Tumor-derived model biobanks comprise patient-derived xenografts, organoids, cell models or cultures, and selected paired derivatives linked to clinical, pathological, molecular, and functional data. In China, patient-derived organoid and xenograft resources have expanded through clinical and academic studies, enterprise-operated platforms, and conventional hospital biobank support for clinical sourcing and quality management. Published studies demonstrate disease-focused living resources in common tumors as well as selected premalignant and less common settings. Clinical and academic groups provide clinically annotated specimens and outcome context, whereas enterprise-operated platforms describe model-generation workflows, functional testing modules, database interfaces, and preclinical service capacity. Together, these activities suggest a transition from project-based model collections toward translational research infrastructure. However, public catalogues, model-level quality descriptors, case-model-data linkage, and access mechanisms remain uneven. This review summarizes representative Chinese resources and enterprise platform types, discusses international benchmark functions for model-biobank maturity, and emphasizes quality transparency for external verification and resource discovery. Future development should strengthen minimum information fields, quality reporting, and governance mechanisms that allow model resources to be discovered and used under appropriate access control.
Lian-Hai Zhang, Ying Hu, Haixin Li et al.· Biopreservation and Biobanki...· 0 citations
BACKGROUND
Extrachromosomal DNA (ecDNA), as a dynamic genetic vector, enables tumor cells to exhibit enhanced adaptability under chemotherapeutic stress. However, its functional role in tumor malignancy and the development of drug resistance in gastric cancer (GC) remains unclear.
OBJECTIVE
This study aims to investigate the relationship between chemotherapy and ecDNA in GC, and explore its potential as a novel therapeutic target.
METHODS
We first analyzed our clinical data to reveal associations between ecDNA induction by chemotherapy and metastatic progression. Then we investigated the role of ecDNA in mediating chemoresistance and malignant phenotypes in cisplatin-resistant cell models using WGS, SEM, western blot, qPCR, flow cytometry, and immunofluorescence.
RESULTS
We found that neoadjuvant chemotherapy (NAC) promoted ecDNA formation from linear amplicons, which was associated with increased tumor mutational burden, poorer survival, and higher distant metastasis risk. The generation of ecDNA in GC was more likely to originate from chromosomes 5, 7, 8, 9, and 12. In cisplatin-resistant models, ecDNA emergence promoted various malignant phenotypes, including DNA damage repair, G1 arrest, autophagy, proliferation, migration, and invasion, which were attenuated by ecDNA inhibition. EcDNA inhibitors delayed acquired resistance in wild-type cells and showed combinatorial activity with cisplatin in resistant GC, supporting clinical potential.
CONCLUSION
Our study revealed that cisplatin could promote ecDNA generation, which enhanced malignant phenotypes, including cell proliferation, motility and drug resistance, and was associated with poorer patient prognosis. Targeting ecDNA with inhibitors could reverse these effects, supporting further preclinical evaluation.
Huanbo Zhu, Liang Chen, Longtao Huangfu et al.· Journal of Advanced Research· 0 citations
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