The breast tumour is a complex ecosystem comprising malignant cancer cells and surrounding immune and stromal cells. Cancer immunotherapy in the last 15 years has shed light on targeting immune cells to reinstate anti-tumour immunity in patients. However, the immune targets employed in current clinical trials for breast cancer patients are predominantly limited to T cell immune checkpoints (Debien et al., 2023), while much of the immune repertoire remains unexplored. To identify potential targets in the immune microenvironment of breast cancer, two spectral flow cytometry panels were established to characterise both myeloid and lymphoid changes in precancerous tissue and tumours using six genetically engineered mouse models. Some models showed significant changes in immune populations at the hyperplastic stage, suggesting a host immune response to early neoplasia. At the tumour stage, the composition of local immune components underwent profound changes: neutrophils represented the most dominant population in some models, whereas macrophages prevailed in others. Along with the myeloid expansion, the lymphoid compartment displayed enhanced proliferation, over-activation, and potential exhaustion. Interestingly, comparisons across tumours revealed intra-model heterogeneity as well as model-specific immune remodelling features. To further resolve the heterogeneity and dynamics within the myeloid population in mouse mammary gland oncogenesis, single-cell RNA sequencing (scRNA-seq) was exploited. The myeloid molecular subset proportions shifted during tumour formation, and the same subset dominated in tumours of three models. Using immunofluorescence confocal microscopy, we revealed distinct myeloid subsets with differential spatial pattern, indicating diverse roles played by myeloid subsets in breast cancer development. These findings highlight extensive and intricate remodelling of the immune microenvironment during tumorigenesis with implications for new immunotherapy targets.