Phenotypic diversity and cell state transition (i.e., acquisition of a CD44+/CD24- cell state or exposure to TGF-beta) can spur intra-tumor genetic heterogeneity and contribute to acquired resistance.

Copy number alteration heterogeneity exists in many shapes and forms in breast cancer genomes and single-cell genomics is a powerful tool to further our understanding of its nature and significance.

The unraveling of distinct mammary tumor hierarchies in various mouse models of breast cancer emphasizes the need to account for specific cell states with potentially varying therapeutic vulnerabilities in tumors.

Tumor morphological patterns are linked to distinct transcriptional profiles and may indicate the need for a multi-site tumor sampling in gene expression-based studies.

ScRNA-seq of diverse pheochromocytoma patients reveals distinct microenvironment characteristics and supports an informative molecular classification system.

A new, high-throughput in vivo MHC-I peptide minigene library platform shows that the naive immune system cannot eliminate cells presenting immunogenic antigens found at low frequencies within a growing tumor.

Tumor-growth-factor-beta signaling helps cancer cells to evolve and become resistant to drugs by down-regulating accurate DNA repair.

Combined analyses of transcriptome and chromatin accessibility elucidated the mechanisms underlying cancer cell lines response to antitumor candidates and provided a versatile perturbation-informed basal signature able to predict drug sensitivity.

Integrated molecular analysis demonstrated that colorectal cancer can be classified into four molecular subtypes (proliferative, immunomodulatory, immunosuppressed, and immune-excluded subtypes), providing valuable insight into the intricate relationship between tumor microenvironment heterogeneity and various clinical phenotypes.

A neutrophil-CAF-tumor cell IL-1β/IL-6/STAT-3 signaling axis in the pancreatic tumor microenvironment underlies the association between neutrophil-to-lymphocyte ratio dynamics and pathologic response in patients with pancreatic ductal adenocarcinoma undergoing neoadjuvant therapy.