Breast cancer (BC) is a prevalent disease in our country. BC are classified into molecular subtypes based on gene expression variations: normal breast-like, luminal A, luminal B, HER2, and basal-like. We previously reported significant differences in TP73 methylation among these subtypes. Luminal A tumors often show unmethylated TP73, while all basal-like tumors exhibit methylated TP73. The p73 protein is structurally and functionally similar to the p53 tumor protein. However, the TP73 gene produces multiple isoforms that have antagonistic properties. Here, we analyzed the expression differences of TP73 exons in the TCGA breast cancer RNASeq dataset using EdgeR tools. This allowed us to identify the prevalent isoforms expressed in each BC subtype. Additionally, we examined the expression and subcellular localization of the TA-p73 and ΔNp73 isoforms in 137 invasive breast tumors and 5 BC cell lines using immunohistochemistry and immunofluorescence techniques. Our results revealed that TP73 is overexpressed in all BC subtypes. Surprisingly, this up-regulation depends mostly on the over-expression of exons corresponding to the TAp73-specific domains. Notably, significant downregulation of the 4th exon was observed in all subtypes, suggesting a differential gene promoter usage favoring TAp73 isoform expression. Furthermore, we found that the TA-p73 isoform predominantly localized in the nucleus of luminal BC tumors, while basal-like and ErbB2+ tumors exhibited cytoplasmic expression. In contrast, the ΔNp73 isoform was mainly localized in the cytoplasm of all breast tumor subtypes. Additionally, the TA-p73 isoform was mostly nuclear in luminal BC cell lines, whereas it was primarily cytoplasmic in basal-like cell lines. These findings provide valuable insights into the expression patterns and subcellular localization of TP73 isoforms in different BC subtypes, highlighting the complex biology of TP73 and its potential implications for prognosis and treatment.