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Pancreatic Ductal Adenocarcinoma (PDAC) is a devastating disease with poor clinical outcomes, which is mainly because of delayed disease detection, resistance to chemotherapy, and lack of specific targeted therapies. The disease's development involves complex interactions among immunological, genetic, and environmental factors, yet its molecular mechanism remains elusive. A major challenge in understanding PDAC etiology lies in unraveling the genetic profiling that governs the PDAC network.

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Background: Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal diseases. Although several chemotherapy regimens have been developed over the past decades, few targeted therapies have shown a significant improvement in overall survival, partly due to the identification of PDAC as a single disease.

Methods: Combining metabolomic analysis and immunohistochemistry staining with Oil Red O staining, analysis for the oxygen consumption rate and extracellular acidification rate, we stratified pancreatic cancer cells into two subtypes.

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Among the various types of pancreatic cancers, pancreatic ductal adenocarcinoma (PDAC) is the most lethal and aggressive, due to its tendency to metastasize quickly and has a particularly low five-year survival rate. Carbohydrate antigen 19-9 (CA 19-9) is the only biomarker approved by the Food and Drug Administration for PDAC and has been a focal point in diagnostic strategies, but its sensitivity and specificity are not sufficient for early and accurate detection. To address this issue, we introduce a synergistic approach combining CA 19-9 levels with a graphene oxide (GO)-based blood test.

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Unlabelled: Immune escape is a critical hallmark of cancer progression and underlies resistance to multiple immunotherapies. However, it remains unclear when the genetic events associated with immune escape occur during cancer development. Here, we integrate functional genomics studies of immunomodulatory genes with a tumor evolution reconstruction approach to infer the evolution of immune escape across 38 cancer types from the Pan-Cancer Analysis of Whole Genomes dataset.

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Background: The combination of local therapy with lenvatinib and programmed cell death protein-1 (PD-1) inhibitors represents an emerging treatment paradigm for unresectable hepatocellular carcinoma (uHCC). Our study sought to investigate the interrelationship between gut microbiota and intratumoral microbiota in the context of triple therapy, with a view to identifying potential biological markers.

Methods: The gut microbial community profiles of patients with primary untreated hepatocellular carcinoma (HCC) and those treated with local therapy combined with lenvatinib and PD-1 inhibitors were analyzed by 16S rRNA gene amplicon sequencing.

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