Special Issue "Cancer Metabolism"

A special issue of Metabolites (ISSN 2218-1989).

Deadline for manuscript submissions: closed (28 February 2017)

Special Issue Editor

Guest Editor
Dr. Madhu Basetti

Cancer Research UK Cambridge Institute, University of Cambridge, Robinson way, Cambridge CB2 ORE, UK
Website | E-Mail
Interests: NMR, cancer; metabolomics, bioinformatics, system biology, tumour metabolism

Special Issue Information

Dear Colleague,

In the 1920’s a German scientist Warburg reported abnormal metabolism of tumour cells that resulted in a shift from ATP generation through oxidative phosphorylation to ATP generation through glycolysis, even in the presence of oxygen. Despite this, over the past 6 decades molecular biology has been the major focus of cancer research. The past decade has seen a revival of interest to better understand cancer metabolism and its association with oncogenes/tumour suppressor genes. The recent interesting findings of glycolysis, glutaminolysis, serine/glycine metabolism, amino acids metabolism, lipid and membrane lipid metabolism, enzymes in TCA cycle mutations in cancer cells has led to a renewed interest in the field of cancer metabolism. The emergence of systems biology, following the publication of the complete human genome, has focused on the integration of information from gene regulation with the molecular phenotypes of proteins (including enzymes) and metabolites. A more complete understanding of cancer metabolism will be essential to define the underlying cellular networks and proper targets for developing anti-cancer treatments. To this end, we are in the process of bringing a special issue of Cancer Metabolism in the online journal of Metabolites. The submission deadline is 28th February 2016.

In view of your expertise in the field of cancer metabolism, we would like to invite you for your contribution in this special issue dedicated to Cancer Metabolism. This will be of a great help for the all researchers working in this field.

Dr. Madhu Basetti
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 850 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Cancer metabolism
  • Warburg effect
  • Glycolysis
  • Oncogenes
  • Tumour suppressor genes
  • Tumour micro environment
  • Chemotherapy
  • Immunotherapy
  • Metabolomics
  • Genomics
  • Proteomics

Published Papers (7 papers)

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Editorial

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Open AccessEditorial Special Issue: Cancer Metabolism
Metabolites 2017, 7(3), 41; https://doi.org/10.3390/metabo7030041
Received: 5 August 2017 / Revised: 5 August 2017 / Accepted: 7 August 2017 / Published: 9 August 2017
Cited by 1 | PDF Full-text (155 KB) | HTML Full-text | XML Full-text
Abstract
This special issue is designed to present the latest research findings and developments in the field of cancer metabolism. Cancer is a complex disease and a common term used for more than 100 diseases, whereas metabolism describes a labyrinth of complex biochemical pathways
[...] Read more.
This special issue is designed to present the latest research findings and developments in the field of cancer metabolism. Cancer is a complex disease and a common term used for more than 100 diseases, whereas metabolism describes a labyrinth of complex biochemical pathways in the cell. It is essential to understand metabolism in the context of cancer for the early detection of disease biomarkers and to find proper targets for potential treatments. The articles presented in this issue cover metabolic aspects of brain tumours, breast tumours, paraganglioma, and the metabolic activity of tumour suppressor gene p53. Full article
(This article belongs to the Special Issue Cancer Metabolism)

Research

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Open AccessArticle Metabolomics of Therapy Response in Preclinical Glioblastoma: A Multi-Slice MRSI-Based Volumetric Analysis for Noninvasive Assessment of Temozolomide Treatment
Metabolites 2017, 7(2), 20; https://doi.org/10.3390/metabo7020020
Received: 31 March 2017 / Revised: 30 April 2017 / Accepted: 15 May 2017 / Published: 18 May 2017
Cited by 1 | PDF Full-text (15122 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Glioblastoma (GBM) is the most common aggressive primary brain tumor in adults, with a short survival time even after aggressive therapy. Non-invasive surrogate biomarkers of therapy response may be relevant for improving patient survival. Previous work produced such biomarkers in preclinical GBM using
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Glioblastoma (GBM) is the most common aggressive primary brain tumor in adults, with a short survival time even after aggressive therapy. Non-invasive surrogate biomarkers of therapy response may be relevant for improving patient survival. Previous work produced such biomarkers in preclinical GBM using semi-supervised source extraction and single-slice Magnetic Resonance Spectroscopic Imaging (MRSI). Nevertheless, GBMs are heterogeneous and single-slice studies could prevent obtaining relevant information. The purpose of this work was to evaluate whether a multi-slice MRSI approach, acquiring consecutive grids across the tumor, is feasible for preclinical models and may produce additional insight into therapy response. Nosological images were analyzed pixel-by-pixel and a relative responding volume, the Tumor Responding Index (TRI), was defined to quantify response. Heterogeneous response levels were observed and treated animals were ascribed to three arbitrary predefined groups: high response (HR, n = 2), TRI = 68.2 ± 2.8%, intermediate response (IR, n = 6), TRI = 41.1 ± 4.2% and low response (LR, n = 2), TRI = 13.4 ± 14.3%, producing therapy response categorization which had not been fully registered in single-slice studies. Results agreed with the multi-slice approach being feasible and producing an inverse correlation between TRI and Ki67 immunostaining. Additionally, ca. 7-day oscillations of TRI were observed, suggesting that host immune system activation in response to treatment could contribute to the responding patterns detected. Full article
(This article belongs to the Special Issue Cancer Metabolism)
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Review

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Open AccessReview Magnetic Resonance Spectroscopy for Detection of 2-Hydroxyglutarate as a Biomarker for IDH Mutation in Gliomas
Metabolites 2017, 7(2), 29; https://doi.org/10.3390/metabo7020029
Received: 12 April 2017 / Revised: 12 June 2017 / Accepted: 12 June 2017 / Published: 19 June 2017
Cited by 8 | PDF Full-text (2395 KB) | HTML Full-text | XML Full-text
Abstract
Mutations in the isocitrate dehydrogenase (IDH)1/2 genes are highly prevalent in gliomas and have been suggested to play an important role in the development and progression of the disease. Tumours harbouring these mutations exhibit a significant alteration in their metabolism resulting in the
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Mutations in the isocitrate dehydrogenase (IDH)1/2 genes are highly prevalent in gliomas and have been suggested to play an important role in the development and progression of the disease. Tumours harbouring these mutations exhibit a significant alteration in their metabolism resulting in the aberrant accumulation of the oncometabolite 2-hydroxygluarate (2-HG). As well as being suggested to play an important role in tumour progression, 2-HG may serve as a surrogate indicator of IDH status through non-invasive detection using magnetic resonance spectroscopy (MRS). In this review, we describe the recent efforts in developing MRS methods for detection and quantification of 2-HG in vivo and provide an assessment of the role of the 2-HG in gliomagenesis and patient prognosis. Full article
(This article belongs to the Special Issue Cancer Metabolism)
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Open AccessReview Breast Tissue Metabolism by Magnetic Resonance Spectroscopy
Metabolites 2017, 7(2), 25; https://doi.org/10.3390/metabo7020025
Received: 13 April 2017 / Revised: 31 May 2017 / Accepted: 31 May 2017 / Published: 7 June 2017
Cited by 5 | PDF Full-text (2095 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Metabolic alterations are known to occur with oncogenesis and tumor progression. During malignant transformation, the metabolism of cells and tissues is altered. Cancer metabolism can be studied using advanced technologies that detect both metabolites and metabolic activities. Identification, characterization, and quantification of metabolites
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Metabolic alterations are known to occur with oncogenesis and tumor progression. During malignant transformation, the metabolism of cells and tissues is altered. Cancer metabolism can be studied using advanced technologies that detect both metabolites and metabolic activities. Identification, characterization, and quantification of metabolites (metabolomics) are important for metabolic analysis and are usually done by nuclear magnetic resonance (NMR) or by mass spectrometry. In contrast to the magnetic resonance imaging that is used to monitor the tumor morphology during progression of the disease and during therapy, in vivo NMR spectroscopy is used to study and monitor tumor metabolism of cells/tissues by detection of various biochemicals or metabolites involved in various metabolic pathways. Several in vivo, in vitro and ex vivo NMR studies using 1H and 31P magnetic resonance spectroscopy (MRS) nuclei have documented increased levels of total choline containing compounds, phosphomonoesters and phosphodiesters in human breast cancer tissues, which is indicative of altered choline and phospholipid metabolism. These levels get reversed with successful treatment. Another method that increases the sensitivity of substrate detection by using nuclear spin hyperpolarization of 13C-lableled substrates by dynamic nuclear polarization has revived a great interest in the study of cancer metabolism. This review discusses breast tissue metabolism studied by various NMR/MRS methods. Full article
(This article belongs to the Special Issue Cancer Metabolism)
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Open AccessReview Regulation of Metabolic Activity by p53
Metabolites 2017, 7(2), 21; https://doi.org/10.3390/metabo7020021
Received: 7 April 2017 / Revised: 16 May 2017 / Accepted: 16 May 2017 / Published: 20 May 2017
Cited by 13 | PDF Full-text (1888 KB) | HTML Full-text | XML Full-text
Abstract
Metabolic reprogramming in cancer cells is controlled by the activation of multiple oncogenic signalling pathways in order to promote macromolecule biosynthesis during rapid proliferation. Cancer cells also need to adapt their metabolism to survive and multiply under the metabolically compromised conditions provided by
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Metabolic reprogramming in cancer cells is controlled by the activation of multiple oncogenic signalling pathways in order to promote macromolecule biosynthesis during rapid proliferation. Cancer cells also need to adapt their metabolism to survive and multiply under the metabolically compromised conditions provided by the tumour microenvironment. The tumour suppressor p53 interacts with the metabolic network at multiple nodes, mostly to reduce anabolic metabolism and promote preservation of cellular energy under conditions of nutrient restriction. Inactivation of this tumour suppressor by deletion or mutation is a frequent event in human cancer. While loss of p53 function lifts an important barrier to cancer development by deleting cell cycle and apoptosis checkpoints, it also removes a crucial regulatory mechanism and can render cancer cells highly sensitive to metabolic perturbation. In this review, we will summarise the major concepts of metabolic regulation by p53 and explore how this knowledge can be used to selectively target p53 deficient cancer cells in the context of the tumour microenvironment. Full article
(This article belongs to the Special Issue Cancer Metabolism)
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Open AccessReview Metabolic Portraits of Breast Cancer by HR MAS MR Spectroscopy of Intact Tissue Samples
Metabolites 2017, 7(2), 18; https://doi.org/10.3390/metabo7020018
Received: 18 March 2017 / Revised: 20 April 2017 / Accepted: 9 May 2017 / Published: 16 May 2017
Cited by 4 | PDF Full-text (1905 KB) | HTML Full-text | XML Full-text
Abstract
Despite progress in early detection and therapeutic strategies, breast cancer remains the second leading cause of cancer-related death among women globally. Due to the heterogeneity and complexity of tumor biology, breast cancer patients with similar diagnosis might have different prognosis and response to
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Despite progress in early detection and therapeutic strategies, breast cancer remains the second leading cause of cancer-related death among women globally. Due to the heterogeneity and complexity of tumor biology, breast cancer patients with similar diagnosis might have different prognosis and response to treatment. Thus, deeper understanding of individual tumor properties is necessary. Cancer cells must be able to convert nutrients to biomass while maintaining energy production, which requires reprogramming of central metabolic processes in the cells. This phenomenon is increasingly recognized as a potential target for treatment, but also as a source for biomarkers that can be used for prognosis, risk stratification and therapy monitoring. Magnetic resonance (MR) metabolomics is a widely used approach in translational research, aiming to identify clinically relevant metabolic biomarkers or generate novel understanding of the molecular biology in tumors. Ex vivo proton high-resolution magic angle spinning (HR MAS) MR spectroscopy is widely used to study central metabolic processes in a non-destructive manner. Here we review the current status for HR MAS MR spectroscopy findings in breast cancer in relation to glucose, amino acid and choline metabolism. Full article
(This article belongs to the Special Issue Cancer Metabolism)
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Open AccessReview Mitochondrial Deficiencies in the Predisposition to Paraganglioma
Metabolites 2017, 7(2), 17; https://doi.org/10.3390/metabo7020017
Received: 30 March 2017 / Revised: 27 April 2017 / Accepted: 30 April 2017 / Published: 4 May 2017
Cited by 6 | PDF Full-text (622 KB) | HTML Full-text | XML Full-text
Abstract
Paragangliomas and pheochromocytomas are rare neuroendocrine tumours with a very strong genetic component. It is estimated that around 40% of all cases are caused by a germline mutation in one of the 13 predisposing genes identified so far. Half of these inherited cases
[...] Read more.
Paragangliomas and pheochromocytomas are rare neuroendocrine tumours with a very strong genetic component. It is estimated that around 40% of all cases are caused by a germline mutation in one of the 13 predisposing genes identified so far. Half of these inherited cases are intriguingly caused by mutations in genes encoding tricarboxylic acid enzymes, namely SDHA, SDHB, SDHC, SDHD, and SDHAF2 genes, encoding succinate dehydrogenase and its assembly protein, FH encoding fumarate hydratase, and MDH2 encoding malate dehydrogenase. These mutations may also predispose to other type of cancers, such as renal cancer, leiomyomas, or gastro-intestinal stromal tumours. SDH, which is also the complex II of the oxidative respiratory chain, was the first mitochondrial enzyme to be identified having tumour suppressor functions, demonstrating that 80 years after his initial proposal, Otto Warburg may have actually been right when he hypothesized that low mitochondrial respiration was the origin of cancer. This review reports the current view on how such metabolic deficiencies may lead to cancer predisposition and shows that the recent data may lead to the development of innovative therapeutic strategies and establish precision medicine approaches for the management of patients affected by these rare diseases. Full article
(This article belongs to the Special Issue Cancer Metabolism)
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