98%
921
2 minutes
20
The approval of anticancer therapeutic strategies is still slowed down by the lack of models able to faithfully reproduce in vivo cancer physiology. On one hand, the conventional in vitro models fail to recapitulate the organ and tissue structures, the fluid flows, and the mechanical stimuli characterizing the human body compartments. On the other hand, in vivo animal models cannot reproduce the typical human tumor microenvironment, essential to study cancer behavior and progression. This study reviews the cancer-on-chips as one of the most promising tools to model and investigate the tumor microenvironment and metastasis. We also described how cancer-on-chip devices have been developed and implemented to study the most common primary cancers and their metastatic sites. Pros and cons of this technology are then discussed highlighting the future challenges to close the gap between the pre-clinical and clinical studies and accelerate the approval of new anticancer therapies in humans.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10436436 | PMC |
http://dx.doi.org/10.1186/s13036-023-00372-6 | DOI Listing |
J Oncol Pharm Pract
September 2025
Department of Research & Development, Squad Medicine and Research (SMR), Amadalavalasa, Andhra Pradesh, India.
Cancer vaccines represent a transformative shift in oncology, aiming to prevent malignancies or treat established cancers by training the immune system to recognize tumor-specific or tumor-associated antigens. This review explores the diverse platforms and mechanisms supporting cancer vaccines, ranging from prophylactic vaccines such as HPV and hepatitis B vaccines that have significantly reduced virus-related cancers to therapeutic vaccines like Sipuleucel-T and T-VEC that extend survival in prostate cancer and melanoma. Vaccine types are classified, and delivery platforms including mRNA, peptide, dendritic cell and viral vector-based approaches are examined alongside pivotal clinical trial outcomes.
View Article and Find Full Text PDFCancer Immunol Res
September 2025
Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, United States.
Antibody-based therapies have revolutionized cancer treatment but have several limitations. These include: down-regulation of the target antigen; mutation of the target epitope; or in the case of antibody drug conjugates (ADCs), resistance to the chemotherapy warhead. Since TROP2-targeted therapy with ADCs yields responses in TROP2+ solid tumors but lacks the durability observed with other immunotherapy-based approaches, we developed novel TROP2-targeting chimeric antigen receptor (CAR) T cells as an alternative.
View Article and Find Full Text PDFCancer Immunol Res
September 2025
University of Pennsylvania, Philadelphia, PA, United States.
Pancreatic ductal adenocarcinoma (PDA) is defined by a myeloid-enriched microenvironment and has shown remarkable resistance to immune checkpoint blockade (e.g., PD-1 and CTLA-4).
View Article and Find Full Text PDFInt J Surg
September 2025
BK21 FOUR KNU Convergence Educational Program of Biomedical Sciences for Creative Future Talents, Department of Biomedical Sciences, School of Medicine, Kyungpook National University, Daegu, Republic of Korea.
Thyroid cancer, a prevalent endocrine malignancy, is influenced by its tumor microenvironment (TME), with cancer-associated fibroblasts (CAFs) playing a pivotal role in disease progression. Molecularly, CAFs orchestrate a pro-tumorigenic niche via cytokine secretion and extracellular matrix (ECM) stiffening, underscoring their targetability. Therapeutic strategies, including small molecule inhibitor-based therapies, immune-based therapies, nanoparticle-based approaches, and combination regimens, have been evaluated for their efficacy in disrupting CAF functionality.
View Article and Find Full Text PDFACS Appl Mater Interfaces
September 2025
MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, College of Biophotonics, School of Optoelectronic Science and Engineering, South China Normal University, No.55 West Zhongshan Avenue, Tianhe District, Guangzhou 510631, Guangdong, China.
While reactive oxygen species (ROS)-dependent chemodynamic therapy (CDT) and photodynamic therapy (PDT) hold promise for cancer treatment, their efficacy remains constrained by tumor microenvironment (TME) barriers: glutathione (GSH) overexpression, insufficient HO supply, and hypoxia. To address these limitations, we engineered a Trojan horse-inspired MnO-shelled CaO nanoreactor (CaO/MnO-Ce6-PEG) by employing a sequential TME reprogramming strategy, triggering a cascading ROS storm for enhanced CDT and PDT. The outer MnO layer first depletes GSH through redox conversion, exposing the CaO core hydrolysis, and subsequently providing HO for CDT and O for ameliorating hypoxia to boost Ce6-mediated PDT.
View Article and Find Full Text PDF