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Biomedicines
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Chronic Respiratory Diseases and Lung Cancers: From Pathophysiology to Novel...
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Chronic Respiratory Diseases and Lung Cancers: From Pathophysiology to Novel Diagnostic and Therapeutic Approaches

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 29606

Special Issue Editors

Dr. Magdalena Radecka

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Guest Editor
Institute of Physical Chemistry of the Polish Academy of Sciences, 01-224 Warsaw, Poland
Interests: chronic obstructive pulmonary disease diagnostic; molecular biology; cancer biology; antitumoral compounds; zebrafish; cap analog-mRNA; aging; 3D culture; microfluidic; bioprinting
Special Issues, Collections and Topics in MDPI journals
Dr. Karolina H. Czarnecka-Chrebelska

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Guest Editor
Department of Biomedicine and Genetics, Medical University of Lodz, Lodz, Poland
Interests: epigenetics related to thyroid and lung carcinogenesis; autoimmune diseases; chronic stress; molecular biology; miRNA and cfDNA circulating biomarkers; liquid biopsy; microbiota analysis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Chronic respiratory diseases (CRDs) are complex multifactorial disorders involving the airways and other lung structures. Some of the most common CRDs are chronic obstructive pulmonary disease (COPD), lung fibrosis, asthma, occupational lung diseases, pneumoconiosis, pulmonary hypertension, and lung cancers. The disease can be caused by long-term exposure to tobacco smoke or irritating gases; other risk factors include air pollution, occupational chemicals, dust, and frequent lower respiratory infections during childhood.

The development of reliable markers for an early and accurate diagnosis and prediction of response to prescribed treatment is essential for the correct management of CRDs. CRDs are not fully curable; however, various forms of treatment that help to dilate major air passages and improve shortness of breath can help to control symptoms and increase the quality of life for people with such diseases.

Long-term exposure to smoke, gases, or dust (e.g., asbestos) can cause prolonged lung tissue irritation, inflammation, and fibrosis, leading to the formation of neoplasms of the respiratory tract and intrathoracic organs. The presence of moderate or severe obstructive lung disease is a significant predictor of lung cancer (LC) in the long term. Moreover, in smokers with airflow obstruction, LC incidence rises up to fivefold. COPD has been recognized as an independent risk factor for LC, predominantly for squamous cell carcinoma. Prolonged lung tissue irritation and inflammation, mitochondrial dysfunction, and premature aging related to smoking and lung dysbiosis are the processes underlying both CRD and LC. Over the last few years, personalized medicine has emerged as a medical care approach that uses a novel technology to personalize treatments according to the particular CRD and LC patient’s medical needs.

Investigating pulmonary pathology has been fundamental for understanding clinical disease, remains essential to diagnosing disease, and is required in drug and device development.

We invite research papers that will consolidate our understanding of this. The Special Issue will publish full research articles, comprehensive reviews, and shorter perspective articles on all aspects related to the theme of chronic respiratory diseases and lung cancers: from pathophysiology to novel diagnostic and therapeutic approaches.

Dr. Magdalena Radecka
Dr. Karolina H. Czarnecka-Chrebelska
Guest Editors

Manuscript Submission Information

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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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • chronic respiratory failure
  • occupational lung diseases
  • obstructive pulmonary disease (COPD)
  • asthma
  • pulmonary hypertension
  • bronchiectasis
  • interstitial lung disease
  • cystic fibrosis, lung fibrosis
  • lung distraction
  • pneumoconiosis
  • lung cancer
  • lung microbiota
  • smoking

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Published Papers (6 papers)

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Research

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14 pages, 6618 KiB  
Article
The Lipid Profile and Biochemical Parameters of COPD Patients in Relation to Smoking Status
by Cristina Vicol, Ioana Buculei, Oana Elena Melinte, Mona Elisabeta Dobrin, Emanuel Ioan Stavarache, Cristina-Maria Gavrilescu, Paraschiva Postolache, Daniela Matei and Antigona Trofor
Biomedicines 2022, 10(11), 2936; https://doi.org/10.3390/biomedicines10112936 - 15 Nov 2022
Cited by 7 | Viewed by 2987
Abstract
Tobacco consumption is the most incriminated and studied risk factor for Chronic obstructive pulmonary disease (COPD), but other factors such as air pollution, are also linked to this disease. One of the known aspects of this chronic lung disease is that its occurrence [...] Read more.
Tobacco consumption is the most incriminated and studied risk factor for Chronic obstructive pulmonary disease (COPD), but other factors such as air pollution, are also linked to this disease. One of the known aspects of this chronic lung disease is that its occurrence is mainly due to the chronic inflammation of the airways. Lipid metabolism seems to be affected by smoking, with studies showing a correlation between this habit and high levels of triglycerides and low levels of high-density lipoprotein cholesterol (HDL-CHOL). Uric acid concentration is thought to reflect the antioxidative capacity of the body because it is the most abundant aqueous antioxidant. The aim of this study was to investigate the lipid profile and biochemical parameters of COPD patients in relation to smoking status. The present study was conducted between 2020 and 2021 in the Clinical Hospital of Pneumology in Iasi, Romania. Patients diagnosed with COPD (n = 52) were included and divided in three groups depending on their smoking status: non-smokers, smokers and ex-smokers. The obtained results show low correlations between COPD stages and serum uric acid concentrations (r = 0.4; p ˂ 0.05), smoking status (smoker/non-smoker/ex-smoker) and total serum cholesterol values (r = 0.45; p ˂ 0.05), but also between serum urea concentrations and the number of packs-years for the smoker/ex-smoker groups (r = 0.45, p ˂ 0.05). Smoking was associated with changes in the lipid profile of smokers and ex-smokers, along with increased low-density lipoprotein cholesterol (LDL-CHOL) and low serum uric acid values. Full article
(This article belongs to the Special Issue Chronic Respiratory Diseases and Lung Cancers: From Pathophysiology to Novel Diagnostic and Therapeutic Approaches)
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13 pages, 1112 KiB  
Article
Risk of Malignancy in Patients with Asthma-COPD Overlap Compared to Patients with COPD without Asthma
by Barbara Bonnesen, Pradeesh Sivapalan, Alexander Jordan, Johannes Wirenfeldt Pedersen, Christina Marisa Bergsøe, Josefin Eklöf, Louise Lindhardt Toennesen, Sidse Graff Jensen, Matiullah Naqibullah, Zaigham Saghir and Jens-Ulrik Stæhr Jensen
Biomedicines 2022, 10(7), 1463; https://doi.org/10.3390/biomedicines10071463 - 21 Jun 2022
Cited by 3 | Viewed by 2078
Abstract
Chronic inflammation such as asthma may lead to higher risks of malignancy, which may be inhibited by anti-inflammatory medicine such as inhaled corticosteroids (ICS). The aim of this study was to evaluate if patients with asthma-Chronic Obstructive Pulmonary Disease (COPD) overlap have a [...] Read more.
Chronic inflammation such as asthma may lead to higher risks of malignancy, which may be inhibited by anti-inflammatory medicine such as inhaled corticosteroids (ICS). The aim of this study was to evaluate if patients with asthma-Chronic Obstructive Pulmonary Disease (COPD) overlap have a higher risk of malignancy than patients with COPD without asthma, and, secondarily, if inhaled corticosteroids modify such a risk in a nationwide multi-center retrospective cohort study of Danish COPD-outpatients with or without asthma. Patients with asthma-COPD overlap were propensity score matched (PSM) 1:2 to patients with COPD without asthma. The endpoint was cancer diagnosis within 2 years. Patients were stratified depending on prior malignancy within 5 years. ICS was explored as a possible risk modifier. We included 50,897 outpatients with COPD; 88% without prior malignancy and 20% with asthma. In the PSM cohorts, 26,003 patients without prior malignancy and 3331 patients with prior malignancy were analyzed. There was no association between asthma-COPD overlap and cancer with hazard ratio (HR) = 0.92, CI = 0.78–1.08, p = 0.31 (no prior malignancy) and HR = 1.04, CI = 0.85–1.26, and p = 0.74 (prior malignancy) as compared to patients with COPD without asthma. ICS did not seem to modify the risk of cancer. In conclusion, in our study, asthma-COPD overlap was not associated with an increased risk of cancer events. Full article
(This article belongs to the Special Issue Chronic Respiratory Diseases and Lung Cancers: From Pathophysiology to Novel Diagnostic and Therapeutic Approaches)
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Review

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20 pages, 638 KiB  
Review
The Usefulness of Nanotechnology in Improving the Prognosis of Lung Cancer
by Gabriela Bordeianu, Nina Filip, Andrei Cernomaz, Bogdan Veliceasa, Loredana Liliana Hurjui, Alin Constantin Pinzariu, Mihaela Pertea, Andreea Clim, Mihai Vasile Marinca and Ionela Lacramioara Serban
Biomedicines 2023, 11(3), 705; https://doi.org/10.3390/biomedicines11030705 - 24 Feb 2023
Cited by 2 | Viewed by 3004
Abstract
Lung cancer remains a major public health problem both in terms of incidence and specific mortality despite recent developments in terms of prevention, such as smoking reduction policies and clinical management advances. Better lung cancer prognosis could be achieved by early and accurate [...] Read more.
Lung cancer remains a major public health problem both in terms of incidence and specific mortality despite recent developments in terms of prevention, such as smoking reduction policies and clinical management advances. Better lung cancer prognosis could be achieved by early and accurate diagnosis and improved therapeutic interventions. Nanotechnology is a dynamic and fast-developing field; various medical applications have been developed and deployed, and more exist as proofs of concepts or experimental models. We aim to summarize current knowledge relevant to the use of nanotechnology in lung cancer management. Starting from the chemical structure-based classification of nanoparticles, we identify and review various practical implementations roughly organized as diagnostic or therapeutic in scope, ranging from innovative contrast agents to targeted drug carriers. Available data are presented starting with standards of practice and moving to highly experimental methods and proofs of concept; particularities, advantages, limits and future directions are explored, focusing on the potential impact on lung cancer clinical prognosis. Full article
(This article belongs to the Special Issue Chronic Respiratory Diseases and Lung Cancers: From Pathophysiology to Novel Diagnostic and Therapeutic Approaches)
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31 pages, 1685 KiB  
Review
Biological and Genetic Mechanisms of COPD, Its Diagnosis, Treatment, and Relationship with Lung Cancer
by Karolina H. Czarnecka-Chrebelska, Debjita Mukherjee, Sofya V. Maryanchik and Magdalena Rudzinska-Radecka
Biomedicines 2023, 11(2), 448; https://doi.org/10.3390/biomedicines11020448 - 3 Feb 2023
Cited by 26 | Viewed by 16283
Abstract
Chronic obstructive pulmonary disease (COPD) is one of the most prevalent chronic adult diseases, with significant worldwide morbidity and mortality. Although long-term tobacco smoking is a critical risk factor for this global health problem, its molecular mechanisms remain unclear. Several phenomena are thought [...] Read more.
Chronic obstructive pulmonary disease (COPD) is one of the most prevalent chronic adult diseases, with significant worldwide morbidity and mortality. Although long-term tobacco smoking is a critical risk factor for this global health problem, its molecular mechanisms remain unclear. Several phenomena are thought to be involved in the evolution of emphysema, including airway inflammation, proteinase/anti-proteinase imbalance, oxidative stress, and genetic/epigenetic modifications. Furthermore, COPD is one main risk for lung cancer (LC), the deadliest form of human tumor; formation and chronic inflammation accompanying COPD can be a potential driver of malignancy maturation (0.8–1.7% of COPD cases develop cancer/per year). Recently, the development of more research based on COPD and lung cancer molecular analysis has provided new light for understanding their pathogenesis, improving the diagnosis and treatments, and elucidating many connections between these diseases. Our review emphasizes the biological factors involved in COPD and lung cancer, the advances in their molecular mechanisms’ research, and the state of the art of diagnosis and treatments. This work combines many biological and genetic elements into a single whole and strongly links COPD with lung tumor features. Full article
(This article belongs to the Special Issue Chronic Respiratory Diseases and Lung Cancers: From Pathophysiology to Novel Diagnostic and Therapeutic Approaches)
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14 pages, 303 KiB  
Review
Adenocarcinomas of the Lung and Neurotrophin System: A Review
by Alberto Ricci, Claudia Salvucci, Silvia Castelli, Antonella Carraturo, Claudia de Vitis and Michela D’Ascanio
Biomedicines 2022, 10(10), 2531; https://doi.org/10.3390/biomedicines10102531 - 10 Oct 2022
Cited by 8 | Viewed by 2512
Abstract
Neurotrophins (NTs) represent a group of growth factors with pleiotropic activities at the central nervous system level. The prototype of these molecules is represented by the nerve growth factor (NGF), but other factors with similar functions have been identified, including the brain derived-growth [...] Read more.
Neurotrophins (NTs) represent a group of growth factors with pleiotropic activities at the central nervous system level. The prototype of these molecules is represented by the nerve growth factor (NGF), but other factors with similar functions have been identified, including the brain derived-growth factor (BDNF), the neurotrophin 3 (NT-3), and NT-4/5. These growth factors act by binding specific low (p75) and high-affinity tyrosine kinase (TrkA, TrkB, and TrkC) receptors. More recently, these growth factors have shown effects outside the nervous system in different organs, particularly in the lungs. These molecules are involved in the natural development of the lungs, and their homeostasis. However, they are also important in different pathological conditions, including lung cancer. The involvement of neurotrophins in lung cancer has been detailed most for non-small cell lung cancer (NSCLC), in particular adenocarcinoma. This review aimed to extensively analyze the current knowledge of NTs and lung cancer and clarify novel molecular mechanisms for diagnostic and therapeutic purposes. Several clinical trials on humans are ongoing using NT receptor antagonists in different cancer cell types for further therapeutic applications. The pharmacological intervention against NT signaling may be essential to directly counteract cancer cell biology, and also indirectly modulate it in an inhibitory way by affecting neurogenesis and/or angiogenesis with potential impacts on tumor growth and progression. Full article
(This article belongs to the Special Issue Chronic Respiratory Diseases and Lung Cancers: From Pathophysiology to Novel Diagnostic and Therapeutic Approaches)

Other

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10 pages, 5324 KiB  
Brief Report
HLA-DRB1*14:54 Is Associated with Pulmonary Alveolar Proteinosis: A Retrospective Real-World Audit
by Mengqian Li, Qinglin Liu, Weiwen Wang and Lili Jiang
Biomedicines 2023, 11(11), 2909; https://doi.org/10.3390/biomedicines11112909 - 27 Oct 2023
Cited by 1 | Viewed by 1489
Abstract
Background: Pulmonary alveolar proteinosis (PAP) is a rare pulmonary disease characterized by abnormal accumulation of pulmonary surfactant lipids in alveoli or terminal bronchioles, leading to increased infection risk and progressive respiratory failure. Approximately more than 90% of all cases are autoimmune PAP (aPAP). [...] Read more.
Background: Pulmonary alveolar proteinosis (PAP) is a rare pulmonary disease characterized by abnormal accumulation of pulmonary surfactant lipids in alveoli or terminal bronchioles, leading to increased infection risk and progressive respiratory failure. Approximately more than 90% of all cases are autoimmune PAP (aPAP). Since one of the predisposing factors has been identified as genes located within the major-histocompatibility-complex region, an investigation of human leukocyte antigen (HLA) alleles associated with the risk of aPAP is warranted. Methods: We retrospectively studied 60 patients pathologically diagnosed with PAP from 2019 to 2022. Patients were divided into the aPAP group or secondary PAP (sPAP) group according to their clinical information. Qualified DNA was extracted from the paraffin-embedded tissue of 28 patients, and the PCR-sequence-based typing method was used for HLA-DRB1 genotyping. Results: A similar HLA-DRB1 allele profile (including the HLA-DRB1*08:03) between the aPAP group and sPAP group was revealed, except that HLA-DRB1*14:54, which has never been reported in aPAP patients, was only detected in the aPAP group rather than the sPAP group (19.4% vs. 0.0%, p = 0.030). Under inhaled granulocyte-macrophage colony-stimulating factor therapy, more clinical remission was observed in HLA-DRB1*14:54 carriers rather than in HLA-DRB1*08:03 carriers (80.0% vs. 57.1%). Conclusions: Our real-world study revealed for the first time that a population with HLA-DRB1*14:54 was subject to aPAP, and HLA-DRB1*14:54 might imply a response in aPAP patients to inhaled granulocyte-macrophage colony-stimulating factor in aPAP patients. Full article
(This article belongs to the Special Issue Chronic Respiratory Diseases and Lung Cancers: From Pathophysiology to Novel Diagnostic and Therapeutic Approaches)
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