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.

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.

Quorum sensing enables heterogeneous production of autoinducers in microbial populations, suggesting an alternative mechanism to stochastic gene expression in bistable gene-regulatory circuits to control phenotypic heterogeneity.

Using unique data from five longitudinal UK birth cohorts, four distinct subsets of genetic variants were identified as differentially associated across wheezing phenotypes from infancy to adolescence with little evidence of genetic associations spanning across different phenotypes.

Network topology and gene expression patterns in small cell lung cancer reveal two mutually opposing teams of regulators that enable multistability and consequent non-genetic heterogeneity, a clinically unsolved challenge.

Computational approach to identify reproducible genetic interactions in cancer reveals that they are enriched among protein–protein interaction pairs.

Very local molecular patterns impart precise changes in the local mechanics of individual cell-cell junctions.

Re-analysis of large gene expression datasets with state-of-the-art quantification methods reveals additional candidate genes mediating complex trait associations.

A gradient of Mib1-Dll4 within multinucleated muscle fibers maintains a continuum of metastable states within the muscle stem cell pool during tissue homeostasis.

In large vaccine trials conducted in dengue-endemic Asia and Latin America, the CYD-TDV tetravalent dengue vaccine shows limited variation in intra-serotype efficacy in the target population for vaccination (>9 years).