期刊
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER
卷 1870, 期 1, 页码 67-75出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbcan.2018.04.011
关键词
Pancreatic cancer; Autophagy; Metabolism; Microenvironment; Macropinocytosis
资金
- National Cancer Institute [R01CA157490, R01CA188048, P01CA117969]
- ACS [RSG-13-298-01-TBG]
- NIH [R01GM095567]
- Lustgarten Foundation
- NATIONAL CANCER INSTITUTE [R01CA157490, P01CA117969, R01CA188048, R35CA232124] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM095567] Funding Source: NIH RePORTER
Pancreatic ductal adenocarcinoma (PDA) is an aggressive cancer that is highly refractory to the current standards of care. The difficulty in treating this disease is due to a number of different factors, including altered metabolism. In PDA, the metabolic rewiring favors anabolic reactions which supply the cancer cell with necessary cellular building blocks for unconstrained growth. Furthermore, PDA cells display high levels of basal autophagy and macropinocytosis. KRAS is the driving oncogene in PDA and many of the metabolic changes are downstream of its activation. Together, these unique pathways for nutrient utilization and acquisition result in metabolic plasticity enabling cells to rapidly adapt to nutrient and oxygen fluctuations. This remarkable adaptability has been implicated as a cause of the intense therapeutic resistance. In this review, we discuss metabolic pathways in PDA tumors and highlight how they contribute to the pathogenesis and treatment of the disease.
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