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Many data already suggested that cancer and IPF are underlined by a number of common pathogenic biologic pathways. However, fewer data regards the interconnections, in terms of synergy or increased toxicities, of drugs used in cancer and IPF. Particularly, how the specific therapy influences the concurrent condition and prognostic factors of response in patients with both lung cancer and IPF are far to be clarified. Similarly, identification of features of IPF patients with higher risk of developing pulmonary adverse events when treated with chemotherapy, immune checkpoint inhibitors, TKIs, or radiotherapy is of primary importance in clinical practice.We will discuss the scientific rationale, based on the extensive analysis of literature data, by consulting several databases for combining anticancer and antifibrotic treatments and for the design of novel therapeutic strategies. The role of immunotherapy in cancer aroused in IPF context will be discussed with specific interested, based on the continuously increasing role of immune checkpoint inhibition against lung tumors.This work will help to improve knowledge, based on a multidisciplinary perspective, on IPF and cancer patients, which identify an unmet clinical need. A better management during each phase of disease progression will require the design innovative trials and the development of new drugs and molecules both in the oncologic and respiratory medicine pipeline.

Introduction: Landscape of Extensive Stage (ES)-SCLC treatment has been largely unchanged over the years. Chemotherapy, mostly based on cisplatin and etoposide, remained the standard-of-care for patients with ES-SCLC, without any additional improvement in outcomes for almost 40 years. In this scenario, immune check points inhibitors have emerged marking a turning point in cancer treatment and more recently for SCLC.Areas covered: Aim of the paper is to discuss ICIs impact on ES-SCLC treatment algorithms, review current clinical trials and explore future perspectives.Expert opinion: A growing body of evidence supports ICI-containing regimens as a new mainstay of ES-SCLC treatment. Whether subgroups of SCLC patients may have greater survival benefits from ICIs treatment needs to be better defined. Understanding the impact of tumor microenvironment and identifying reliable predictive and/or prognostic biomarkers will be fundamental to move towards a personalized treatment approach leading to improved survival.

Lung cancer (LC) and chronic obstructive pulmonary disease (COPD) represent leading causes of morbidity and mortality worldwide. Common risk factors lead to an increased inflammatory response, enhances oxidative stress, and changes in lung microenvironment contributing to fine-tuned interaction between these respiratory disorders. Despite evidence that COPD represents a main risk factor for LC, assessment of LC risk features among COPD patients is not routinely considered in the clinical practice. In LC patients concurrent COPD may impact on clinical scenario influencing the response to treatment. Better understanding LC and COPD coexistence may impact on clinical scenario influencing therapeutic approach. In this review, we describe the basis of this network and how the complex interplay between these respiratory disorders affects the clinical decision-making process.

BACKGROUND AND OBJECTIVE: Translational research is a source of continuous innovation in medicine, more particularly for clinical research on new treatment modalities in idiopathic pulmonary fibrosis (IPF) patients. However, the heterogeneity of the disease is well recognized, and different pathological and molecular settings have been identified. The molecular mechanisms by which IPF proceeds in time and space remains poorly understood. Although some IPF features are reminiscent of cancer, the dynamics of malignant divergent clonal selective pressure and heterogeneity clearly differ from those occurring in IPF. This is reflected in the absence of patient proper selection and stratification to biological agents (pirfenidone, nintedanib) which limit therapeutic efficacy. Consequently, increased costs are related to the clinical management of advanced IPF patients. Steady collaboration and fluid communication between pneumo-oncologists, radiologists and molecular biologists is a clear priority for the correct interpretation of tests and the definition of effective personalized strategies against this orphan disease. The present work aims at providing the most relevant hints shared by cancer and IPF. METHODS: A systematic literature review was performed to identify all relevant data. The examined databases were Scopus, Web of Science, Cochrane, Google Scholar, and PubMed. The last search was run on January 5, 2022. We have primarily conducted separated research for lung cancer, IPF, genetics, epigenetics, surgery in IPF and cancer. KEY CONTENT AND FINDINGS: The data here presented mainly focus on gene mutations, epigenetics and novel therapeutic approaches. Moreover, epidemiology, prognostic variables and in new treatment strategies adopted in patients with IPF and lung cancer are discussed as well. CONCLUSIONS: Overall, the findings of this narrative review will be of help in defining the key molecular features that could applied in IPF setting with promising rationale to improve therapy and to better manage those cases carrying IPF and cancer concomitantly.

Obesity, through adipose tissue (AT) inflammation and dysregulation, represents a critical factor for COVID-19; here, we investigated whether serum levels of adiponectin, HMW oligomers, leptin, and resistin are modulated and/or correlated with clinical and biochemical parameters of severe COVID-19 patients. This study included 62 severe COVID-19 patients; 62 age and sex-matched healthy subjects were recruited as a control group. Anthropometric and biochemical parameters were obtained and compared. Adiponectin, HMW oligomers, leptin, and resistin were analyzed by ELISA. The adiponectin oligomerization state was visualized by Western blotting. When compared to healthy subjects, total adiponectin levels were statistically lower in severe COVID-19 while, in contrast, the levels of leptin and resistin were statistically higher. Interestingly, HMW adiponectin oligomers negatively correlated with leptin and were positively associated with LUS scores. Resistin showed a positive association with IL-6, IL-2R, and KL-6. Our data strongly support that adipose tissue might play a functional role in COVID-19. Although it needs to be confirmed in larger cohorts, adiponectin HMW oligomers might represent a laboratory resource to predict patient seriousness. Whether adipokines can be integrated as a potential additional tool in the evolving landscape of biomarkers for the COVID-19 disease is still a matter of debate. Other studies are needed to understand the molecular mechanisms behind adipokine’s involvement in COVID-19. © 2023 by the authors.

Background: Limited evidence exists regarding adverse modifications affecting cardiovascular and pulmonary function in physical active adults affected by COVID-19, especially in athletic populations. We aimed to describe the clinical presentation of COVID-19 in a cohort of competitive athletes, as well as spirometry and echocardiography findings and cardio-respiratory performance during exercise. Methods: Twenty-four competitive athletes with COVID-19 were recruited for this study after ending self-isolation and confirmation of negative laboratory results. All athletes underwent clinical evaluation, spirometry, echocardiography and cardiopulmonary exercise testing (CPET). These data were compared to a group of healthy control athletes. Results: Anosmia was the most frequent symptom present in 70.83% patients, followed by myalgia, fatigue and ageusia. The most frequent persisting symptoms were anosmia 11 (45.83%) and ageusia 8 (33.33%). Compared to controls, COVID-19 patients presented lower FEV1%: 97.5 (91.5–108) vs. 109 (106–116) p = 0.007. Peak Oxygen Uptake (VO2) in COVID-19 patients was 50.1 (47.7–51.65) vs. 49 (44.2–52.6) in controls (p = 0.618). Conclusions: Reduced exercise capacity was not identified and pulmonary and cardiovascular function are not impaired during early recovery phase in a population of physical active adults except FEV1 reduction.

Lung cancer still represents the leading cause of cancer-related death, globally. Likewise, malnutrition and inactivity represent a major risk for loss of functional pulmonary capacities influencing overall lung cancer severity. Therefore, the adhesion to an appropriate health lifestyle is crucial in the management of lung cancer patients despite the subtype of cancer. This review aims to summarize the available knowledge about dietary approaches as well as physical activity as the major factors that decrease the risk towards lung cancer, and improve the response to therapies. We discuss the most significant dietary schemes positively associated to body composition and prognosis of lung cancer and the main molecular processes regulated by specific diet schemes, functional foods and physical activity, i.e., inflammation and oxidative stress. Finally, we report evidence demonstrating that dysbiosis of lung and/or gut microbiome, as well as their interconnection (the gut–lung axis), are strictly related to dietary patterns and regular physical activity playing a key role in lung cancer formation and progression, opening to the avenue of modulating the microbiome as coadjuvant therapy. Altogether, the evidence reported in this review highlights the necessity to consider non-pharmacological interventions (nutrition and physical activity) as effective adjunctive strategies in the management of lung cancer.

Background: Chronic obstructive pulmonary disease (COPD) is characterized by the presence of air flow limitation and exacerbations caused by inflammation. Recently, blood neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) have been shown to be valuable predictors of inflammatory conditions and are used for risk stratification of different diseases. During COPD exacerbation, NLR and PLR are associated to mortality, ICU occupancy and need for NIV. Methods: We therefore conducted a retrospective study in stable COPD patients to evaluate the role of NLR in phenotyping COPD patients. The study included COPD patients ≥ 40 years, current or former smokers (pack/years ≥10) with documented FEV1/FVC Results: From 66 consecutive COPD patients, 46 met the inclusion criteria. 8 (17.4%) patients were group A, 21 (45.6%) group B, 2 (4.3%) group C, 15 (32.6%) group D. Mean NLR was 2.86±1.76; Mean PLR was 136.9±77.0. The cut-off value of NLR was arbitrarily defined based on the upper quartile point as 3.3. Patients with high NLR showed lower FEV1 (p= 0.036), FVC (p=0.048), with more symptoms (p=0.029) and worse COPD stage (p=0.01). Interestingly, patients with high NLR were more likely under ICS treatment (p=0.059). A PLR ratio cut-off of 158.0 discriminated patients more symptomatic (p=0.01) and with worse disease stage (p=0.01). Conclusions: NLR and PLR are independently associated with disease severity in stable COPD.

Latest evidences from literature suggest that SARS-CoV-2 disease 2019 (COVID-19) is commonly complicated with coagulopathy and that disseminated intravascular coagulation is present in the majority of deceased patients. Particularly, conventional coagulation parameters appear to be significantly altered in patients with poor prognosis. A wide-ranging cross- talk between coagulative haemostasis and inflammation, as well as the activation of coagulation cascade during viral infections, are well established. Another important evidence which may explain coagulation disorders in COVID-19 is the increase of thrombus formation under conditions of hypoxia. Despite the exact pathophysiological mechanism of coronavirus-induced thromboembolism needs to be further investigated, this finding suggests that it is good practice to assess the risk of thrombosis in COVID-19 patients to improvethe clinical management in terms of anticoagulation therapy. Anticoagulants, mainly low-molecular-weight heparin (LMWH), should be tailored in patients meeting sepsis induced coagulopathy (SIC) criteria or with markedly elevated D-dimer. In this context, further studies are needed to optimise the decision making in therapeutic approach.

The elderly may represent a specific cluster of high-risk patients for developing COVID-19 with rapidly progressive clinical deterioration. Indeed, in older individuals, immunosenescence and comorbid disorders are more likely to promote viral-induced cytokine storm resulting in life-threatening respiratory failure and multisystemic involvement. Early diagnosis and individualized therapeutic management should be developed for elderly subjects based on personal medical history and polypharmacotherapy. Our review examines the pathogenesis and clinical implications of ageing in COVID-19 patients; finally, we discuss the evidence and controversies in the management in the long-stay residential care homes and aspects of end-of-life care for elderly patients with COVID-19.

Pulmonary hypertension is an umbrella term including many different disorders causing an increase of the mean pulmonary arterial pressure (mPAP) ≥ 25 mmHg. Recent data revealed a strong association between obesity and pulmonary hypertension. Adiponectin is a protein synthetized by the adipose tissue with pleiotropic effects on inflammation and cell proliferation, with a potential protective role on the pulmonary vasculature. Both in vivo and in vitro studies documented that adiponectin is an endogenous modulator of NO production and interferes with AMP-activated protein kinase (AMPK) activation, mammalian target of rapamycin (mTOR), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κβ) signaling preventing endothelial dysfunction and proliferation. Furthermore, adiponectin ameliorates insulin resistance by mediating the biological effects of peroxisome proliferator-activated receptor-gamma (PPARγ). Therefore, adiponectin modulation emerged as a theoretical target for the treatment of pulmonary hypertension, currently under investigation. Recently, consistent data showed that hypoglycemic agents targeting PPARγ as well as renin⁻angiotensin system inhibitors and mineralocorticoid receptor blockers may influence pulmonary hemodynamics in different models of pulmonary hypertension.

Elderly patients represent the majority of lung cancer cases, but they are often under-represented in clinical cancer treatment trials or excluded from studies because of comorbidities. Due to lack of data, treatment options for this population must be carefully evaluated and preliminary assessment should aim to stratify patients into different risk subgroups. In early NSCLC stages, surgery remains the best therapeutic option in low-moderate risk patients. Conversely, in patients unfit for surgery or in advanced stages, chemotherapy and radiotherapy should be considered as they may offer benefits in terms of clinical outcomes. Recent developments in targeting driver genes mutations as well as immune checkpoints have opened novel horizon in lung cancer management and systematic investigation in elderly population is required. In this review, we examined the more recent results of the literature about the therapeutic scenario in limited and advanced lung cancer stages in elderly and very elderly population.

Ischemic heart disease is currently a major cause of mortality and morbidity worldwide. Nevertheless, the actual therapeutic scenario does not target myocardial cell regeneration and consequently, the progression toward the late stage of chronic heart failure is common. Endothelial progenitor cells (EPCs) are bone marrow-derived stem cells that contribute to the homeostasis of the endothelial wall in acute and chronic ischemic disease. Calcium modulation and other molecular pathways (NOTCH, VEGFR, and CXCR4) contribute to EPC proliferation and differentiation. The present review provides a summary of EPC biology with a particular focus on the regulatory pathways of EPCs and describes promising applications for cardiovascular cell therapy.