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Peer-reviewedCC BY 4.0Oncogene

Phylogenetic and phylodynamic approaches to understanding the evolution of non-small cell lung cancer using single-cell sequencing

  • Teng Li1,2
  • Xianghan Li2
  • Yiran Zou2
  • Thomas K. F. Wong2,3
  • Michael J. Campa4
  • Elizabeth B. Gottlin4
  • Edward F. Patz4,5,6
  • Allen Rodrigo1,2
6 affiliations
  1. 1School of Biological Sciences, University of Auckland, Auckland, New Zealand
  2. 2Research School of Biology, Australian National University, Canberra, ACT Australia
  3. 3School of Computing, Australian National University, Canberra, ACT Australia
  4. 4Department of Radiology, Duke University Medical Center, Durham, NC USA
  5. 5Duke Cancer Institute, Duke University Medical Center, Durham, NC USA
  6. 6Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC USA
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Abstract

Characterizing the genealogy of tumor cells and their population dynamics is central to our understanding of the evolution of cancer. While direct monitoring of the tumor evolutionary process is impractical, we leverage advances in phylogenetics and phylodynamics to explore the evolutionary dynamics of non-small cell lung cancer (NSCLC) using single-cell whole exome sequencing data from 351 tumor cells across 11 NSCLC patients, predominantly focusing on the primary tumors and early stages of NSCLC. Our results reveal distinct phylogenetic tree shapes and evolutionary trajectories across different stages of NSCLC evolution. However, this intricate and multi-phase evolutionary process cannot be fully elucidated by current tumor models. Herein, we hypothesize that tumors progress through the following phases: (1) an initial rapid expansion through Big Bang-like growth, (2) a prolonged plateau period of non-progression with possible accumulation of neutral substitutions, (3) a subsequent phase where adaptive substitutions accumulate gradually, (4) a bottleneck event where selectively advantageous subclones acquire invasive capabilities (characterized by a pattern of punctuated evolution), and, potentially, a rapid expansion leading to metastasis. This work highlights the use of single-cell phylogenetics and phylodynamics for interpreting the evolution of NSCLC, with potential in predicting cancer progression, resistance mechanisms, and treatment response.

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Cite

BibTeXRIS
BibTeX
@article{li2026phylogenetic,
  title = {{Phylogenetic and phylodynamic approaches to understanding the evolution of non-small cell lung cancer using single-cell sequencing}},
  author = {Teng Li and Xianghan Li and Yiran Zou and Thomas K. F. Wong and Michael J. Campa and Elizabeth B. Gottlin and Edward F. Patz and Allen Rodrigo},
  journal = {Oncogene},
  year = {2026},
  month = sep,
  doi = {10.1038/s41388-026-03997-1},
  url = {https://doi.org/10.1038/s41388-026-03997-1},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Phylogenetic and phylodynamic approaches to understanding the evolution of non-small cell lung cancer using single-cell sequencing
AU  - Teng Li
AU  - Xianghan Li
AU  - Yiran Zou
AU  - Thomas K. F. Wong
AU  - Michael J. Campa
AU  - Elizabeth B. Gottlin
AU  - Edward F. Patz
AU  - Allen Rodrigo
PY  - 2026
DA  - 2026/09/24
JO  - Oncogene
DO  - 10.1038/s41388-026-03997-1
UR  - https://doi.org/10.1038/s41388-026-03997-1
AB  - Characterizing the genealogy of tumor cells and their population dynamics is central to our understanding of the evolution of cancer. While direct monitoring of the tumor evolutionary process is impractical, we leverage advances in phylogenetics and phylodynamics to explore the evolutionary dynamics of non-small cell lung cancer (NSCLC) using single-cell whole exome sequencing data from 351 tumor cells across 11 NSCLC patients, predominantly focusing on the primary tumors and early stages of NSCLC. Our results reveal distinct phylogenetic tree shapes and evolutionary trajectories across different stages of NSCLC evolution. However, this intricate and multi-phase evolutionary process cannot be fully elucidated by current tumor models. Herein, we hypothesize that tumors progress through the following phases: (1) an initial rapid expansion through Big Bang-like growth, (2) a prolonged plateau period of non-progression with possible accumulation of neutral substitutions, (3) a subsequent phase where adaptive substitutions accumulate gradually, (4) a bottleneck event where selectively advantageous subclones acquire invasive capabilities (characterized by a pattern of punctuated evolution), and, potentially, a rapid expansion leading to metastasis. This work highlights the use of single-cell phylogenetics and phylodynamics for interpreting the evolution of NSCLC, with potential in predicting cancer progression, resistance mechanisms, and treatment response.
SN  - 0950-9232
SN  - 1476-5594
ER  -