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Tumor-associated macrophages (TAMs) are one of the major immune cell types in the TME. Stromal cells and cancerous epithelial cells have bidirectional crosstalk that creates a desmoplastic stroma within the microenvironment, thus promoting tumor progression and chemoresistance 10, 11, 12. However, PDOs are mainly epithelial and lack the tumor microenvironment (TME) in PDAC, which is characterized by the infiltration of immune cells and fibroblasts. Pancreatic organoids can be developed from pancreatic tissue samples obtained via fine-needle biopsy (FNB), and patient-derived organoids (PDOs) from PDAC could help advance PM in PDAC 9. Tissue-derived stem cells can self-organize themselves into sphere-shaped organoids composed predominantly of epithelial cells 8. Unlike primary cells, organoids can be propagated long-term ex vivo, allowing for the study of patient-specific cancer readouts. Organoids are progenitor cells that possess the phenotype of the tissue of origin. Instead, a personalized approach (precision medicine, PM) that uses tumor-related information to predict the drug response can be used.Īdvances in three-dimensional (3D) culture techniques have enabled the formation of organoids from patient tissues, bringing us closer to individualized PM in pancreatic cancer 7. The lack of a remarkable clinical response is partly due to the large molecular heterogeneity among PDAC patients consequently, only a small subset of patients who may potentially benefit from these drugs are included in clinical trials. Multiple targeted therapies with promising preclinical profiles have emerged over the past decade, but no drug has been shown to exert an expected response in the setting of a clinical trial. These challenges suggest that there is an urgent need to identify effective treatments for combating this deadly cancer.
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Unfortunately, improved FOLFIRINOX with gemcitabine as an adjuvant did not increase survival rates 6.
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FOLFIRINOX, a combination of fluorouracil, leucovorin, irinotecan, and oxaliplatin, has been used to treat metastatic PDAC patients, although this method has not shown ideal outcomes 5. Surgical resection combined with chemoradiation may improve the survival rate however, it is still not above 20–25% 4. The survival rate has only increased from 3 to 10% in the last five decades, and surgery remains the only possible curative strategy 3. It is anticipated to be the second leading cause of cancer-related death in the USA by 2040 2, 3. PDAC is considered the most fatal of all cancers and is associated with an abysmal prognosis. Pancreatic ductal adenocarcinoma (PDAC) accounts for 93% of cancers arising from the pancreas 1. However, targeting stroma in our tumor-chip model resulted in a significant increase in the chemotherapy effect on cancer cells, thus validating the use of this tumor-chip device for drug testing. When primary cancer cells in monoculture were subjected to stroma-depleting agents, there was no effect on cancer cell viability. Establishing PDOs in a multicellular microfluidic chip device prolongs cellular function and longevity and successfully establishes a complex organotypic tumor environment that incorporates desmoplastic stroma and immune cells. This study developed a tumor-chip device engineered to mimic the PDAC TME by incorporating PDOs and stromal cells, specifically pancreatic stellate cells and macrophages. The development of patient-derived organoids (PDOs) has opened the door for improved personalized medicine since PDOs are derived directly from patient tumors, thus preserving the tumors’ unique behaviors and genetic phenotypes. Current in vitro techniques insufficiently replicate the intricate stromal components of PDAC tumor microenvironments (TMEs) and fail to model a given tumor’s unique genetic phenotype. The heterogeneity of PDAC tumor composition has complicated treatment and stalled success in clinical trials. The patient population suffering from pancreatic ductal adenocarcinoma (PDAC) presents, as a whole, with a high degree of molecular tumor heterogeneity.