Metabolic signatures in pancreatic ductal adenocarcinoma: diagnostic and therapeutic implications

被引:2
|
作者
Gong, Ruining [1 ,2 ]
Hu, Yonglu [3 ]
Yu, Qian [1 ]
Fang, Lin [4 ]
Ren, He [1 ,5 ]
机构
[1] Qingdao Univ, Shandong Prov Key Lab Clin Res Pancreat Dis, Ctr GI Canc Diag & Treatment Tumor Immunol & Cytot, Med Res Ctr,Affiliated Hosp, Qingdao 266003, Peoples R China
[2] Qingdao Univ, Dept Gastroenterol, Affiliated Hosp, Qingdao 266003, Peoples R China
[3] Qingdao Univ, Dept Endocrinol, Affiliated Hosp, Qingdao 266003, Peoples R China
[4] Qingdao Univ, Affiliated Hosp, Phase Clin Res Ctr 1, Qingdao 266003, Peoples R China
[5] Qingdao Univ, Shandong Prov Key Lab Clin Res Pancreat Dis, Ctr GI Canc Diag & Treatment Tumor Immunol & Cytot, Med Res Ctr,Affiliated Hosp, Qingdao 266003, Peoples R China
基金
中国国家自然科学基金;
关键词
Diagnosis; Metabolism; Pancreatic ductal adenocarcinoma; Treatment; Tumor microenvironment; PHASE-II; MITOCHONDRIAL METABOLISM; GLUTAMINE-METABOLISM; AUTOPHAGY INHIBITION; TUMOR METABOLISM; PROGNOSTIC VALUE; F-18-FDG PET/CT; ONCOGENIC KRAS; CANCER GROWTH; CELLS;
D O I
10.1097/JP9.0000000000000146
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Pancreatic ductal adenocarcinoma (PDAC) is the prototypical aggressive cancer that develops in nutrient-deficient and hypoxic microenvironment. PDAC overcomes these restrictions by employing unconventional tactics for the procurement and usage of fuel sources. The substantial reprogramming of PDAC cell metabolism is driven by oncogene-mediated cell-autonomous pathways. PDAC cells use glucose, glutamine, and lipids for energy and depend on autophagy and macropinocytosis for survival and growth. They also interact metabolically with non-cancerous cells, aiding tumor progression. Many clinical trials focusing on altered metabolism are ongoing. Understanding the metabolic regulation of PDAC cells will not only help to increase understanding of the mechanisms of disease progression but also provide insights for the development of new diagnostic and therapeutic approaches.
引用
收藏
页码:185 / 195
页数:11
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