Neoantigens in Chronic Obstructive Pulmonary Disease and Lung Cancer: A Point of View

Zeneyedpour, Lona; Dekker, Lennard J. M.; Hoff, Jenny J M van Sten-van T; Burgers, Peter C.; Hacken, Nick H. T. ten; Luider, Theo M.

doi:10.1002/prca.201800093

Cited by 11 publications

(11 citation statements)

References 60 publications

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“…We and others previously showed that mutations in proteins in both cell cultures and tissues could be detected by mass spectrometry, including the IDH1 mutation, but for these measurements, an enrichment by immunoprecipitation of the mutated protein was required. 21,22 In the current study, we show that using the newest-generation mass spectrometry equipment, this step can be omitted. Using this assay, the IDH1 mutation could be confirmed in all IDH1 mut cultures and most of the tissues.…”

Section: ■ Discussionmentioning

confidence: 75%

Effects of the IDH1 R132H Mutation on the Energy Metabolism: A Comparison between Tissue and Corresponding Primary Glioma Cell Cultures

et al. 2022

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The R132H mutation in the metabolic enzyme isocitrate dehydrogenase 1 (IDH1) is the most important prognostic factor for the survival of glioma patients. Subsequent studies led to the discovery of a panel of enzymes mainly involved in glutamate anaplerosis and aerobic glycolysis that change in abundance as a result of the IDH1 mutation. To further study these changes, appropriate glioma models are required that accurately mimic in vivo metabolism. To investigate how metabolism is affected by in vitro cell culture, we here compared surgically obtained snap-frozen glioma tissues with their corresponding primary glioma cell culture models with a previously developed targeted mass spectrometry proteomic assay. We determined the relative abundance of a panel of metabolic enzymes. Results confirmed increased glutamate use and decreased aerobic glycolysis in resected IDH1 R132H glioma tissue samples. However, these metabolic profiles were not reflected in the paired glioma primary cell cultures. We suggest that culture conditions and tumor microenvironment play a crucial role in maintaining the in vivo metabolic situation in cell culture models. For this reason, new models that more closely resemble the in vivo microenvironment, such as threedimensional cell co-cultures or organotypic multicellular spheroid models, need to be developed and investigated.

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Section: ■ Discussionmentioning

confidence: 75%

Effects of the IDH1 R132H Mutation on the Energy Metabolism: A Comparison between Tissue and Corresponding Primary Glioma Cell Cultures

et al. 2022

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“…TP53 is one of the most well-known tumour suppressor and exerts multi-functional roles in controlling cell cycle checkpoints, apoptosis and DNA repair ( 40 ). In smokers with COPD, down-regulation of TP53 and p53-related signaling transduction may lead to lung tumorigenesis ( 41 ). Thus, these genes are reasonable as core targets for chenpi preventing COPD and its progression to lung cancer.…”

Section: Discussionmentioning

confidence: 99%

The mechanism and candidate compounds of aged citrus peel (chenpi) preventing chronic obstructive pulmonary disease and its progression to lung cancer

Zhou

Kui

et al. 2021

Food & Nutrition Research

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Background: Chronic obstructive pulmonary disease (COPD) is an important risk factor for developing lung cancer. Aged citrus peel (chenpi) has been used as a dietary supplement for respiratory diseases in China. Objective: To explore the mechanism and candidate compounds of chenpi preventing COPD and its progression to lung cancer. Methods: The active components and potential targets of chenpi were retrieved from the Traditional Chinese Medicine Systems Pharmacology (TCMSP) database. Disease-associated targets of COPD and lung cancer were collected in the Gene Cards and TTD database. The component-target network and PPI network were constructed using the Cytoscape 3.8.0 software. David database was used for GO and KEGG enrichment analysis. The main active components were verified by using the autodock Vina 1.1.2 software. Mouse lung cancer with COPD was induced by cigarette smoking (CS) combined with urethane injection to confirm preventing the effect of hesperetin (the candidate compound of chenpi) on COPD progression to lung cancer and its underlying mechanisms. Results: The network analysis revealed that the key active components of chenpi (nobiletin, naringenin, hesperetin) regulate five core targets (AKT1, TP53, IL6, VEGFA, MMP9). In addition, 103 potential pathways of chenpi were identified. Chenpi can prevent COPD and its progression to lung cancer by getting involved in the PI3K-Akt signaling pathway and MAPK signaling pathway. Molecular docking indicated that hesperetin had better binding activity for core targets. In mouse lung cancer with COPD, treatment with hesperetin dose-dependently improved not only lung tissue injury in COPD but also carcinoma lesions in lung cancer. Meanwhile, hesperetin could suppress the protein expression of AKT1, IL6, VEGFA, MMP9 and up-regulate the protein expression of TP53, and thus reduced the risk of COPD progression to lung cancer. Conclusion: Hesperetin is a candidate compound of chenpi that helps in preventing COPD and its progression to lung cancer by regulating AKT1, IL6, VEGFA, MMP9 and TP53.

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“…The accumulation of the products of apoptosis cause reduced phagocytic capacities of macrophages and production of suppressory cytokines, among others TGFβ [ 37 ]. Thus, emphysema seems to be not only structural, but also immune disease [ 58 , 59 ].…”

Section: Pathogenesis and Common Pathwaysmentioning

confidence: 99%

Lung Cancer in the Course of COPD-Emerging Problems Today

Uliński

Kwiecień

Domagała‐Kulawik

2022

Cancers

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Tobacco smoking remains the main cause of tobacco-dependent diseases like lung cancer, chronic obstructive pulmonary disease (COPD), in addition to cardiovascular diseases and other cancers. Whilst the majority of smokers will not develop either COPD or lung cancer, they are closely related diseases, occurring as co-morbidities at a higher rate than if they were independently triggered by smoking. A patient with COPD has a four- to six-fold greater risk of developing lung cancer independent of smoking exposure, when compared to matched smokers with normal lung function. The 10 year risk is about 8.8% in the COPD group and only 2% in patients with normal lung function. COPD is not a uniform disorder: there are different phenotypes. One of them is manifested by the prevalence of emphysema and this is complicated by malignant processes most often. Here, we present and discuss the clinical problems of COPD in patients with lung cancer and against lung cancer in the course of COPD. There are common pathological pathways in both diseases. These are inflammation with participation of macrophages and neutrophils and proteases. It is known that anticancer immune regulation is distorted towards immunosuppression, while in COPD the elements of autoimmunity are described. Cytotoxic T cells, lymphocytes B and regulatory T cells with the important role of check point molecules are involved in both processes. A growing number of lung cancer patients are treated with immune check point inhibitors (ICIs), and it was found that COPD patients may have benefits from this treatment. Altogether, the data point to the necessity for deeper analysis and intensive research studies to limit the burden of these serious diseases by prevention and by elaboration of specific therapeutic options.

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Neoantigens in Chronic Obstructive Pulmonary Disease and Lung Cancer: A Point of View

Cited by 11 publications

References 60 publications

Effects of the IDH1 R132H Mutation on the Energy Metabolism: A Comparison between Tissue and Corresponding Primary Glioma Cell Cultures

Effects of the IDH1 R132H Mutation on the Energy Metabolism: A Comparison between Tissue and Corresponding Primary Glioma Cell Cultures

The mechanism and candidate compounds of aged citrus peel (chenpi) preventing chronic obstructive pulmonary disease and its progression to lung cancer

Lung Cancer in the Course of COPD-Emerging Problems Today

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