ArticleCancer management and research2026
Saikosaponin D Induced Apoptosis and Anti-Tumor Effect Enhancing Chemotherapy Sensitivity of Gemcitabine in Patient-Derived Cholangiocarcinoma Organoids.
Article in Cancer management and research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Cholangiocarcinoma (CCA), an aggressive malignancy with limited therapeutic options and poor survival rates, poses an urgent clinical challenge necessitating innovative therapeutic strategies. Saikosaponin D (SSd), a bioactive compound derived from Methods: Four PDCO models were established from surgical tumor tissues and metastatic ascites of CCA patients. Histological, immunohistochemical (Cytokeratin 7, Cytokeratin 19 and Ki-67), and immunofluorescence analyses validated the fidelity of organoids to the primary tumors. Drug sensitivity testing evaluated SSd (0.001-50µM) and gemcitabine alone or in combination (ratios 1:1, 1:2, 1:4) using dose-response curves and combination index (CI) analysis. Apoptosis mechanisms were assessed via TUNEL staining, caspase-3 activity assays, and the JC-1 assay for the mitochondrial membrane potential. Results: SSd exhibited dose-dependent growth inhibition across PDCOs, with half-maximal inhibitory concentration (IC50) values ranging from 0.9µM to 13µM. Gemcitabine showed IC50 values spanning 0.03µM to 11.1µM. Notably, the SSd-gemcitabine combination at 1:4 ratio demonstrated synergistic effects (CI=0.0005), significantly reducing organoid viability. Ascites-derived PDCOs (eg, CCA182) displayed lower sensitivity to SSd, correlating with prior chemotherapy exposure. Apoptosis induction by SSd was confirmed through increased TUNEL-positive cells, elevated caspase-3 activity, and mitochondrial depolarization. Histological and molecular profiles of PDCOs closely mirrored those of the primary tumors, preserving spatial heterogeneity (eg, glandular structures in tissue-derived PDCOs vs compact morphology in ascites-derived models). Conclusion: The combination of SSd and gemcitabine exerts a synergistic antitumor effect in patient-derived cholangiocarcinoma organoids through activating caspase-3 and triggering mitochondrial dysfunction-mediated apoptosis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.