ArticleNature genetics2025
Characterizing the evolutionary dynamics of cancer proliferation in single-cell clones with SPRINTER.
Article in Nature genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Trial
- Eco-Evolutionary Dynamics of Proliferation Heterogeneity: A Phenotype-Structured Model for Tumor Growth and Treatment Response.Bulletin of mathematical biology · 2026Article
- Agent-Based Simulations of Lung Tumor Evolution Suggest That Ongoing Cell Competition Drives Realistic Clonal Expansions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- CNVeil resolves haplotype-specific copy number and uncovers subclonal architecture hidden from total copy number profiling in single-cell cancer genomes.bioRxiv : the preprint server for biology · 2026Article
- Tumor heterogeneity: development, mechanisms, and therapeutic implications.Signal transduction and targeted therapy · 2026Review
- 3D chromatin architecture-related genes orchestrate LUAD evolution and therapy resistance: insights from integrative machine learning and spatial single-cell mapping.Functional & integrative genomics · 2026Article
- Prediction of Ki-67 expression in hepatocellular carcinoma: a dual-center study based on T2-weighted imaging habitat analysis.Radiology and oncology · 2026Article
- Single-Cell and Spatial Omics: Methods and Applications.MedComm · 2026Review
- Epithelial-to-mesenchymal transition as a central driver of tumor cell plasticity.Nature cancer · 2026Review
- A hormetic transcriptional program coregulates invasion, proliferation and dormancy to define metastatic potential.Nature communications · 2026Article
- Organoids glimpse: the nexus for diverse tumor heterogeneity.Frontiers in cell and developmental biology · 2026Review
- Targeting tumor transition windows.Exploration of targeted anti-tumor therapy · 2026Review
- From residual risk to precision intervention: the evolving role of minimal residual disease in breast cancer management.Cancer biology & medicine · 2025Review
- Review
Corrections and comments
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Authors and funding
26 authors.
Funding
Abstract
Proliferation is a key hallmark of cancer, but whether it differs between evolutionarily distinct clones co-existing within a tumor is unknown. We introduce the Single-cell Proliferation Rate Inference in Non-homogeneous Tumors through Evolutionary Routes (SPRINTER) algorithm that uses single-cell whole-genome DNA sequencing data to enable accurate identification and clone assignment of S- and G2-phase cells, as assessed by generating accurate ground truth data. Applied to a newly generated longitudinal, primary-metastasis-matched dataset of 14,994 non-small cell lung cancer cells, SPRINTER revealed widespread clone proliferation heterogeneity, orthogonally supported by Ki-67 staining, nuclei imaging and clinical imaging. We further demonstrated that high-proliferation clones have increased metastatic seeding potential, increased circulating tumor DNA shedding and clone-specific altered replication timing in proliferation- or metastasis-related genes associated with expression changes. Applied to previously generated datasets of 61,914 breast and ovarian cancer cells, SPRINTER revealed increased single-cell rates of different genomic variants and enrichment of proliferation-related gene amplifications in high-proliferation clones.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.