SPECIAL ISSUE: Cancer metabolism: models, mechanisms and targets
Summary: The guest editors of this Special Collection discuss recent advances in the field of cancer metabolism, as well as the challenges faced as this exciting research progresses.
A MODEL FOR LIFE
AT A GLANCE
Summary: This ‘At a Glance’ review and accompanying poster address how tumors can negatively affect immune cells through depletion of critical nutrients or through production of toxic metabolic products.
Microenvironmental regulation of cancer cell metabolism: implications for experimental design and translational studies
Summary: Here, we discuss the model systems for cancer metabolism studies and highlight their key strengths and pitfalls in addressing different questions, such as how the microenvironment affects cancer metabolism and response to therapy.
Summary: In this Review, the authors focus on the regulation of NO levels by the synthesis and availability of arginine, and on the implications of this metabolic regulation to cancer biology and therapy.
Summary: Extracellular metabolites can mediate cell communication and change transcriptional and functional aspects of tumor and normal cells. This Review focuses on how these metabolic cues affect the immune system with a special focus on tumor-associated macrophages.
Summary: This Review summarizes recent findings about multifaceted metabolic enzymes with non-canonical activities outside their core biochemical functions, and how they may provide new therapeutic strategies for cancers.
Summary: In this Review the authors summarize recent findings on how specific metabolic cues modulate and influence the behaviour, genome and epigenome of metastatic cancer cells. They also discuss how the crosstalk between metabolism and the epigenome of metastatic cells can be harnessed to develop new anti-metastatic therapies.
Synergistic antiproliferative effects of an mTOR inhibitor (rad001) plus gemcitabine on cholangiocarcinoma by decreasing choline kinase activity
Summary: Rad001 plus gemcitabine exerts a synergistic antitumor effect on cholangiocarcinoma irrespective of KRAS mutation status, with underlying mechanisms involving activation of the death receptor, mitochondrial pathways and downregulated choline kinase activity.
A novel zebrafish intestinal tumor model reveals a role for cyp7a1-dependent tumor–liver crosstalk in causing adverse effects on the host
Summary: The authors genetically dissect the adverse effects on the host in a new model of zebrafish intestinal tumor.