Deciphering Breast Cancer: Spatial and Molecular Insights into Tumor Evolution

In recognition of Breast Cancer Awareness Month, join us for a live webinar to uncover the complexity of tumor biology and the surprising resilience of normal tissue. This event will feature two expert-led presentations: one demonstrating how protein multiplexing and quantitative imaging uncover the hidden heterogeneity of breast tumors, and another examining how natural tissue remodeling can both suppress and influence oncogenic transformation. A live discussion and Q&A session will follow, giving you the opportunity to engage directly with leading researchers and gain valuable insights to improve cancer diagnosis, guide therapy decisions, and inform prevention strategies. All sessions will be available on demand, allowing flexible access for continued learning and engagement.

 

 

Heterogeneity is a noted feature in breast cancer and has a potential impact on cancer diagnosis, decision-making for therapy and resistance to treatment.  While morphological differences in the cancer epithelium is a recognized pathologic feature, biomarker presence and intensity are generally measured in the clinical pathology lab by a bulk assessment derived from immunohistochemical (IHC) staining.  [SEE FULL ABSTRACT]

 

 

 

Oncogenic clones frequently emerge in normal tissues as we age, progressively colonizing their host tissues for decades while remaining fully functional. This suggests that tissues possess a remarkable capacity to manage the presence of mutant cells while maintaining functional and morphological normalcy.  [SEE FULL ABSTRACT]

 

 

Learning Objectives

 

 

Don’t miss this opportunity to hear directly from leading experts as they share cutting-edge research on tumor heterogeneity and natural tissue resistance in breast cancer. Register today to secure your spot and gain new insights to advance your spatial biology research.

 

 

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Heterogeneity is a noted feature in breast cancer and has a potential impact on cancer diagnosis, decision-making for therapy and resistance to treatment.  While morphological differences in the cancer epithelium is a recognized pathologic feature, biomarker presence and intensity are generally measured in the clinical pathology lab by a bulk assessment derived from immunohistochemical (IHC) staining.  Using protein multiplexing and quantitative image analysis, we assessed inter-tumoural heterogeneity of single cell phenotypes within each molecular subtype.  Using a collection of lumpectomies that were processed using whole-mount histopathology techniques, the degree of intra-tumoural heterogeneity was also evaluated.  These quantitative analytical tools for high-dimensional protein multiplex will be described and their utilizations in spatial biology investigations will be illustrated.

 

 

Oncogenic clones frequently emerge in normal tissues as we age, progressively colonizing their host tissues for decades while remaining fully functional. This suggests that tissues possess a remarkable capacity to manage the presence of mutant cells while maintaining functional and morphological normalcy.

 

This phenomenon is particularly surprising in heavily remodeled tissues, such as the breast tissue, where oncogenic clones are effectively kept in check. The mammary epithelium is dynamically remodeled throughout the different stages of reproduction, which include consecutive estrous cycles, pregnancy, lactation, and involution. Using genetically engineered mouse models combined with lineage tracing and intravital microscopy, we investigated how these different reproductive stages influence the fate and behavior of cells carrying oncogenic mutations, and how these life events could therefore influence breast cancer risk.

 

After sporadic induction of different oncogenes, coupled to fluorophore expression, we identified intrinsic tissue-resistance mechanisms against oncogenic transformation at the cell and tissue level. By coupling these cellular dynamics with live intravital recordings of pathway activity using signaling reporters and timed single-cell transcriptomics, we further elucidated the molecular pathways driving this tissue-intrinsic resistance to oncogenic transformation.