An integrated 4249 marker FISH/RH map of the canine genome

Breen, Matthew; Hitte, Christophe; Lorentzen, Travis D.; Thomas, Rachael; Cadieu, Édouard; Sabacan, Leah; Scott, A.; Evanno, Gwénaëlle; Parker, Heidi G.; Kirkness, Ewen F.; Hudson, R Ichard R.; Guyon, Richard; Mahairas, Gregory G.; Gelfenbeyn, Boris; Fraser, Claire M.; André, Catherine; Galibert, Francis; Ostrander, Elaine A.

doi:10.1186/1471-2164-5-65

Cited by 107 publications

(68 citation statements)

References 36 publications

(65 reference statements)

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“…To verify that each BAC pool had a unique cytogenetic location in healthy cells, all were first hybridized to metaphase preparations from six clinically healthy dogs, generated by conventional mitogen stimulation of peripheral lymphocytes (Breen et al 1999). Single locus probe (SLP) multicolor FISH analysis was performed as described previously (Breen et al 2004). …”

Section: Methodsmentioning

confidence: 99%

Comparative cytogenetic characterization of primary canine melanocytic lesions using array CGH and fluorescence in situ hybridization

Poorman

Borst

Moroff³

et al. 2014

Chromosome Res

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Melanocytic lesions originating from the oral mucosa or cutaneous epithelium are common in the general dog population, with up to 100,000 diagnoses each year in the USA. Oral melanoma is the most frequent canine neoplasm of the oral cavity, exhibiting a highly aggressive course. Cutaneous melanocytomas occur frequently, but rarely develop into a malignant form. Despite the differential prognosis, it has been assumed that subtypes of melanocytic lesions represent the same disease. To address the relative paucity of information about their genomic status, molecular cytogenetic analysis was performed on the three recognized subtypes of canine melanocytic lesions. Using array comparative genomic hybridization (aCGH) analysis, highly aberrant distinct copy number status across the tumor genome for both of the malignant melanoma subtypes was revealed. The most frequent aberrations included gain of dog chromosome (CFA) 13 and 17 and loss of CFA 22. Melanocytomas possessed fewer genome wide aberrations, yet showed a recurrent gain of CFA 20q15.3–17. A distinctive copy number profile, evident only in oral melanomas, displayed a sigmoidal pattern of copy number loss followed immediately by a gain, around CFA 30q14. Moreover, when assessed by fluorescence in situ hybridization (FISH), copy number aberrations of targeted genes, such as gain of c-MYC (80 % of cases) and loss of CDKN2A (68 % of cases), were observed. This study suggests that in concordance with what is known for human melanomas, canine melanomas of the oral mucosa and cutaneous epithelium are discrete and initiated by different molecular pathways.

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Section: Methodsmentioning

confidence: 99%

Comparative cytogenetic characterization of primary canine melanocytic lesions using array CGH and fluorescence in situ hybridization

Poorman

Borst

Moroff³

et al. 2014

Chromosome Res

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“…FISH analysis was performed using bacterial artificial chromosome (BAC) clones from the CHORI-82 canine BAC library (http://bacpac.chori.org, BACPAC Resources, Children’s Hospital Oakland Research Institute, Oakland, CA), containing the full coding sequence of the VEGFA gene (clone 152L05) and associated receptor ( VEGFR2/KDR , clone 34E11). FISH probes for VEGFA and VEGFR2/KDR were generated by incorporation of fluorescent-conjugated nucleotides into BAC DNA using nick translation, and their unique chromosomal location was verified by conventional FISH analysis of chromosome preparations from clinically healthy dogs (Breen et al 2004). Thin (5 micron) sections from FFPE tissue blocks were floated onto positively charged slides and deparaffinised with xylene.…”

Section: Methodsmentioning

confidence: 99%

Genomic profiling reveals extensive heterogeneity in somatic DNA copy number aberrations of canine hemangiosarcoma

et al. 2014

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Canine hemangiosarcoma is a highly aggressive vascular neoplasm associated with extensive clinical and anatomical heterogeneity and a grave prognosis. Comprehensive molecular characterization of hemangiosarcoma may identify novel therapeutic targets and advanced clinical management strategies, but there are no published reports of tumor-associated genome instability and disrupted gene dosage in this cancer. We performed genome-wide microarray-based somatic DNA copy number profiling of 75 primary intra-abdominal hemangiosarcomas from five popular dog breeds that are highly predisposed to this disease. The cohort exhibited limited global genomic instability, compared to other canine sarcomas studied to date, and DNA copy number aberrations (CNAs) were predominantly of low amplitude. Recurrent imbalances of several key cancer-associated genes were evident; however the global penetrance of any single CNA was low and no distinct hallmark aberrations were evident. Copy number gains of dog chromosomes 13, 24 and 31, and loss of chromosome 16, were the most recurrent CNAs involving large chromosome regions, but their relative distribution within and between cases suggests they most likely represent passenger aberrations. CNAs involving CDKN2A, VEGFA and the SKI oncogene were identified as potential driver aberrations of hemangiosarcoma development, highlighting potential targets for therapeutic modulation. CNA profiles were broadly conserved between the five breeds, although subregional variation was evident, including a near two-fold lower incidence of VEGFA gain in Golden Retrievers versus other breeds (22% versus 40%). These observations support prior transcriptional studies suggesting that the clinical heterogeneity of this cancer may reflect the existence of multiple, molecularly-distinct subtypes of canine hemangiosarcoma.

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“…We also used the dog map information in order to improve the localization of the TWIST1 gene in the cat chromosome. We used the 4249 marker FISH/RH map of the canine genome for chromosome 14 from Breen et al [39] and the FISH/RH maps available from the same author at http://cvm.ncsu.edu/mbs/breen/dog_map.htm. (c) Chromosome ideograms showing the TWIST1 gene localization in several species analysed in the present work.…”

Section: Gene Localizationmentioning

confidence: 99%

“…(c) Chromosome ideograms showing the TWIST1 gene localization in several species analysed in the present work. [37][38] and the 4249 marker FISH/RH map of the canine genome for the 14 chromosome [39] and the FISH/RH maps available at http://cvm.ncsu.edu/mbs/breen/dog_map.htm. With this comparative analysis it was possible to in silico map the TWIST1 gene to the q21.3 band from cat chromosome A2 (Fig.…”

Section: Gene Localizationmentioning

confidence: 99%

TWIST1 Gene: First Insights in Felis Catus

2014

Advances in Genome Science

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TWIST1 is thought to be a novel oncogene. Understanding the molecular mechanisms regulating the TWIST1 gene expression profiles in tumor cells may give new insights regarding prognostic factors and novel therapeutic targets in veterinary oncology. In the present study we partially isolated the TWIST1 gene in Felis catus and performed comparative studies. Several primer combinations were used based on the alignments of homologous DNA sequences. After PCR amplification, three bands were obtained, purified and sequenced. Several bioinformatic tools were utilized to carry out the comparative studies. Higher similarity was found between the isolated TWIST1 gene in Felis catus and Homo sapiens (86%) than between Homo sapiens and Rattus norvegicus or Mus musculus (75%). Partial amino acid sequence showed no change in the four species analyzed. This confirmed that coding sequences presented high similarity (~96%) between man and cat. These results give the first insights regarding the TWIST1 gene in cat but further studies are required in order to establish, or not, its role in tumor formation and progression in veterinary oncology.

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An integrated 4249 marker FISH/RH map of the canine genome

Cited by 107 publications

References 36 publications

Comparative cytogenetic characterization of primary canine melanocytic lesions using array CGH and fluorescence in situ hybridization

Comparative cytogenetic characterization of primary canine melanocytic lesions using array CGH and fluorescence in situ hybridization

Genomic profiling reveals extensive heterogeneity in somatic DNA copy number aberrations of canine hemangiosarcoma

TWIST1 Gene: First Insights in Felis Catus

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