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PLoS One ; 10(5): e0126371, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-25955013

RESUMO

BACKGROUND: Copy number aberrations frequently occur during the development of many cancers. Such events affect dosage of involved genes and may cause further genomic instability and progression of cancer. In this survey, canine SNP microarrays were used to study 117 canine mammary tumours from 69 dogs. RESULTS: We found a high occurrence of copy number aberrations in canine mammary tumours, losses being more frequent than gains. Increased frequency of aberrations and loss of heterozygosity were positively correlated with increased malignancy in terms of histopathological diagnosis. One of the most highly recurrently amplified regions harbored the MYC gene. PTEN was located to a frequently lost region and also homozygously deleted in five tumours. Thus, deregulation of these genes due to copy number aberrations appears to be an important event in canine mammary tumour development. Other potential contributors to canine mammary tumour pathogenesis are COL9A3, INPP5A, CYP2E1 and RB1. The present study also shows that a more detailed analysis of chromosomal aberrations associated with histopathological parameters may aid in identifying specific genes associated with canine mammary tumour progression. CONCLUSIONS: The high frequency of copy number aberrations is a prominent feature of canine mammary tumours as seen in other canine and human cancers. Our findings share several features with corresponding studies in human breast tumours and strengthen the dog as a suitable model organism for this disease.


Assuntos
Neoplasias Mamárias Animais/patologia , PTEN Fosfo-Hidrolase/genética , Proteínas Proto-Oncogênicas c-myc/genética , Alelos , Animais , Aberrações Cromossômicas , Colágeno Tipo IX/genética , Hibridização Genômica Comparativa , Citocromo P-450 CYP2E1/genética , Variações do Número de Cópias de DNA , Cães , Feminino , Humanos , Inositol Polifosfato 5-Fosfatases , Perda de Heterozigosidade , Neoplasias Mamárias Animais/metabolismo , Monoéster Fosfórico Hidrolases/genética , Ploidias , Polimorfismo de Nucleotídeo Único
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