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Journal ArticleDOI

Lipid metabolism and lung cancer.

TLDR
The basis of lipid metabolism in lung cancer is reviewed, potential biomarkers are suggested, and potential therapeutic agents based on bioactive compounds such as cerulenin, SCD1, ACLY inhibitors, statins, polyphenolic compounds, etc.
Abstract
Lung cancer is currently one of the most serious health issues in developed and developing countries. There are multiple available treatment options; however survival still remains very poor. Despite metabolism alteration being one of the hallmarks described in human cancer, lipid metabolism disorders are less known. They are recently becoming more important in this setting and therefore achieving a deeper knowledge might be helpful to obtain new strategies to accurate diagnosis, estimate prognosis, and develop therapeutic agents based on bioactive compounds such as cerulenin, SCD1, ACLY inhibitors, statins, polyphenolic compounds, etc. The present paper reviews the basis of lipid metabolism in lung cancer and suggests potential biomarkers. Further investigation is crucial to improve our knowledge in this area.

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Journal ArticleDOI

Lipid metabolism reprogramming and its potential targets in cancer

TL;DR: SREBP cleavage-activating protein is a key transporter in the trafficking and activation of SREBPs as well as a critical glucose sensor, thus linking glucose metabolism and de novo lipid synthesis and Targeting altered lipid metabolic pathways has become a promising anti-cancer strategy.
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Alterations of Lipid Metabolism in Cancer: Implications in Prognosis and Treatment.

TL;DR: The impact of obesity and related tumor microenviroment alterations as modifiable risk factors in cancer is analyzed, focusing on the lipid alterations co-occurring during tumorigenesis, and the value of precision technologies and its application to target lipid metabolism in cancer are discussed.
Journal ArticleDOI

YAP and TAZ in Lung Cancer: Oncogenic Role and Clinical Targeting

TL;DR: The most recent advances made in YAP and TAZ biology in lung cancer are discussed and, more importantly, on the newly discovered mechanisms of YAPand TAZ inhibition in lung cancers as well as their clinical implications.
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Autophagy modulates lipid metabolism to maintain metabolic flexibility for Lkb1-deficient Kras-driven lung tumorigenesis

TL;DR: It is found that autophagy ablation was synthetically lethal during Lkb1-deficient lung tumorigenesis in both tumor initiation and tumor growth, and this strongly suggest that autophile inhibition could be a strategy for treating LKB1- deficient lung tumors.
Journal ArticleDOI

Lipid metabolism in cancer progression and therapeutic strategies

TL;DR: Recent evidence implicating the contribution of lipid metabolic reprogramming in cancer to cancer progression is reviewed, the molecular mechanisms underlying lipid metabolism rewiring in cancer, and potential therapeutic strategies directed toward lipid metabolism in cancer are discussed.
References
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Journal ArticleDOI

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The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers

TL;DR: No reduction in the incidence of lung cancer among male smokers is found after five to eight years of dietary supplementation with alpha-tocopherol or beta carotene, and this trial raises the possibility that these supplements may actually have harmful as well as beneficial effects.
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Effects of a combination of beta carotene and vitamin a on lung cancer and cardiovascular disease

TL;DR: After an average of four years of supplementation, the combination of beta carotene and vitamin A had no benefit and may have had an adverse effect on the incidence of lung cancer and on the risk of death from lung cancer, cardiovascular disease, and any cause in smokers and workers exposed to asbestos.
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