Literature DB >> 34722470

The Potential Role of Changes in the Glucose and Lipid Metabolic Pathways in Gastrointestinal Cancer Progression: Strategy in Cancer Therapy.

Gordon A Ferns1, Milad Shahini Shams Abadi2,3, Ahmad Raeisi4, Mohammad-Hassan Arjmand3,5.   

Abstract

BACKGROUND: Changes in cell metabolism are a well-known feature of some cancers, and this may be involved in the etiology of tumor formation and progression, as well as tumor heterogeneity. These changes may affect fatty acid metabolism and glycolysis and are required to provide the increase in energy necessary for the high rate of proliferation of cancer cells. Gastrointestinal cancers remain a difficult-to-treat cancer, particularly as they are usually diagnosed at a late stage of disease and are associated with poor outcomes.
SUMMARY: Recently, the changes in the metabolic pathways, including the expression of the rate-limiting enzymes involved, have been considered to be a potential target for therapy for gastrointestinal tumors. KEY MESSAGE: A combination of routine chemotherapy drugs with metabolic inhibitors may improve the effectiveness of treatment.
Copyright © 2021 by S. Karger AG, Basel.

Entities:  

Keywords:  Cancer metabolism; Gastrointestinal tumors; Glucose metabolism; Lipid metabolism

Year:  2021        PMID: 34722470      PMCID: PMC8546445          DOI: 10.1159/000517771

Source DB:  PubMed          Journal:  Gastrointest Tumors        ISSN: 2296-3774


  82 in total

Review 1.  Tumor cell metabolism: an integral view.

Authors:  Susana Romero-Garcia; Jose Sullivan Lopez-Gonzalez; José Luis Báez-Viveros; Dolores Aguilar-Cazares; Heriberto Prado-Garcia
Journal:  Cancer Biol Ther       Date:  2011-12-01       Impact factor: 4.742

2.  Energy boost: the Warburg effect returns in a new theory of cancer.

Authors:  Ken Garber
Journal:  J Natl Cancer Inst       Date:  2004-12-15       Impact factor: 13.506

3.  GLUT-1 expression and response to chemoradiotherapy in rectal cancer.

Authors:  Sarah Brophy; Katherine M Sheehan; Deborah A McNamara; Joseph Deasy; David J Bouchier-Hayes; Elaine W Kay
Journal:  Int J Cancer       Date:  2009-12-15       Impact factor: 7.396

Review 4.  Tumors as organs: complex tissues that interface with the entire organism.

Authors:  Mikala Egeblad; Elizabeth S Nakasone; Zena Werb
Journal:  Dev Cell       Date:  2010-06-15       Impact factor: 12.270

5.  Phosphofructokinase type 1 kinetics, isoform expression, and gene polymorphisms in cancer cells.

Authors:  Rafael Moreno-Sánchez; Alvaro Marín-Hernández; Juan Carlos Gallardo-Pérez; Héctor Quezada; Rusely Encalada; Sara Rodríguez-Enríquez; Emma Saavedra
Journal:  J Cell Biochem       Date:  2012-05       Impact factor: 4.429

6.  Tricarballylate and hydroxycitrate: substrate and inhibitor of ATP: citrate oxaloacetate lyase.

Authors:  J A Watson; M Fang; J M Lowenstein
Journal:  Arch Biochem Biophys       Date:  1969-12       Impact factor: 4.013

7.  HMGCR is necessary for the tumorigenecity of esophageal squamous cell carcinoma and is regulated by Myc.

Authors:  Chenxi Zhong; Limin Fan; Feng Yao; Jianxin Shi; Wentao Fang; Heng Zhao
Journal:  Tumour Biol       Date:  2014-01-05

Review 8.  Fatty acid synthase as a potential therapeutic target in cancer.

Authors:  Richard Flavin; Stephane Peluso; Paul L Nguyen; Massimo Loda
Journal:  Future Oncol       Date:  2010-04       Impact factor: 3.404

9.  Inhibition of fatty acid oxidation by etomoxir impairs NADPH production and increases reactive oxygen species resulting in ATP depletion and cell death in human glioblastoma cells.

Authors:  Lisa S Pike; Amy L Smift; Nicole J Croteau; David A Ferrick; Min Wu
Journal:  Biochim Biophys Acta       Date:  2011-06

Review 10.  MYC-induced cancer cell energy metabolism and therapeutic opportunities.

Authors:  Chi V Dang; Anne Le; Ping Gao
Journal:  Clin Cancer Res       Date:  2009-10-27       Impact factor: 12.531

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