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Open AccessJournal ArticleDOI

Essential Role for Oxidative Phosphorylation in Cancer Progression

Maria Chiara Maiuri, +1 more
- 06 Jan 2015 - 
- Vol. 21, Iss: 1, pp 11-12
TLDR
It is demonstrated that only mtDNA-depleted cancer cells capable of recovering mtDNA from the host form metastasizing cancers in vivo, revealing an essential requirement for oxidative phosphorylation in tumor progression.
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This article is published in Cell Metabolism.The article was published on 2015-01-06 and is currently open access. It has received 44 citations till now. The article focuses on the topics: Tumor progression & Cancer.

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Citations
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Journal ArticleDOI

The interplay between cell signalling and the mevalonate pathway in cancer

TL;DR: This Review summarizes recent advances and discusses unique opportunities for immediately targeting this metabolic vulnerability in cancer with agents that have been approved for other therapeutic uses, such as the statin family of drugs, to improve outcomes for cancer patients.
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Metformin in patients with advanced pancreatic cancer: a double-blind, randomised, placebo-controlled phase 2 trial

TL;DR: Addition of a conventional anti-diabetic dose of metformin does not improve outcome in patients with advanced pancreatic cancer treated with gemcitabine and erlotinib and future research should focus on patients with hyperinsulinaemia and patients with tumours showing markers of sensitivity to energetic stress.
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Targeting glucose metabolism to suppress cancer progression: prospective of anti-glycolytic cancer therapy.

TL;DR: This review aimed to present the most recent data on the emerging drug candidate targeting enzymes and intermediates involved in glucose metabolism to provide therapeutic opportunities and challenges for antiglycolytic cancer therapy.
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Modeling the Genetic Regulation of Cancer Metabolism: Interplay between Glycolysis and Oxidative Phosphorylation

TL;DR: It is proposed that the hybrid phenotype contributes to metabolic plasticity, allowing cancer cells to adapt to various microenvironments, and design cancer therapies targeting metabolism.
References
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Journal ArticleDOI

Mitochondria and cancer

TL;DR: Cancer cells then reprogramme adjacent stromal cells to optimize the cancer cell environment and activate out-of-context programmes that are important in development, stress response, wound healing and nutritional status.
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Mitochondrial mutations in cancer.

TL;DR: The mtDNA mutations in tumors may fall into two main classes: (1) severe mutations that inhibit OXPHOS, increase reactive oxygen species (ROS) and promote tumor cell proliferation and (2) milder mutations that may permit tumors to adapt to new environments.
Journal ArticleDOI

Human mitochondrial DNA: roles of inherited and somatic mutations

TL;DR: Insight into the roles of mtDNA mutations in a wide variety of diseases is discussed, highlighting the interesting genetic characteristics of the mitochondrial genome and challenges in studying its contribution to pathogenesis.
Journal ArticleDOI

Metabolic targets for cancer therapy

TL;DR: The intimate relationship between metabolism and malignancy is discussed, focusing on strategies through which this central aspect of tumour biology might be turned into cancer's Achilles heel.
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