American Association for Cancer Research
00085472can171461-sup-183444_3_supp_4263540_vw5qwj.xlsx (768.02 kB)

Supplementary Table S1 to S7 from Clonality, Heterogeneity, and Evolution of Synchronous Bilateral Ovarian Cancer

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posted on 2023-03-31, 01:02 authored by Xia Yin, Ying Jing, Mei-Chun Cai, Pengfei Ma, Yi Zhang, Cong Xu, Meiying Zhang, Wen Di, Guanglei Zhuang

Supplementary Table S1. Clinical characteristics of unilateral and bilateral ovarian cancer patients.Supplementary Table S2: Sequencing statistics.Supplementary Table S3: All somatic exonic alterations.Supplementary Table S4: Sanger sequencing validation of mutations in SBOCs.Supplementary Table S5: Predisposition genes.Supplementary Table S6: Driver mutation analysis.Supplementary Table S7: Clonal numbers inferred by PyClone or SciClone analyses.


National Natural Science Foundation of China

State Key Laboratory of Oncogenes and Related Genes

Shanghai Jiao Tong University

Shanghai Municipal Education Commission

Shanghai Institutions of Higher Learning

Shanghai Rising-Star Program

Shanghai Municipal Commission of Health and Family Planning

Shanghai Key Laboratory of Gynecologic Oncology

Science and Technology Commission of Shanghai Municipality



Synchronous bilateral ovarian cancer (SBOC) represents a relatively frequent occurrence and clinically relevant diagnostic dilemma. Delineation of its clonal architecture, genetic heterogeneity, and evolutionary trajectories may have important implications for prognosis and management of patients with SBOC. Here, we describe the results of next-generation whole-exome or whole-genome sequencing of specimens from 12 SBOC cases and report that bilateral tumors from each individual display a comparable number of genomic abnormalities and similar mutational signatures of single-nucleotide variations. Clonality indices based on tumor-specific alterations supported monoclonal origins of SBOC. Each of the ovarian lesions was nevertheless oligoclonal, with inferred metastatic tumors harboring more subclones than their primary counterparts. The phylogenetic structure of SBOC indicated that most cancer cell dissemination occurred early, when the primary carcinoma was still relatively small (<100 million cells). Accordingly, the mutation spectra and mutational signatures of somatic variants exhibited pronounced spatiotemporal differences in each patient. Overall, these findings suggest that SBOCs are clonally related and form through pelvic spread rather than independent multifocal oncogenesis. Metastatic dissemination is often an early event, with dynamic mutational processes leading to divergent evolution and intratumor and intertumor heterogeneity, ultimately contributing substantially to phenotypic plasticity and diverse clinical course in SBOC. Cancer Res; 77(23); 6551–61. ©2017 AACR.

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