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Patient-derived organoids represent a novel platform to recapitulate the cancer cells in the patient tissue. While cancer heterogeneity has been extensively studied by a number of omics approaches, little is known about the spatiotemporal kinase activity dynamics. Here we applied a live imaging approach to organoids derived from 10 pancreatic ductal adenocarcinoma (PDAC) patients to comprehensively understand their heterogeneous growth potential and drug responses.

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Microbiome and metabolome analysis in smoking and non-smoking pancreatic ductal adenocarcinoma patients.

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Department of Gastroenterology, Qilu Hospital of Shandong University, 107 Wenhuaxi Road, Jinan, Shandong Province, 250012, China.

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Methods: SBCs and triple-negative invasive ductal carcinoma patients (TN-IDCs) were enrolled from three cancer centers between January 2011 and December 2020. SBCs were further divided into two subgroups: those with triple negativity (TN-SBCs) and those without (non-TN-SBCs).

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Organoids, tissue slices and organotypic cultures: advancing our understanding of pancreatic ductal adenocarcinoma through in vitro and ex vivo models.

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Amsterdam UMC location University of Amsterdam, Laboratory of Experimental Oncology and Radiobiology, Amsterdam, the Netherlands; Cancer Center Amsterdam, Cancer Biology, Amsterdam, the Netherlands. Electronic address:

Pancreatic ductal adenocarcinoma (PDAC) has one of the worst prognoses of all common solid cancers. For the large majority of PDAC patients, only systemic therapies with very limited efficacy are indicated. In addition, immunotherapies have not brought the advances seen in other cancer types.

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Pancreatic ductal adenocarcinoma (PDAC) has a minimal (<15%) 5-year existence, in part due to resistance to chemoradiotherapy. Previous research reveals the impact of paricalcitol (P) and hydroxychloroquine (H) on altering the lysosomal fusion, decreasing stromal burden, and triggering PDAC to chemotherapies. This investigation aims to elucidate the molecular properties of the H and P combination and their potential in sensitizing PDAC to gemcitabine (G).

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