KRAS: feeding pancreatic cancer proliferation

By Kirsten L. Bryant, J. Mancias, Alec C. Kimmelman, C. Der. TIBS -Trends in Biochemical Sciences. Regular ed, 2014

622 citations recorded by the source corpus.

Oncogenic KRAS mutation is the signature genetic event in the progression and growth of pancreatic ductal adenocarcinoma (PDAC), an almost universally fatal disease. Although it has been appreciated for some time that nearly 95% of PDAC harbor mutationally activated KRAS, to date no effective treatments that target this mutant protein have reached the clinic. A number of studies have shown that oncogenic KRAS plays a central role in controlling tumor metabolism by orchestrating multiple metabolic changes including stimulation of glucose uptake, differential channeling of glucose intermediates, reprogrammed glutamine metabolism, increased autophagy, and macropinocytosis. Here we review these recent findings and address how they may be applied to develop new PDAC treatments.

Subfields: Molecular Biology, Oncology, Surgery

View Paper: https://www.semanticscholar.org/paper/7a6ff61e7a97572dd42e6d04f8bf25fa153b9d73

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In Molecular Biology

1. K. Rossman
2. C. Der

In Oncology

1. K. Rossman
2. G. A. Hobbs
3. C. Der

Citations in the corpus

• RAS isoforms and mutations in cancer at a glance (2016, background): “There are substantial cell culture and mouse model analyses that support the driving role of four families (i.e. RAF, PI3K, RalGEF and TIAM1) in RASdriven oncogenesis (Bryant et al., 2014).”
• The Roles of Autophagy in Cancer (2018, neutral): “mitochondria and decreases cell growth [88,89,90].”