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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A Metabolic Reprogramming Amino Acid Polymer as an Immunosurveillance Activator and Leukemia Targeting Drug Carrier for T‐Cell Acute Lymphoblastic Leukemia
Changlian Li,Xinru You,Xi Xu,Bing Wu,Yuye Liu,Tong Tong,Jie Chen,Yishan Li,Chunlei Dai,Zhitao Ye,Xiaobin Tian,Yan Wei,Zechen Hao,Linjia Jiang,Jun Wu,Meng Zhao +15 more
TL;DR: A novel amino acid metabolite nanomedicine is invented to treat T‐ALL through the combination of leukemic cell targeting and immunosurveillance stimulation.
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Preclinical studies on metal based anticancer drugs as enabled by integrated metallomics and metabolomics
Luis Galvez,Mate Rusz,Michaela Schwaiger-Haber,Yasin El Abiead,Gerrit Hermann,Ute Jungwirth,Walter Berger,Bernhard K. Keppler,Bernhard K. Keppler,Michael A. Jakupec,Michael A. Jakupec,Gunda Koellensperger +11 more
TL;DR: A novel -omics workflow enabling the parallel study of platinum drug uptake and its distribution between nucleus/protein and small molecule fraction along with metabolic changes after different treatment time points is introduced.
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Deubiquitinase PSMD14 promotes ovarian cancer progression by decreasing enzymatic activity of PKM2.
TL;DR: In this article, the function and mechanism of deubiquitinating enzyme 26S proteasome non-ATPase regulatory subunit 14 (PSMD14) in the progression of ovarian cancer (OV), the deadliest gynecological cancer, still remains to be characterized.
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Targeting glioma-initiating cells via the tyrosine metabolic pathway
Daisuke Yamashita,Joshua D. Bernstock,Galal A. Elsayed,Hirokazu Sadahiro,Ahmed Mohyeldin,Gustavo Chagoya,Adeel Ilyas,James Mooney,Dagoberto Estevez-Ordonez,Shinobu Yamaguchi,Victoria L. Flanary,James R. Hackney,Krishna P. Bhat,Harley I. Kornblum,Harley I. Kornblum,Nicola Zamboni,Sung Hak Kim,E. Antonio Chiocca,Ichiro Nakano +18 more
TL;DR: Metabolic heterogeneity in both HGG tumor tissues and GBM sphere culture models was identified, and analyses suggested that tyrosine metabolism may serve as a possible therapeutic target in GBM, particularly in the tumor core.
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The Metabolic Inhibitor CPI-613 Negates Treatment Enrichment of Ovarian Cancer Stem Cells.
Chiara Bellio,Celeste DiGloria,David R. Spriggs,Rosemary Foster,Whitfield B. Growdon,Bo R. Rueda +5 more
TL;DR: The results suggest that CPI-613 preferentially targets ovarian CSCs and could be a candidate to augment current treatment strategies to extend either progression-free or overall survival of OvCa.
References
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