ArticleCell genomics2026
Co-mapping clonal and transcriptional heterogeneity in somatic evolution via GoT-Multi.
Article in Cell genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Scalable genotyping in fixed transcriptomes resolves clonal heterogeneity via single-cell sequencing.bioRxiv : the preprint server for biology · 2026Article
- Integrating Single-Cell Sequencing and Proteomics to Unravel Stem Cell Heterogeneity: Implications for Precision Regenerative Medicine.Stem cell reviews and reports · 2026Review
- How somatic evolution affects health.Nature ecology & evolution · 2026Article
- Charting clonal evolution and behavior with GoT-Multi.Cell genomics · 2026Article
- Emerging Approaches in Breast Cancer: From Molecular Mechanisms to Diagnosis and Therapeutic Strategies.Oncology research · 2026Review
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Authors and funding
15 authors.
Funding
Abstract
Somatic evolution leads to clonal heterogeneity, which fuels cancer progression and therapy resistance. To decipher the consequences of clonal heterogeneity, we require a method that deconvolutes complex clonal architectures and their downstream transcriptional states. We developed Genotyping of Transcriptomes for multiple targets and sample types (GoT-Multi), a high-throughput, formalin-fixed paraffin-embedded (FFPE) tissue-compatible single-cell multi-omics for co-detection of multiple somatic genotypes and whole transcriptomes. We developed an ensemble-based machine learning pipeline to optimize genotyping. We applied GoT-Multi to frozen or FFPE samples of Richter transformation, a progression of chronic lymphocytic leukemia to therapy-resistant large B cell lymphoma. GoT-Multi detected heterogeneous cancer cell states with genotypic data of 27 mutations, enabling clonal architecture reconstruction linked with their transcriptional programs. Distinct subclonal genotypes, including therapy-resistant mutations, converged on an inflammatory state. Other subclones displayed enhanced proliferation and/or MYC program. Thus, GoT-Multi revealed that distinct genotypic identities may converge on similar transcriptional states to mediate therapy resistance.
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