We have previously demonstrated that the SRC-family kinase LYN is expressed in mammary tumours from a BRCA1 loss-of-function-dependent mouse mammary tumour model, as well as in the cells of origin of such tumours, the mammary luminal epithelial stem/progenitor cells, and in human basal-like/hormone receptor negative breast cancers. We have also shown that suppressing LYN kinase activity in BRCA1-defective cell lines, as well as in in vitro cultures of Brca1-null mouse mammary tumours, is deleterious to their growth. Here, we have examined the interaction between LYN kinase and BRCA1 loss-of-function in an in vivo mouse mammary tumour model, using conditional knockout Brca1 and Lyn alleles. Comparison of tumour cohorts carrying Brca1 conditional alleles on a p53 heterozygous background and also either wild type, heterozygous or homozygous for the conditional Lyn allele, demonstrated that homozygous conditional Lyn cohorts had a small, but significant, decrease in median survival time compared to the other genotypes. However, this was confounded by the development of multiple tumours in some animals, and continued expression of LYN in some Lynfl/fl tumours (as well as low levels of LYN in some Lynwt/wt tumours). We therefore carried out a transcriptomic analysis of Lynwt/wt, Lynfl/wt and Lynfl/fl tumours, identifying differentially expressed genes between tumour groups categorised on the basis of supervised (comparison between tumours with high and low Lyn levels as measured directly by RNAseq) and unsupervised (Principal Component Analysis-based) methods. There was substantial overlap between tumours determined by the supervised and unsupervised approaches, suggesting levels of Lyn expression were, at least in part, responsible for biological differences between the tumours. The analysis also showed that Lyn high tumours had a significantly slower doubling time than Lyn low tumours and were enriched in inflammatory pathways and canonical NfkB signalling. Taken together with our previous findings, these results suggest a context-dependency to LYN signalling in mammary epithelial tumour cells, similar to its biology in B-cells.