With its primarily whole chromosome alterations tumor T47 was reminiscent of the simplex type, while T30 resembled the complex type I or “sawtooth” pattern and T49 belonged to the complex Type II or “firestorm” type. These genomic architectural classes were extended into eight subgroups and it was shown that the level of complexity of aberrations is an independent prognostic marker. Further research is needed to show whether there is a significant sub-group of canine tumors that display no gross amplifications or deletions. Several well-described cancer genes were affected by chromosomal and segmental copy-number changes in the five different tumor genomes. Tumor T47 carried an additional copy of chromosome CFA1. Gains of CFA1 were also detected in studies of other dog cancers and the proto-oncogene MYB has been mapped to this chromosome. MYB amplification has been found at high frequencies in human hereditary breast cancer. The protein is highly expressed in estrogen receptor positive breast tumors and the enhanced expression hinders apoptosis and differentiation of the cancer cells. Interestingly, the osteosarcoma T30 was the only tumor showing an amplification of CFA13 containing the Sibutramine HCl oncogenes cMYC and KIT. cMYC amplifications and CFA13 gains have been detected in canine and human cancers before. Interestingly, the tumor-suppressor gene BRCA1 was slightly amplified in T30. FGFR1 is amplified in the osteosarcoma T30 but deleted in the tubulopapillary carcinoma T52. FGFR1 amplification contributes to high metastatic potential and resistance to endocrine therapy of human breast carcinomas and is thought to be a major contributor to the poor prognosis of the luminal B subtype. Nevertheless, a downregulation of FGFR1 expression has been previously described for canine metastatic mammary carcinomas as compared with non-metastatic and normal mammary tissue. PTEN located on chromosome CFA26, was also deleted in the T30 genome, which is in line with earlier reports of human and canine mammary gland cancers. This tumor was the only one sequenced harboring a HER2/ERBB2 amplification. As assessed by ddPCR, four out of twenty tumors carried a HER2/ERBB2 amplification, which is consistent with data for human breast cancer, where the amplification has an incidence. HER2/ERBB2 overexpression is detected in canine mammary tumors to varying extends. Results seem to depend on the method of detection, since methods do not always correlate perfectly. In addition T30 carried a deletion of chromosome 22, on which the retinoblastoma-associated protein gene is located. Together, with the deletion of the RB1 regulator genes CDKN2A-CDKN2B in two of the other samples the Rb pathway was affected in 60% of the analyzed tumors. The high prevalence of abnormalities of genes of the Rb pathway has been described for canine malignancies elsewhere. Taken together the genomic aberrations seen in the five tumor genomes are heterogeneous and show Sipeimine similarities as well as differences to the conditions described in human breast cancers. Based on former comparisons between canine and human CNI a total overlap of the affected genomic regions cannot be expected. Some recurrent CNIs are species-specific because they arise from evolutionary unstable hypervariable regions as found for example on human chromosome 8p23.1.