Project description:This is a bulk RNA sequencing dataset of pancreatic tumors of varying disease grades from genetically engineered PDAC-bearing KPC mice (Pdx-1+/Cre; Kras+/LSL-G12D; Trp53+/LSL-R172H) (n = 24), and healthy controls (n = 11). KPC-derived tissues comprised early PDAC (only pancreatic remodeling and/or preinvasive lesions) to advanced disease (PDAC grades 2, 3, and 4). Mice resulting from KPC strain breeding, which did not carry Pdx-1+/Cre but only Kras+/LSL-G12D and/or Trp53+/LSL-R172H-mutations, or which carried no mutation at all, served as control animals. To identify the changes in pancreatic gene expression during PDAC development, bulk RNAseq was performed on harvested pancreatic tissues.
2025-11-25 | GSE290898 | GEO
Project description:CRKP strains sequencing
| PRJNA1106931 | ENA
Project description:RNA-seq of klebsiella and KPC-2 CRKP
Project description:Carbapenem-resistant Klebsiella pneumoniae (CRKP), particularly the K64 serotype, poses a severe clinical threat due to its high virulence and multidrug resistance. In this study, we investigated the gene expression profiles of host lung tissues to understand the pathogenesis of K64-CRKP infection and the therapeutic mechanism of Dep44, a capsule-degrading depolymerase. An acute pneumonia mouse model was established via intranasal infection with K64-CRKP. We performed high-throughput RNA sequencing (RNA-seq) on lung tissues from four experimental groups: the negative control group (healthy mice), the positive control group (K64-CRKP infected model), the treatment group (infected mice treated with Dep44), and the drug control group (healthy mice treated with Dep44). The analysis aims to elucidate the host immune response to K64-CRKP infection and evaluate how Dep44 treatment modulates these transcriptomic changes to exert its therapeutic effect.
Project description:Cadherin 11 (Cdh11), a cell-to-cell adhesion molecule, has been suggested to promote tumor growth and immunosuppression in PDAC, and Cdh11 inhibition significantly extended survival in mice with PDAC. However, the mechanisms by which Cdh11 deficiency influences PDAC progression and anti-tumor immune responses has yet to be fully elucidated. To investigate Cdh11-deficiency induced changes in PDAC tumor microenvironment (TME), we crossed p48-Cre; LSL-KrasG12D/+; LSL-Trp53R172H/+ (KPC) mice with Cdh11+/- mice and performed single-cell RNA sequencing (scRNA-seq) of the non-immune (CD45-) and immune (CD45+) compartment of KPC tumor bearing Cdh11 proficient (KPC-Cdh11+/+) and Cdh11 deficient (KPC-Cdh11+/-) mice.
2025-05-01 | GSE233915 | GEO
Project description:Whole genome sequencing of 6 CRKP strains
| PRJNA983204 | ENA
Project description:Whole genome sequencing of 6 CRKP strains
Project description:Chromosomal abnormalities are important causes of miscarriages. To delinate the chromosomal abnormalities in miscarriages, 564 miscarriages were collected and analyzed using single nucleotide polymorphism (SNP) array. 336 (59.6%) miscarriages were with abnormal copy number variations (CNVs), including 325 (57.6%) miscarriages with pathogenic CNVs and 11 (2%) miscarriages with variations of unknown significance (VOUS). The remaining 228 (40.4%) miscarriages had no clinically relevant chromosomal variants.