Insight into the potential candidate genes and signaling pathways involved in lymphoma progression in dogs using a comprehensive whole blood transcriptome analysis
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ABSTRACT:
PROVIDER: PRJNA803741 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17893383_1.fastq.gz | Fastqsanger.gz | |||
| SRR17893383_2.fastq.gz | Fastqsanger.gz | |||
| SRR17893384_1.fastq.gz | Fastqsanger.gz | |||
| SRR17893384_2.fastq.gz | Fastqsanger.gz | |||
| SRR17893385_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: This goal of this study was to explore the important genes and pathways involved in canine lymphoma progression and understand the underlying molecular using RNA-Sequencing. Methods: RNAs acquired from seven pairs of lymphoma and non-lymphoma blood samples were sequenced from different breeds of dogs. Sequencing reads were preprocessed, aligned with the reference genome, assembled and expressions were estimated through bioinformatics approaches. Result: A total of 625 differentially expressed genes (DEGs) were identified between lymphoma and non–lymphoma samples, including 347 up–regulated DEGs such as SLC38A11, SCN3A, ZIC5 etc. and 278 down–regulated DEGs such as LOC475937, CSMD1, KRT14 etc. Especially, the pathway of PI3K-Akt signaling, which was directly related to the lymphoma, was enriched in KEGG analysis. In the protein-protein interaction network, CDK1 was found to be a top hub gene with highest degree of connectivity in lymphoma samples. Conclusion: We found important candidate genes and pathways for further testing in canine lymphoma.
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2010-05-22 | E-GEOD-18317 | biostudies-arrayexpress
Project description:DNA structural variation (SV) comprises a major portion of genetic diversity, but its biological impact is unclear. We propose that the genetic history and extraordinary phenotypic variation of dogs make them an ideal mammal in which to study the effects of SV on biology and disease. The hundreds of existing dog breeds were created by selection of extreme morphological and behavioral traits. And along with those traits, each breed carries increased risk for different diseases. We used array CGH to create the first map of DNA copy number variation (CNV) or SV in dogs. The extent of this variation, and some of the gene classes affected, are similar to those of mice and humans. Most canine CNVs affect genes, including disease and candidate disease genes, and are thus likely to be functional. We identified many CNVs that may be breed or breed class specific. Cluster analysis of CNV regions showed that dog breeds tend to group according to breed classes. Our combined findings suggest many CNVs are (1) in linkage disequilibrium with flanking sequence, and (2) associated with breed specific traits. We discuss how a catalog of structural variation in dogs will accelerate the identification of the genetic basis of canine traits and diseases, beginning with the use of whole genome association and candidate CNV/gene approaches. Chen WK, Swartz JD, Rush LJ, Alvarez, CE. Mapping DNA structural variation in dogs. Genome Res. 2009. 19: 500 509 PMID: 19015322
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Project description:Background: Congenital portosystemic shunts are developmental anomalies of the vascular system that cause portal blood to bypass the liver. Large-breed dogs are reported to have a predisposition for intrahepatic portosystemic shunts (IHPSS) and small-breed dogs a predisposition for extrahepatic portosystemic shunts (EHPSS). While the physiological consequences of the two types of shunt are identical, the metabolic pathways involved are probably different. The aim of this study was to gain insight into the metabolic pathways involved in the different types of portosystemic shunting. Results: Microarray analysis of mRNA expression in liver tissue from dogs with EHPSS and IHPSS revealed that the expression of 26 genes was altered in either IHPSS or EHPSS samples compared with that in liver samples from control dogs. Quantitative real-time PCR of these genes in 14 IHPSS, 17 EHPSS, and 8 control liver samples revealed a significantly different expression of ACBP, CCBL1, GPC3, HAMP, PALLD, VCAM1, and WEE1. Immunohistochemistry studies revealed that the pattern of VCAM1 and WEE1 protein expression supports the involvement of these proteins in the development of EHPSS and IHPSS, respectively. Conclusions: We identified a small list of genes possibly involved in two genetically different types of portosystemic shunt with identical pathophysiological consequences. WEE1 was found to be aberrantly expressed at an RNA and protein level in dogs with IHPSS. A decreased VCAM1 expression may play a role in the development of intrahepatic portal vascularization in dogs with EHPSS.
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