cell proliferation, whereas Pdx-1 stimulates both M-NM-1- and M-NM-2-cell proliferation. Furthermore, cyclins D1/D2 are upregulated by Pdx-1 but not by Nkx6.1, and inhibition of cdk4 blocks Pdx-1- but not Nkx6.1-stimulated islet cell proliferation. Genes regulated by Pdx-1 and not Nkx6.1 were identified by microarray analysis. Two members of the transient receptor potential cation (TRPC) channel family, TRPC3 and TRPC6, are upregulated by Pdx-1 overexpression, and siRNA-mediated knockdown of TRPC3/6 or TRPC6 alone inhibits Pdx-1-induced but not Nkx6.1-induced islet cell proliferation. Pdx-1 also stimulates ERK1/2 phosphorylation, an effect partially blocked by knockdown of TRPC3/6, and blockade of ERK1/2 activation with a MEK1/2 inhibitor partially impairs Pdx-1-stimulated proliferation. These studies define a pathway by which overexpression of Pdx-1 activates islet cell proliferation that is distinct from and additive to a pathway activated by Nkx6.1. We identified genes that were upregulated or downregulated at 48 h with Pdx-1 overexpression as compared to untreated and M-NM-2gal controls. We set up a microarray using primary rat islets that were left untreated or transduced with adenoviruses overexpressing M-NM-2gal or Pdx-1 for 48 h.

2013-09-01 | E-GEOD-49786 | biostudies-arrayexpress

Quantification strategy for PDX MS data

Project description:Data interpreting of PDX proteome is still a problem because with the growth of human cancerous tissue in an immunodeficient mouse, the endothelial cells and fibroblasts from the host mouse replaced human stromal components, making PDX sample a mixture of human and mouse cells. In this study, we created four human and mouse protein mixtures with different human protein percentages as the standard testing sets. We established an easy algorithm to fit the known proportions and used this strategy on a pair of PDX samples. Our data suggested that our new algorithm is feasible and may help to offer more information on PDX proteome data analysis.

2022-05-19 | PXD008611 | Pride

RNAseq analysis of meso PDX models

Project description:We investigated the gene expression changes in a library of meso PDX models.

2022-06-17 | E-MTAB-11783 | biostudies-arrayexpress

ChIP-Chip and SACO Analysis of Pdx-1 binding in NIT-1 Insulinoma Cells

Project description:The BCBC Promoter Chip 5B was used to identify genomic targets of Pdx-1 binding. Genomic DNA from mouse NIT-1 insulinoma cells was immunoprecipitated with a Pdx-1 Antibody, PCR amplified, and labeled to the chip. All hybridizations were versus a common reference sample which was a labeled IgG IP. Additionally a Pdx1 SACO library for NIT-1 cells was generated.

2014-11-21 | E-MTAB-3126 | biostudies-arrayexpress

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