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Keywords {🔍}

cancer, pancreatic, pubmed, article, google, scholar, cas, cells, central, metabolism, cell, metabolic, gemcitabine, tumor, clinical, glycolysis, glucose, patients, addition, acid, growth, res, acids, microenvironment, fatty, amino, resistance, expression, role, progression, kras, autophagy, study, regulation, wang, chemoresistance, lactate, phase, therapy, pathway, treatment, inhibition, chemotherapy, survival, oncol, effect, tumors, cholesterol, clin, adenocarcinoma,

Topics {✒️}

nox/ros/nf-kappab/stat3 signaling cascade ccl18/nf-kb/vcam-1 pathway myc/pgc-1alpha balance determines modulating kras-e-cadherin pathway paracrine hgf/c-met enhances ribonucleotide reductase subunit-m2 erythrocyte-entrapped l-asparaginase ubiquitin-specific peptidase 9x article download pdf myeloid-derived suppressor cells tumour-derived lactic acid proper atp/adp ratio enhances gemcitabine-induced regression secrete high-energy metabolites mir-21-mediated metabolic alteration patient-level meta-analysis treatment-related adverse events plasma l-asparagine starvation early breast cancer mutant kras/galectin-3/αvβ3 complex growth-induced solid stress folfirinox versus gemcitabine/nab-paclitaxel cell-intrinsic lysosomal lipolysis converts gln-derived glu gemcitabine-resistant pancreatic cancer blocking iqgap1-mapk interaction altered energy metabolism nanovector-albumin-bound paclitaxel high-level free cholesterol kras-driven mapk pathway ribonucleotide reductase m2 suppress anti-tumor immunity combining β-lapachone full access secrete autophagy-derived alanine nano albumin bound-paclitaxel ribulose-5-phosphate-3-epimerase rpia mit/tfe proteins promote mitochondria-translocated pgk1 functions moderate ros generation anabolic glucose metabolism induces er stress kras-driven overexpressed enzymes gln-dependently activate mtor biochim biophys acta mutant kras-driven cancers inhibit gemcitabine-induced apoptosis affect host metabolism pi3k/akt signaling upregulation locally advanced disease

Questions {❓}

• Nature and nurture: what determines tumor metabolic phenotypes?
• The Warburg effect: how does it benefit cancer cells?

Schema {🗺️}

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         headline:Metabolism of pancreatic cancer: paving the way to better anticancer strategies
         description:Pancreatic cancer is currently one of the most lethal diseases. In recent years, increasing evidence has shown that reprogrammed metabolism may play a critical role in the carcinogenesis, progression, treatment and prognosis of pancreatic cancer. Affected by internal or external factors, pancreatic cancer cells adopt extensively distinct metabolic processes to meet their demand for growth. Rewired glucose, amino acid and lipid metabolism and metabolic crosstalk within the tumor microenvironment contribute to unlimited pancreatic tumor progression. In addition, the metabolic reprogramming involved in pancreatic cancer resistance is also closely related to chemotherapy, radiotherapy and immunotherapy, and results in a poor prognosis. Reflective of the key role of metabolism, the number of preclinical and clinical trials about metabolism-targeted therapies for pancreatic cancer is increasing. The poor prognosis of pancreatic cancer patients might be largely improved after employing therapies that regulate metabolism. Thus, investigations of metabolism not only benefit the understanding of carcinogenesis and cancer progression but also provide new insights for treatments against pancreatic cancer.
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      headline:Metabolism of pancreatic cancer: paving the way to better anticancer strategies
      description:Pancreatic cancer is currently one of the most lethal diseases. In recent years, increasing evidence has shown that reprogrammed metabolism may play a critical role in the carcinogenesis, progression, treatment and prognosis of pancreatic cancer. Affected by internal or external factors, pancreatic cancer cells adopt extensively distinct metabolic processes to meet their demand for growth. Rewired glucose, amino acid and lipid metabolism and metabolic crosstalk within the tumor microenvironment contribute to unlimited pancreatic tumor progression. In addition, the metabolic reprogramming involved in pancreatic cancer resistance is also closely related to chemotherapy, radiotherapy and immunotherapy, and results in a poor prognosis. Reflective of the key role of metabolism, the number of preclinical and clinical trials about metabolism-targeted therapies for pancreatic cancer is increasing. The poor prognosis of pancreatic cancer patients might be largely improved after employing therapies that regulate metabolism. Thus, investigations of metabolism not only benefit the understanding of carcinogenesis and cancer progression but also provide new insights for treatments against pancreatic cancer.
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         Pancreatic cancer
         Metabolism
         Chemoresistance
         Gemcitabine
         Radioresistance
         Immunosuppression
         Clinical trials
         Cancer Research
         Oncology
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