Exercise prescription for symptoms and quality of life improvements in lung cancer patients: a systematic review.

PURPOSE: The purpose of this study was to conduct a systematic review to assess the effect of exercise on symptoms and quality of life in lung cancer patients. METHODS: We conducted a systematic review using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. PubMed, Medline, Embase, Scopus, Web of Science, and SciELO were searched for studies published from January 1998 to January 2019. The review included all randomized controlled trials that evaluated the effect of exercise on symptoms and quality of life of lung cancer patients. Two reviewers independently assessed the quality of all the included studies using the Physiotherapy Evidence Database scale. RESULTS: In total, ten studies (835 participants) met all inclusion criteria. Three studies investigated the effect of exercise after lung resection, whereas four studies investigated it as a pre-surgery intervention. Two studies investigated the effect of exercise in patients under systemic treatment only, and one study included patients on diverse treatment plans. Exercise protocols consisted of different combinations of strength, aerobic, and inspiratory muscle training. Two trials, including 101 participants, found significant difference in quality of life between groups, favoring the intervention group; and five trials, including 549 participants, found significant inter-group differences in isolated symptoms, also favoring the intervention group. CONCLUSIONS: Exercise can lead to improvements of symptoms and of quality of life in lung cancer survivors. Providing resistance training combined with high-intensity interval aerobic exercise after lung resection seems to be particularly effective. Further studies are warranted to investigate exercise for patients with poor performance status.

Ankyrin-B dysfunction predisposes to arrhythmogenic cardiomyopathy and is amenable to therapy.

Arrhythmogenic cardiomyopathy (ACM) is an inherited arrhythmia syndrome characterized by severe structural and electrical cardiac phenotypes, including myocardial fibrofatty replacement and sudden cardiac death. Clinical management of ACM is largely palliative, owing to an absence of therapies that target its underlying pathophysiology, which stems partially from our limited insight into the condition. Following identification of deceased ACM probands possessing ANK2 rare variants and evidence of ankyrin-B loss of function on cardiac tissue analysis, an ANK2 mouse model was found to develop dramatic structural abnormalities reflective of human ACM, including biventricular dilation, reduced ejection fraction, cardiac fibrosis, and premature death. Desmosomal structure and function appeared preserved in diseased human and murine specimens in the presence of markedly abnormal ß-catenin expression and patterning, leading to identification of a previously unknown interaction between ankyrin-B and ß-catenin. A pharmacological activator of the WNT/ß-catenin pathway, SB-216763, successfully prevented and partially reversed the murine ACM phenotypes. Our findings introduce what we believe to be a new pathway for ACM, a role of ankyrin-B in cardiac structure and signaling, a molecular link between ankyrin-B and ß-catenin, and evidence for targeted activation of the WNT/ß-catenin pathway as a potential treatment for this disease.

Successful Intravascular Correction of Intratumoral Pseudoaneurysm by Erosion of the Aorta in a Patient with Thoracic Giant Cell Tumor of Bone Responding to Denosumab.

Giant cell tumor of bone (GCT) is a rare, locally aggressive neoplasm characterized by the presence of giant cells with osteoclast activity. Its biology involves the overexpression of the Receptor Activator of Nuclear Factor kB Ligand (RANKL) by osteoclast-like giant cells and tumor stromal cells, which has been shown to be an actionable target in this disease. In cases amenable to surgical resection, very few therapeutic options were available until the recent demonstration of significant activity of the anti-RANK-ligand monoclonal antibody denosumab. Here we present a case of a patient with advanced GCT arising in the spine, recurring after multiple resections and embolization. Following initiation of denosumab, which resulted in unequivocal clinical improvement, computed tomography of the chest done for reassessment purposes revealed an intratumoral pseudoaneurysm by erosion of the aorta, further corrected by endovascular approach and stent placement. Patient had an unremarkable recovery from the procedure and continued benefit from therapy with denosumab and remains on treatment 24 months after the first dose.