ArticleClinical transplantation and research2025
Cellular expansion of hepatocellular carcinoma organoids using decellularized liver scaffolds.
Article in Clinical transplantation and research, 2025. 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: A decellularized liver scaffold (DLS) is a three-dimensional acellular extracellular matrix created by removing cellular components from liver tissue. Hepatocellular carcinoma (HCC) organoids represent a useful experimental model. Methods: HCC organoids from patient-derived xenografts (PDX), liver organoids, and HepG2 cells were expanded by cultivation within a murine DLS. Results: HCC and liver organoids were generated from HCC PDX and human liver tissues, respectively. Expression levels of hepatocyte paraffin 1 (HepPar1), epithelial cell adhesion molecule (EpCAM), alpha-fetoprotein, keratin-7, and keratin-19 were detected in normal liver tissue, HCC tissue, HCC PDX, and HCC organoids. Fifteen murine DLSs were created, and the complete absence of liver cells was confirmed histologically by Masson trichrome and periodic acid-Schiff staining. Culture of HCC organoids in the DLS resulted in the expansion of numerous HCC cells scattered throughout the DLS framework. Keratin-7 expression was abundant, indicating widely dispersed progenitor cells. In contrast, cultivation of HepG2 cells within the DLS resulted in sparse cell distribution throughout the scaffold. Human hepatocyte organoids could not be cultivated successfully within the murine DLS framework. Conclusions: The DLS collagen framework facilitates the proliferation of HCC organoids. Thus, cultivating HCC organoids within a DLS appears to represent an effective method for rapid cell expansion, although it was ineffective for HepG2 cells and liver organoids. Further studies are required to validate the biological and oncological equivalence between seeded HCC organoids and those rapidly expanded within a DLS.
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.