Method Profile
Compare carboplatin and paclitaxel responses across direct ascites organoids and matched xenograft-derived routes.
Assess retention and variation of retrospective platinum-response patterns after model expansion through xenografts.
Five high-grade serous ovarian cancer patients: two platinum sensitive, two resistant and one refractory. Direct malignant-ascites PDOs and matched mouse xenograft-ascites/solid-tumor PDXOs.
Passage-3–9 organoids, 20–30 organoid units per well, 72-hour fixed-dose exposure followed by CellTiter-Glo 3D ATP measurement.
Drug conditions
Carboplatin 1 μM, paclitaxel 10 nM and the combination; 0.1% DMSO vehicle and afatinib 10 μM positive killing control.
Repetition and origin
At least six technical wells per condition and two independent screening runs per model. Xenograft routes are derived from the same patients and retain an animal-expansion stage.
Compare drugs and matched derivation routes within each patient, preserving exceptions rather than assigning all resistant cultures one response.
Five patient sources with three derivation routes; technical wells and screening runs are within-model replicates.
Direct PDO, xenograft-ascites PDXO and solid-tumor PDXO; drug/vehicle/killing controls.
Sensitive and refractory patterns broadly persisted. Resistant patient 2 showed route-dependent paclitaxel response and a 16% combination reduction in solid PDXO, while resistant patient 80 showed a small significant combination-associated viability increase.
Primary study comparisons of the stated models, treatments and measurements.
Organoids from five ovarian cancer patients and their matched xenografts broadly reflected existing platinum-response classifications. Paclitaxel and combination responses varied with derivation route, showing why direct and xenograft-derived cultures are not interchangeable in every condition.
