Abstract
Metabolic programs are rewired in tumors to support growth, progression, and immune evasion. A wealth of work in the past decade has delineated how these metabolic rearrangements are facilitated by signaling pathways downstream of oncogene activation and tumor suppressor loss. More recently, this field has expanded to include metabolic interactions among the diverse cell types that exist within a tumor and how this impacts the immune system. In this special issue, 17 review articles discuss these phenomena, and, alongside four original research manuscripts, the vulnerabilities associated with deregulated metabolic programming are highlighted and examined.
Highlights
Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA
The reprogramming of cellular metabolism is a hallmark feature observed across cancers [1]. Contemporary research in this area has led to the discovery of tumor-specific metabolic mechanisms and illustrated ways that these can serve as selective, exploitable vulnerabilities. In this Editorial, we provide a high-level overview of the central themes from among the 21 review articles and original research studies in the Special Issue on Metabolic Reprogramming and Vulnerabilities in Cancer
A detailed review on the regulation of glucose metabolism in pancreatic cancer is provided by Yan et al [2], nucleotide metabolism by Villa et al [3], and amino acid metabolism by Choi and
Summary
Contemporary research in this area has led to the discovery of tumor-specific metabolic mechanisms and illustrated ways that these can serve as selective, exploitable vulnerabilities. In this Editorial, we provide a high-level overview of the central themes from among the 21 review articles and original research studies in the Special Issue on Metabolic Reprogramming and Vulnerabilities in Cancer. Nutrient acquisition and cancer growth: Metabolic programs are rewired in cancer cells to facilitate macromolecular biosynthesis required for cellular proliferation and tumor growth.
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