Characteristics PDX
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB74764 | ENA |
REPOSITORIES: ENA
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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
Project description:There is a strong need to develop patient-derived xenograft (PDX) tumor models for studying new treatment options for gastric cancer (GC). With low engraftment success, few collections of GC PDX have been reported and molecular basis of the model establishment remain largely unknown. Here we established n=27 PDX models from n=100 GC tumors and compared their characteristics to GC patient tumors based on the recent work done by ACRG and TCGA, to evaluate the representativeness and relevance of the collection for drug testing. We show that MSI, CIN and MSS/TP53- tumors were preferentially established as PDX, while MSS/EMT and EBV not and that PDX models retained histology and molecular subtypes of parental tumors. By using synapse database, we identified 48 druggable alterations that could be investigated with the collection. Counting alterations for these 48 genes in PDX compared to TCGA tumors revealed models frequently classified with heavily altered tumors but well preserved genomic alteration patterns specific of each GC subtype. The molecular analysis of n=8/27 tumors and corresponding PDX at passage P1, P2 and P3 revealed variations in somatic alteration content both at single nucleotide and chromosomal level in highly unstable MSI and CIN tumors, with changes occurring mainly at P1. In two cases, we show likely emergence of rare subclones carrying known oncogenic alterations in KRAS and PIK3CA. Significance. This study presents a resource of fully annotated GC PDX models for anticancer agent testing. We show that beside close resemblance of PDX with parental tumors, not all subtypes are established, and that the clonal selection plays a key role the establishment of certain tumors. This may have a bearing on translation of observations into the clinic and underline the need to frequently survey the molecular characteristics of the PDX models.
2020-07-15 | GSE115637 | GEO
Project description:There is a strong need to develop patient-derived xenograft (PDX) tumor models for studying new treatment options for gastric cancer (GC). With low engraftment success, few collections of GC PDX have been reported and molecular basis of the model establishment remain largely unknown. Here we established n=27 PDX models from n=100 GC tumors and compared their characteristics to GC patient tumors based on the recent work done by ACRG and TCGA, to evaluate the representativeness and relevance of the collection for drug testing. We show that MSI, CIN and MSS/TP53- tumors were preferentially established as PDX, while MSS/EMT and EBV not and that PDX models retained histology and molecular subtypes of parental tumors. By using synapse database, we identified 48 druggable alterations that could be investigated with the collection. Counting alterations for these 48 genes in PDX compared to TCGA tumors revealed models frequently classified with heavily altered tumors but well preserved genomic alteration patterns specific of each GC subtype. The molecular analysis of n=8/27 tumors and corresponding PDX at passage P1, P2 and P3 revealed variations in somatic alteration content both at single nucleotide and chromosomal level in highly unstable MSI and CIN tumors, with changes occurring mainly at P1. In two cases, we show likely emergence of rare subclones carrying known oncogenic alterations in KRAS and PIK3CA. Significance. This study presents a resource of fully annotated GC PDX models for anticancer agent testing. We show that beside close resemblance of PDX with parental tumors, not all subtypes are established, and that the clonal selection plays a key role the establishment of certain tumors. This may have a bearing on translation of observations into the clinic and underline the need to frequently survey the molecular characteristics of the PDX models.
2020-07-15 | GSE115674 | GEO
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
Project description:5 different human ccRCC PDX models treated or not with an anti chemerin monoclonal antibody
2025-07-01 | E-MTAB-15016 | biostudies-arrayexpress
Project description:FOXA1 binding in human breast cancer cells in PDX mice after different treatments
2019-06-01 | GSE101407 | GEO
Project description:We investigated the gene expression changes in a library of meso PDX models.
2022-06-17 | E-MTAB-11783 | biostudies-arrayexpress
Project description:DNA methylation in rhabdomyosarcoma PDX and PDX-derived primary cells
| PRJNA641458 | ENA
Project description:DNA methylation in rhabdomyosarcoma PDX and PDX-derived primary cells
| PRJNA641459 | ENA
Project description:H3K4me3 ChIP-seq from melanoma PDX tumours fed with different diets
2020-05-18 | GSE125822 | GEO