Fundamentals of cancer metabolism
TLDR
A conceptual framework to understand how and why metabolic reprogramming occurs in tumor cells, and the mechanisms linking altered metabolism to tumorigenesis and metastasis will progressively support the development of new strategies to treat human cancer.Abstract:
Tumors reprogram pathways of nutrient acquisition and metabolism to meet the bioenergetic, biosynthetic, and redox demands of malignant cells. These reprogrammed activities are now recognized as hallmarks of cancer, and recent work has uncovered remarkable flexibility in the specific pathways activated by tumor cells to support these key functions. In this perspective, we provide a conceptual framework to understand how and why metabolic reprogramming occurs in tumor cells, and the mechanisms linking altered metabolism to tumorigenesis and metastasis. Understanding these concepts will progressively support the development of new strategies to treat human cancer.read more
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Impact of Inhibition of the Mitochondrial Pyruvate Carrier on the Tumor Extracellular pH as Measured by CEST-MRI.
Chloé Buyse,Nicolas Joudiou,Cyril Corbet,Olivier Feron,Lionel Mignion,Julien Flament,Bernard Gallez +6 more
TL;DR: In this paper, the authors evaluated the impact of a treatment with UK-5099, a mitochondrial pyruvate carrier (MPC) inhibitor on tumor extracellular pH (pHe), using either chemical exchange saturation transfer (CEST)-MRI with iopamidol as pHe probe or 31P-NMR spectroscopy with 3-aminopropylphosphonate (3-APP).
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Metabolic reprogramming related to whole-chromosome instability in models for Hürthle cell carcinoma.
Ruben D. Addie,Sarantos Kostidis,Willem E. Corver,Jan Oosting,Sepideh Aminzadeh-Gohari,René G. Feichtinger,Barbara Kofler,Mehtap Derya Aydemirli,Martin Giera,Hans Morreau +9 more
TL;DR: The data suggests that metabolic reprogramming and a subtle balance between ROS generation and scavenging/conversion of intermediates may be involved in ROS-induced w-CIN in HCC and possibly also in rare cases of follicular thyroid cancer showing a NHG.
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Inhibitor potency varies widely among tumor-relevant human isocitrate dehydrogenase 1 mutants.
Diego Avellaneda Matteo,Grace Wells,Lucas A. Luna,Adam J. Grunseth,Olga Zagnitko,David Scott,An Hoang,Amit Luthra,Manal A. Swairjo,Jamie M. Schiffer,Christal D. Sohl +10 more
TL;DR: This work provides a platform for predicting a patient's therapeutic response and identifies a potential resistance mutation that may arise upon treatment with mutant IDH inhibitors.
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Oxidative stress from DGAT1 oncoprotein inhibition in melanoma suppresses tumor growth when ROS defenses are also breached
Daniel J. Wilcock,Andrew P. Badrock,Chun-wing Wong,Rhys Owen,Melissa Guerin,Andrew D. Southam,Hannah Johnston,Brian A. Telfer,Paul Fullwood,Joanne Watson,Harriet R. Ferguson,Jennifer Ferguson,Gavin R. Lloyd,Andris Jankevics,Warwick B. Dunn,Claudia Wellbrock,P. Lorigan,Craig J. Ceol,Chiara Francavilla,Michael S. Smith,Adam Hurlstone +20 more
TL;DR: In this paper , the authors demonstrate that diacylglycerol O-acyltransferase 1 (DGAT1) is frequently upregulated in melanoma, allowing melanoma cells to tolerate excess FA.
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KRAS Status is Associated with Metabolic Parameters in Metastatic Colorectal Cancer According to Primary Tumour Location
M Tabuso,M Tabuso,Mark Christian,Peter K. Kimani,Kishore Gopalakrishnan,Ramesh P. Arasaradnam +5 more
TL;DR: A subgroup of mCRC patients with KRAS mutated recto-sigmoid cancer may benefit from optimal lipid lowering treatment, and this study evaluated associations between metabolic parameters and KRAS status in metastatic CRC according to a new tumour site classification.
References
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