Pancreatic cancer remains challenging to treat due to its typically late diagnosis and strong resistance to chemotherapy.
Recent research highlights the significant role of oncogenic KRAS in pancreatic cancer. KRAS upregulates the nuclear factor erythroid 2-related factor 2 (NRF2), which is implicated in the disease’s chemoresistance. NRF2 activation leads to metabolic reprogramming, specifically altering glutamine metabolism, which contributes to the cancer’s resistance to treatment and poor patient prognosis.
Targeting glutamine metabolism using glutaminase inhibitors has shown promise in reducing chemoresistance and stress granule formation in KRAS-mutant pancreatic cancer cells.
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