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The complex landscape of pancreatic cancer metabolism
#MMPMID24743516
Sousa CM
; Kimmelman AC
Carcinogenesis
2014[Jul]; 35
(7
): 1441-50
PMID24743516
show ga
Pancreatic ductal adenocarcinomas (PDA) are extremely aggressive cancers and
currently available therapies are only minimally effective in treating this
disease. Tackling this devastating cancer has been a major challenge to the
scientific and medical communities, in part due to its intense therapeutic
resistance. One of the aspects of this tumor that contributes to its aggressive
behavior is its altered cellular metabolism. Indeed, PDA cells seem to possess
the ability to adapt their metabolism to the particular environment to which they
are exposed, including utilizing diverse fuel sources depending on their
availability. Moreover, PDA tumors are efficient at recycling various metabolic
substrates through activation of different salvage pathways such as autophagy and
macropinocytosis. Together, these diverse metabolic adaptations allow PDA cells
to survive and thrive in harsh environments that may lack nutrients and oxygen.
Not surprisingly, given its central role in the pathogenesis of this tumor,
oncogenic Kras plays a critical role in much of the metabolic reprogramming seen
in PDA. In this review, we discuss the metabolic landscape of PDA tumors,
including the molecular underpinnings of the key regulatory nodes, and describe
how such pathways can be exploited for future diagnostic and therapeutic
approaches.
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