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Peer-reviewedCC BYCancer communications (London, England)

Spatiotemporal Analysis of Molecular Continuity in Pathogenesis of Squamous Cell Carcinoma: From Normal Epithelium to Precancerous Lesions and Carcinoma.

  • Lan Lan1,2
  • Xinyu Wang1,2
  • Xiaoqi Jiang1,2
  • Xiangyi Lin1,2
  • Yancheng Lai1,2
  • Wen Tan1,2
  • Shaosen Zhang1,2
  • Dongxin Lin1,2,3
  • Chen Wu1,2,3,4
4 affiliations
  1. 1Department of Etiology and Carcinogenesis, National Cancer Center/National Clinical Research Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, P. R. China.
  2. 2Key Laboratory of Cancer Genomic Biology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, P. R. China.
  3. 3Collaborative Innovation Center for Cancer Personalized Medicine, Nanjing Medical University, Nanjing, Jiangsu, P. R. China.
  4. 4Chinese Academy of Medical Sciences (CAMS) Oxford Institute, Chinese Academy of Medical Sciences, Beijing, P. R. China.
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Abstract

Squamous cell carcinomas (SCCs) develop from the stratified epithelia of the esophagus, head and neck, lung, and skin, providing a tractable model to investigate how altered epithelial fields progress toward invasive cancer. Across SCC subtypes, evolution often begins before overt malignancy, with age- and exposure-associated mutant clones expanding within histologically normal epithelia. As lesions advance, early driver selection becomes coupled to copy number alterations, chromosomal instability, and epigenetic remodeling, whereas later stages are shaped by branching diversification, cellular plasticity, and regionally constrained selection. Despite tissue-specific differences, several recurrent principles emerge, including clonal expansion within mutated normal fields, transition bottlenecks marked by genome-scale instability, and the spatial organization of subclonal architecture and invasive-front states. In this review, we synthesize recent progress in the temporal ordering and spatial patterning of SCC evolution and discuss how genetic alterations, epigenetic remodeling, and tissue ecology jointly drive disease progression. We further highlight the implications for early interception, biomarker development, immune evasion, and evolution-informed prevention and therapy.

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Cite

BibTeXRIS
BibTeX
@article{lan2026spatiotemporal,
  title = {{Spatiotemporal Analysis of Molecular Continuity in Pathogenesis of Squamous Cell Carcinoma: From Normal Epithelium to Precancerous Lesions and Carcinoma.}},
  author = {Lan Lan and Xinyu Wang and Xiaoqi Jiang and Xiangyi Lin and Yancheng Lai and Wen Tan and Shaosen Zhang and Dongxin Lin and Chen Wu},
  journal = {Cancer communications (London, England)},
  year = {2026},
  month = oct,
  doi = {10.34133/cancomm.0051},
  url = {https://europepmc.org/article/MED/42898679},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Spatiotemporal Analysis of Molecular Continuity in Pathogenesis of Squamous Cell Carcinoma: From Normal Epithelium to Precancerous Lesions and Carcinoma.
AU  - Lan Lan
AU  - Xinyu Wang
AU  - Xiaoqi Jiang
AU  - Xiangyi Lin
AU  - Yancheng Lai
AU  - Wen Tan
AU  - Shaosen Zhang
AU  - Dongxin Lin
AU  - Chen Wu
PY  - 2026
DA  - 2026/10/19
JO  - Cancer communications (London, England)
DO  - 10.34133/cancomm.0051
UR  - https://europepmc.org/article/MED/42898679
AB  - Squamous cell carcinomas (SCCs) develop from the stratified epithelia of the esophagus, head and neck, lung, and skin, providing a tractable model to investigate how altered epithelial fields progress toward invasive cancer. Across SCC subtypes, evolution often begins before overt malignancy, with age- and exposure-associated mutant clones expanding within histologically normal epithelia. As lesions advance, early driver selection becomes coupled to copy number alterations, chromosomal instability, and epigenetic remodeling, whereas later stages are shaped by branching diversification, cellular plasticity, and regionally constrained selection. Despite tissue-specific differences, several recurrent principles emerge, including clonal expansion within mutated normal fields, transition bottlenecks marked by genome-scale instability, and the spatial organization of subclonal architecture and invasive-front states. In this review, we synthesize recent progress in the temporal ordering and spatial patterning of SCC evolution and discuss how genetic alterations, epigenetic remodeling, and tissue ecology jointly drive disease progression. We further highlight the implications for early interception, biomarker development, immune evasion, and evolution-informed prevention and therapy.
SN  - 2523-3548
ER  -