Solid cancers are a complex ‘ecosystem’ of diverse cell-types, whose interactions between malignant epithelial, stromal and immune populations are central in defining disease aetiology and response to therapy. Breast cancer is heterogenous and the complexity of the tumour microenvironment, and its interaction with malignant epithelial cells, remains poorly characterized. This limits the development of effective targeted therapies.
To systematically profile the cellular diversity of breast cancers, single-cell RNA sequencing (scRNA-Seq) was applied to 26 primary tumours, spanning all major molecular subtypes. We integrated transcriptomes from over 150,000 individual cells, providing a high-resolution characterization of the neoplastic, immune and stromal landscapes. CITE-SEQ was used on representative cases to profile ~150 cell-surface proteins within the tumour microenvironment. Integrating these modalities identified distinct and novel immune and stromal cellular states that may play critical roles in regulating cancer progression.
Transcriptional heterogeneity of malignant epithelial cells is observed both within and between breast tumours and is an important clinical factor. Further, we have identified confounding mixtures of entrapped normal and malignant epithelial cells within individual tumours. Matched spatial profiling confirms these observations. Large-scale copy-number changes were inferred in each cell to isolate malignant epithelial cells. To explore their transcriptional heterogeneity we developed a single-cell specific extension of the PAM50 molecular subtype classifier, and a meta-gene approach to characterize the regulatory programs of tumour cell-states. Together, these complementary approaches, for the first time, describe distinct and recurring cancer cell populations across diverse breast tumours.
Our study highlights the potential of atlas-scale single-cell projects to unravel the complex cellular heterogeneity within tumours and identify novel cell types and regulatory states underlying carcinogenesis. Such insights will guide the next-generation of therapies, which will likely be based upon an integrated understanding of the neoplastic, stromal and immune states that define a tumour and inform treatment response.