Analysis reveals adaptive therapy influenced tumor dynamics in chemotherapy-resistant ovarian cancer, indicating potential for long-term control.
Sensitive and resistant HGSC populations grow and decline dynamically during treatment and can be tracked in cfDNA from patients with HGSC. A, OVCAR4 and Ov4Cis cells were grown as 50:50 cocultures in low-resource conditions. On day 6, cells were treated with cisplatin (0.1–1 μmol/L) or vehicle (dashed line). Cultures were harvested over time and the ratio of sensitive (green) to resistant (red) cells was measured by flow cytometry over time. Data are shown as mean ± SD, with n = 3 technical replicates. B, Tumor purity–corrected copy number profile for each sample obtained from Patient 1. Gray bars show the copy number (CN) profile of diagnostic samples, and red bars show CN profile of later samples as indicated. Transparent bars show genome segments with no resistance‐specific CNAs (i.e., regions with clonally shared CN or with other CNAs). Resistant proportion of each sample estimated by LiqCNA is shown. Error bars indicate the 95% confidence interval of each estimate. C, Zoomed‐in profiles of selected chromosomes with the most prominent/impactful resistance‐specific CNAs. Driver genes or genes associated with ovarian cancer that overlap with resistance‐specific CNA are indicated by blue vertical lines and listed below each graph.
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Hockings et al. (2025) studied this question.
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