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Gene Regulation and Targeted Therapy in Gastric Cancer Peritoneal Metastasis: Radiological Findings from Dual Energy CT and PET/CT
Published on: January 22, 2018
Progress in Metabolic Studies of Gastric Cancer and Therapeutic Implications
Adriana Romo-Perez1, Guadalupe Dominguez-Gomez2, Alma Chavez-Blanco2
1Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Mexico City, Mexico.
Background:
Worldwide, gastric cancer is ranked the fifth malignancy in incidence and the third malignancy in mortality. Gastric cancer causes an altered metabolism that can be therapeutically exploited.
Objective:
The objective of this study is to provide an overview of the significant metabolic alterations caused by gastric cancer and propose a blockade.
Methods:
A comprehensive and up-to-date review of descriptive and experimental publications on the metabolic alterations caused by gastric cancer and their blockade. This is not a systematic review.
Results:
Gastric cancer causes high rates of glycolysis and glutaminolysis. There are increased rates of de novo fatty acid synthesis and cholesterol synthesis. Moreover, gastric cancer causes high rates of lipid turnover via fatty acid β-oxidation. Preclinical data indicate that the individual blockade of these pathways via enzyme targeting leads to antitumor effects in vitro and in vivo. Nevertheless, there is no data on the simultaneous blockade of these five pathways, which is critical as tumors show metabolic flexibility in response to the availability of nutrients. This means tumors may activate alternate routes when one or more are inhibited. We hypothesize there is a need to simultaneously block them to avoid or decrease the metabolic flexibility that may lead to treatment resistance.
Conclusion:
There is a need to explore the preclinical efficacy and feasibility of combined metabolic therapy targeting the pathways of glucose, glutamine, fatty acid synthesis, cholesterol synthesis, and fatty acid oxidation. This may have therapeutical implications because we have clinically available drugs that target these pathways in gastric cancer.
Insights
Gastric cancer alters metabolism, increasing glycolysis and glutaminolysis. Simultaneously blocking these pathways, along with fatty acid and cholesterol synthesis, may overcome treatment resistance.
Area of Science:
- Oncology
- Metabolic Research
- Cancer Therapeutics
Background:
- Gastric cancer is a leading cause of cancer incidence and mortality globally.
- Cancerous cells exhibit significant metabolic reprogramming that presents therapeutic opportunities.
Purpose of the Study:
- To review metabolic alterations in gastric cancer.
- To propose a blockade of these altered metabolic pathways.
Main Methods:
- Comprehensive review of descriptive and experimental literature.
- Focus on metabolic alterations and their blockade in gastric cancer.
- Not a systematic review.
Main Results:
- Gastric cancer upregulates glycolysis, glutaminolysis, de novo fatty acid and cholesterol synthesis, and fatty acid oxidation.
- Individual pathway blockade shows preclinical antitumor effects.
- Simultaneous blockade of multiple pathways is critical due to tumor metabolic flexibility and potential resistance.
Conclusions:
- Further preclinical investigation of combined metabolic therapy is warranted.
- Targeting glucose, glutamine, fatty acid synthesis, cholesterol synthesis, and fatty acid oxidation pathways is proposed.
- Clinically available drugs exist for these targets, suggesting therapeutic potential.
