Part 1: Exploring the Origins of Tumors

Resolving early tumor-initiating events at single cell resolution

Tumorigenesis starts with the acquisition of a mutation within a single cell.

It is a gradual, multifactorial process driven by genetic, epigenetic, and chromosomal changes that over time disrupt the transcriptional and regulatory mechanisms, granting the cell a selective growth advantage to persist and expand. These accumulations gradually drive the transition from homeostasis to malignancy.

While different models try to explain the complexities identified in the dynamics of cancer cells, what gives a cell its tumorigenic identity is a sequence of disruptions to key biological systems, particularly those regulating cell growth, division, differentiation, and apoptosis.

Single cell RNA sequencing (scRNA-seq) revolutionizes cancer research by enabling individual cell resolution of transcriptional states, lineage relationships, and pathway activities. It provides a unique lens into how cancers originate, evolve, and resist treatment. Unlocking questions that bulk approaches cannot resolve. Below, we outline key research applications of scRNA-seq in tumor biology. 

TLDR: Every tumor begins with cells that take a wrong turn. From that point, accumulating mutations, chromosomal changes, and epigenetic shifts progressively disrupt the systems that regulate growth, differentiation, and cell death. Whether these alterations lead to malignant transformation depends on how they reshape gene expression programs and signaling networks across individual cells. Single cell RNA sequencing makes these early molecular events visible, capturing how cell states diverge, adapt, and evolve. Below, we explore how single cell analysis traces tumor origins, exposes hidden heterogeneity, and reveals the pathways that drive cancer initiation and progression.