Canine tumors
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA376373 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4346330_1.fastq.gz | Fastqsanger.gz | |||
| SRR4346330_2.fastq.gz | Fastqsanger.gz | |||
| SRR4346340_1.fastq.gz | Fastqsanger.gz | |||
| SRR4346340_2.fastq.gz | Fastqsanger.gz | |||
| SRR4346350_1.fastq.gz | Fastqsanger.gz |
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Project description:The recently developed COXEN method (PMID: 17666531) has been used to successfully extrapolate gene signatures of drug sensitivity across different tumor histotypes. We wanted to explore the utility of COXEN to predict chemosensitivity in canine cancer, specifically if we could extrapolate gene signatures identified in human datasets over to canine osteosarcoma tumors. This dataset of canine osteosarcoma tumor samples has available clinical outcome data after patients had infected limbs amputated and were treated with doxorubicin and/or carboplatin. We performed microarray analysis on this panel of tumor samples for validating our COXEN prediction models for doxorubicin or carboplatin sensitivity.
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Project description:<p>The identification of efficient and sensitive biomarkers for non-invasive tests is one of the major challenges in cancer diagnosis. To address this challenge, metabolomics is widely applied for identifying biomarkers that detects abnormal changes in cancer patients. Canine mammary tumors exhibit physiological characteristics identical to those in human breast cancer and serve as a useful animal model to conduct breast cancer research. Here, we aimed to provide a reliable large-scale metabolite dataset collected from dogs with mammary tumors, using proton nuclear magnetic resonance spectroscopy. We identified 55 metabolites in urine samples from 20 benign, 87 malignant, and 49 healthy control subjects. This dataset provides details of mammary tumor-specific metabolites in dogs and insights into cancer-specific metabolic alterations that share similar molecular characteristics.</p>
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Project description:The recently developed COXEN method (PMID: 17666531) has been used to successfully extrapolate gene signatures of drug sensitivity across different tumor histotypes. We wanted to explore the utility of COXEN to predict chemosensitivity in canine cancer, specifically if we could extrapolate gene signatures identified in human datasets over to canine osteosarcoma tumors. This dataset of canine osteosarcoma tumor samples has available clinical outcome data after patients had infected limbs amputated and were treated with doxorubicin and/or carboplatin. We performed microarray analysis on this panel of tumor samples for validating our COXEN prediction models for doxorubicin or carboplatin sensitivity. Chemotherapy naive primary tumors were collected at the time of amputation and archived at the Flint Animal Cancer Center. RNA was extracted from 33 frozen archived tumor samples, followed by microarray analysis. The gene expression data was RMA preprocessed, scaled and were used as a independent test set to evaluate developed prediction models of sensitivity to doxorubicin or carboplatin. Drug predictions were than compared to clinical outcome in these patients that received doxorubicin and/or carboplatin.
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Project description:RNA-Seq of canine transmissible venereal tumors
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Project description:RNA-Seq of canine transmissible venereal tumors (CTVT)
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Project description:Human colorectal cancer (CRC) is one of the better-understood systems for studying the genetics of cancer initiation and progression. To develop a cross-species comparison strategy for identifying CRC causative gene or genomic alterations, we performed array comparative genomic hybridization (aCGH) to investigate copy number abnormalities (CNAs), one of the most prominent lesion types reported for human CRCs, in 10 spontaneously occurring canine CRCs. The results revealed for the first time a strong degree of genetic homology between sporadic canine and human CRCs. First, we saw that between 5 and 22% of the canine genome was amplified/deleted in these tumors, and that, reminiscent of human CRCs, the total altered sequences directly correlated to the tumor’s progression stage, origin, and likely microsatellite instability status. Second, when mapping the identified CNAs onto syntenic regions of the human genome, we noted that the canine orthologs of genes participating in known human CRC pathways were recurrently disrupted, indicating that these pathways might be altered in the canine CRCs as well. Lastly, we observed a significant overlapping of CNAs between human and canine tumors, and tumors from the two species were clustered according to the tumor subtypes but not the species. Significantly, compared with the shared CNAs, we found that species-specific (especially human-specific) CNAs localize to evolutionarily unstable regions that harbor more segmental duplications and interspecies genomic rearrangement breakpoints. These findings indicate that CNAs recurrent between human and dog CRCs may have a higher probability of being cancer-causative, compared with CNAs found in one species only
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Project description:Tumors frequently found in dogs include canine oral tumors, either cancerous or noncancerous. The bloodstream is an important route for tumor metastasis, particularly for late-stage oral melanoma (LOM) and late-stage oral squamous cell carcinoma (LOSCC). The present study aimed to investigate serum peptidome-based biomarkers of dogs with early-stage oral melanoma, LOM, LOSCC, benign oral tumors, chronic periodontitis and healthy controls, using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) and liquid chromatography tandem mass spectrometry.
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Project description:Microarrays was performed in 7 aCGH-matched canine primary tumors (4 DLG2 deleted, 3 DLG2 wild type) to investigate the gene expression profiles associated with DLG2 deletion in canine osteosarcoma.
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Project description:[original title] Metastatic Canine Mammary Carcinomas can be Identified by a Gene Expression Profile that partly Overlaps with Human Breast Cancer Profiles. Introduction: Similar to human breast cancer mammary tumors of the female dog are commonly associated with a fatal outcome due to the development of distant metastases. However, the molecular defects leading to metastasis are largely unknown and the value of canine mammary carcinoma as a model for human breast cancer is unclear. In this study, we analyzed the gene expression signatures associated with mammary tumor metastasis and asked for parallels with the human equivalent. Methods: Messenger RNA expression profiles of twenty-seven lymph node metastasis positive or negative canine mammary carcinomas were established by microarray analysis. Differentially expressed genes were functionally characterized and associated with molecular pathways. The findings were also correlated with published data on human breast cancer. Results: Metastatic canine mammary carcinomas had 1,011 significantly differentially expressed genes when compared to non-metastatic carcinomas. Metastatic carcinomas had a significant up-regulation of genes associated with cell cycle regulation, matrix modulation, protein folding and proteasomal degradation whereas cell differentiation genes, growth factor pathway genes and regulators of actin organization were significantly down-regulated. Interestingly, 265 of the 1,011 differentially expressed canine genes are also related to human breast cancer and, vice versa, parts of a human prognostic gene signature were identified in the expression profiles of the metastatic canine tumors. Conclusions: Metastatic canine mammary carcinomas can be discriminated from non-metastatic carcinomas by their gene expression profiles. More than one third of the differentially expressed genes are also described of relevance for human breast cancer. Many of the differentially expressed genes are linked to functions and pathways which appear to be relevant for the induction and maintenance of metastatic progression and may represent new therapeutic targets. Furthermore, dogs are in some aspects suitable as a translational model for human breast tumors in order to identify prognostic molecular signatures and potential therapeutic targets.
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