Song Wen

Tumor evolution is fundamentally driven by the successive accumulation of somatic driver mutations and subsequent clonal expansion. However, the precise transition from these early alterations to malignancy remains poorly understood. 
It is now well-established that somatic point mutations responsible for human carcinogenesis (e.g., in TP53 or NOTCH1) also drive small clones in normal-looking tissues, while more recent single cell studies revealed that a fraction of normal epithelial cells are aneuploid, exhibiting expanded copy number alteration (CNA) events resembling those found in malignant tumors 
To systematically investigate the role of genomic events and clonal alterations in early tumor evolution, our lab has developed a multidisciplinary approach utilizing post-mortem tissues derived from whole-body donors. 
My PhD research aims to better understand the role of these clonal alterations in early tumor evolution. To establish this I will develop a donor-based pan-organ atlas of genomic alterations in normal human tissues. Furthermore, I will employ established and emerging spatial omics technologies to study interclonal interactions and characterize the functional roles of these clones within the tissue microenvironment.
 

• Master of Science in Oncology at Peking University (2022-2025)
• Bachelor of Clinical Medicine at Chongqing Medical University (2016-2022)
   

• ‘Characteristics of Chinese breast cancer patients with double heterozygosity for BRCA1 and BRCA2 germline pathogenic variants.’ Breast Cancer Res Treat, 2024. (PMID: 38900213)
   

• Lab address: Department of Human Structure and Repair, Unit of Anatomy and Embryology, Corneel Heymanslaan 10, UZP123, 9000 Ghent, Belgium
• Computational Cancer Genomics and Tumor Evolution lab
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• ORCID