Table 1.
Number of biospecimens collected by cancer type.
Fig 1.
Overview of biospecimen collection and resource development.
A total of 666 gynecologic cancer cases were included in the biobank. Among these, 294 cases formed the clinical cohort with informed consent and included retrospective (N = 179) and prospective (N = 115) cases from patients with endometrial, cervical, or ovarian cancers. For each case, biospecimens (tissue, blood, ascites, urine) and clinical data were collected. Derived secondary resources include whole-genome sequencing (WGS) datasets, patient-derived xenografts (PDXs), and tissue microarrays (TMAs). An additional 372 retrospective cases were used for TMA construction (endometrial: N = 301; cervical: N = 71), all under IRB approval and with patient consent. N indicates the number of patients.
Table 2.
Summary of clinical and diagnostic data.
Fig 2.
Establishment and validation of IHOSE cell lines.
(A) Phase-contrast microscopy images of four IHOSE cell lines (designated A–D) at ×40 and ×100 magnification. All cell lines retained epithelial morphology and showed stable proliferative capacity. Scale bar = 1000 µm (×40), 400 µm (×100). (B) PCR-based mycoplasma contamination testing. No contamination was detected in any of the four lines. The positive control (+) confirmed the assay sensitivity.
Fig 3.
Re-implantation–based validation of cryopreserved PDX tumor tissues for biobank deposition.
(A) Schematic overview of the study workflow illustrating establishment of PDX models from gynecologic cancer tissues, serial passaging (P1–P4), cryopreservation of tumor tissues, re-implantation of cryopreserved PDX fragments, and subsequent deposition into the biobank. (B) Tumor growth curves following re-implantation of cryopreserved PDX tissues derived from endometrial cancer (upper panel) and cervical cancer (lower panel). Tumor volumes were measured weekly using digital calipers and plotted over time. The passage number indicated in parentheses (P#) represents the passage of the cryopreserved PDX tissue used for re-implantation, followed by the passage number of the regrown xenograft. (C) Representative gross images of BALB/c nude mice bearing re-implanted PDX tumors (left) and the corresponding harvested xenograft tumors (right). Representative examples from endometrial cancer (PDX-170-P3(P4)) and cervical cancer (PDX-50-P4(P5)) are shown. (D) Representative H&E–stained sections of the original patient tumors (left) and the corresponding re-implanted xenograft tumors (right) are shown. Whole-slide images with higher-magnification insets from endometrial cancer (PDX-170, P4) and cervical cancer (PDX-50, P5) demonstrate preservation of histological features following re-implantation.
Fig 4.
Establishment and characterization of patient-derived ovarian cancer organoids.
(A) Schematic workflow illustrating the overall experimental process: ovarian cancer patient tissues were collected from the hospital, followed by organoid establishment, drug efficacy testing, and data analysis. (B) Brightfield images showing the growth kinetics of patient-derived ovarian cancer organoids (OVC#5) over time. Organoids increased in size and complexity from Day 8 to Day 25. Scale bar = 100 μm. (C) Serial passage of organoids derived from two ovarian cancer patients (OVC#5 and OVC#10). Representative brightfield images of organoids at each passage are shown. Scale bar = 1 mm. (D) Drug sensitivity assays for cisplatin, carboplatin, and nab-paclitaxel in OVC#5 and OVC#10 organoids. Top: Dose–response curves with calculated IC₅₀ values. Bottom: Representative organoid morphology under increasing drug concentrations. (E) Histological comparison between original patient tumor tissues and derived organoids using H&E, pan-cytokeratin (PanCK), and Ki-67 staining. Organoids retained epithelial characteristics and proliferative capacity consistent with their parental tumors. Scale bars = 200 μm (tissue), 100 μm (organoid).
Table 3.
Clinicopathological characteristics of patients in the cervical cancer TMA cohort.
Table 4.
Clinicopathological characteristics of patients in the endometrial cancer TMA cohort.
Fig 5.
In vitro evaluation of JIN-001 in ovarian cancer cell lines.
(A) Baseline response profiles of HOSE and IHOSE cells under non-tumorigenic conditions following treatment with JIN-001. (B) Dose–response curves of OVCAR3 and cisplatin-resistant OVCAR3-CisR cells treated with cisplatin in the presence or absence of JIN-001. (C) Cisplatin dose–response curves of OVCAR3 and OVCAR3-CisR cells in the presence of a fixed concentration of JIN-001 (0.1 µM).