Cancer is a complex disease caused by the accumulation of multiple and successive somatic mutations, resulting in modifications in gene functions that act on specific molecular pathways, such as cycle cell control, apoptosis, differentiation and angeiogenesis. On tumor genome studies one of the aims is to identify new genes related to carcinogenesis, a lot of them possibly restrained on the chromosomal alterations. The breast cancer is an important model to genomic studies because it is a complex and heterogeneous disease, not fully understood yet. In this study, we proposed to evaluate the genomic alterations as gains and losses of DNA segments in ductal invasive breast carcinomas, seeking to identify characteristic genomic profiles of some different subtypes of this cancer. Moreover, we seek to establish a correlation between the genomic alterations found and the occurrence or not of axillary limph nodal involvement at diagnosis. It was investigated 72 breast carcinomas of ductal invasive type. The initial analysis of the tumor group detected the frequent occurrence (>20%) of gains on chromossomes 1q, 8q, 16p and 17q12-q21 region, while recurrent losses were detected mainly at 8p, 11q, 16q and on the chromossomes 13 and 18. It was identified 3828 copy number somatic alterations in genomic segments (SCNAs), with an average number of 53 per tumoral genome and an average size of 6,9 Mb. Loss events showed a higher significantly size (p<0,0001) than gain events, and high amplitude events (amplicons and homozygous losses) affected significantly smaller genomic segments. The genomic profile of SCNA differed also between the breast carcinomas according to the estrogen receptor (ER) expression status it was detected significant difference on the SCNA number per tumoral genome and on the size of this alterations, that were both greater in the group of estrogen receptor negative tumors (ER(-)) when compared to the expressing group (ER(+)). Furthermore, the genomic profile of SCNAs showed that the ER(-) group has a greater variability of affected genomic regions when compared to ER(+) group, with large losses mapped at 4q and 5q, besides focal gains that were identified at 10p and 17q; the ER(+) tumor group showed a high frequency of 16p gain. We also directed the analysis to identify relevant genomic alterations possibly related to the presence of metastasis at axillary lymph nodes at diagnosis [Nx(linf(+))]. Gains were frequent on Nx (linf(+)) tumors at 5p, 7p, 8q 10p and chromosome 19, while a frequent loss was detected at 8p; the carcinomas withouth lymph nodes metastasis exibithed a different profile, with SCNAs concentrated in other regions of the genome such as 1p and 9p losses and 16p gain. The last step of our analysis was to investigate genomic regions affected by high amplitude SCNAs (high copy number gains=amplicons, and homozygous deletions), excluding those already related to the breast tumorigenesis. This analysis was performed only on the breast carcinoma group with lymph node metastasis at diagnosis, since we were seeking to identify potential oncogenes and tumor suppressor genes associated with the cancer progression. Genes mapped on seven regions affected by high amplitude SCNAs were selected to technical validation. These new relevant candidate genes in breast cancer progression are KISS1, ADAMTS3 and HSD17B12 (mapped at amplicons) and ZBTB20, MTAP, ELF5 and RERGL (affected by homozygous deletion). The final purpose of a study like ours is to enlarge the knowledgement to obtain defined gene signatures to each tumor, possibiliting more effective individualized treatments