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Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fibrosing interstitial lung disease (ILD) of unknown aetiology, with a median survival of 2-4 years from the time of diagnosis. Although IPF has unknown aetiology by definition, there have been identified several risks factors increasing the probability of the onset and progression of the disease in IPF patients such as cigarette smoking and environmental risk factors associated with domestic and occupational exposure. Among them, cigarette smoking together with concomitant emphysema might predispose IPF patients to lung cancer (LC), mostly to non-small cell lung cancer (NSCLC), increasing the risk of lung cancer development. To this purpose, IPF and LC share several cellular and molecular processes driving the progression of both pathologies such as fibroblast transition proliferation and activation, endoplasmic reticulum stress, oxidative stress, and many genetic and epigenetic markers that predispose IPF patients to LC development. Nintedanib, a tyrosine-kinase inhibitor, was firstly developed as an anticancer drug and then recognized as an anti-fibrotic agent based on the common target molecular pathway. In this review our aim is to describe the updated studies on common cellular and molecular mechanisms between IPF and lung cancer, knowledge of which might help to find novel therapeutic targets for this disease combination.

Highlights • Chylothorax is an uncommon form of benign pleural effusion. • It may have poor prognosis if not properly treated. • Conservative measures are the first line of treatment for managing chylothorax. • Surgery is considered an option for recurrent chylothorax. • In our recurrent case, octreotide plus talc poudrage was effective., Introduction and importance Chylothorax is an uncommon form of pleural effusion characterized by the presence of chylomicrons, triglycerides and cholesterol in the physical and chemical examination of the pleural fluid. It may have poor prognosis if not properly treated. Currently, conservative measures are the first line of treatment for managing chylothorax. The aim of our study is to show and suggest the use of octreotide in association with talc poudrage as good option to manage post-operative a severe chylothorax. Case presentation A 59-year-old male patient who underwent a replacement of the ascending aorta, aortic hemiarch and surgery of the aortic valve for aortic dissection showed a severe pleural effusion three months after surgery. Because the physical and chemical examination of the pleural fluid revealed high levels of triglycerides and cholesterol, a conservative treatment with pleural drainage, TPN and nihil per os was attempted, with the introduction of 0.3 mg/die of octreotide on day thirty-four. With the application of talc poudrage, the chylothorax completely resolved. Clinical discussion Octreotide has been shown to significantly decrease chylous effusion in many studies, but the dose and duration of therapy have not yet been defined. Our patient responded partially to octreotide after two days of treatment, with the drainage leak reduced to less than 100 mL/day. Conclusion After octreotide treatment associated with talc poudrage, the drainage leak was drastically reduced, suggesting that this could be a useful approach in the management of severe chylous leaks.

Cancer stem cells (CSCs) have been considered the key drivers of cancer initiation and progression due to their unlimited self-renewal capacity and their ability to induce tumor formation. Macrophages, particularly tumor-associated macrophages (TAMs), establish a tumor microenvironment to protect and induce CSCs development and dissemination. Many studies in the past decade have been performed to understand the molecular mediators of CSCs and TAMs, and several studies have elucidated the complex crosstalk that occurs between these two cell types. The aim of this review is to define the complex crosstalk between these two cell types and to highlight potential future anti-cancer strategies.

Challenging the efficacy of checkpoint inhibitors: a new 3D model for a precision medicine approach.