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      Risk of cancer after lung transplantation for COPD

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          Abstract

          Background

          The risk of cancer is increased and affects survival after lung transplantation (LTx), but has not been well characterized in COPD. We aimed to evaluate the incidence and prognosis of cancer following LTx for COPD.

          Methods

          A prospective, population-based study of patients undergoing LTx for end-stage COPD at the two transplantation centers in Sweden between 1990−2013, with follow-up for incident cancer and death, using national registers. The excess risk of cancer was calculated as standardized incidence ratios compared with the general population matched for age, sex, and calendar year. Risk factors for cancer were analyzed using Fine-Gray regression, and survival after cancer diagnosis with Kaplan–Meier.

          Results

          In total, 331 patients (mean age 55.4 years; 64% women; 97% former smokers) were included. At a median follow-up of 2.8 years, 35% of patients had developed cancer and the risk was increased more than 10-fold ([95% CI] 8.1−11.8). The highest excess risks were for non-Hodgkin lymphoma (20.8−66.7), skin cancer (20.3−35.2), lung (11.7−31.2), liver (3.6−51.6), and colorectal cancer (6.1−19.5). Median survival was longer for skin cancer (8 years; 95% CI, 3−15) compared with non-skin cancer (4 years; 95% CI, 2.8−4.8; p<0.001).

          Conclusion

          The cancer risk is markedly increased after LTx for COPD. It could not be predicted by the factors evaluated, but contributed significantly to a negative prognosis.

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          Most cited references 19

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          Lymphomas after solid organ transplantation: a collaborative transplant study report.

          We used the Collaborative Transplant Study database to analyze the incidence, risk, and impact of malignant lymphomas in approximately 200,000 organ transplant recipients. Over a 10-year period, the risk in renal transplant recipients was 11.8-fold higher than that in a matched nontransplanted population (p<0.0001). The majority of lymphomas were diagnosed after the first post-transplant year. Heart-lung transplants showed the highest relative risk (RR 239.5) among different types of organ transplants. In kidney recipients, immunosuppression with cyclosporine did not confer added risk compared with azathioprine/steroid treatment, whereas treatment with FK506 increased the risk approximately twofold. Induction therapy with OKT3 or ATG, but not with anti-IL2 receptor antibodies, increased the risk of lymphoma during the first year. Antirejection therapy with OKT3 or ATG also increased the risk. First-year mortality in renal and heart transplant patients with lymphoma was approximately 40% and 50%, respectively, and showed no improvement in recent years. A pattern of preferential localization to the vicinity of the transplant was noted, and the prognosis of the patient was related to localization. This study highlights the continuing risk for lymphoma with time post-transplantation, the contribution of immunosuppression to increased risk, and continuing poor outcomes in patients with post-transplant lymphoma.
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            The relationship between COPD and lung cancer

            Highlights • COPD is a risk factor for lung cancer beyond their shared aetiology. • Both are driven by oxidative stress. • Both are linked to cellular aging, senescence and telomere shortening. • Both have been linked to genetic predisposition. • Both show altered epigenetic regulation of gene expression.
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              Low lung function and incident lung cancer in the United States: data From the First National Health and Nutrition Examination Survey follow-up.

              Obstructive lung disease and lung cancer are tobacco-related diseases that can remain clinically silent until late in the disease process. We sought to define the risk for incident lung cancer among a national cohort of US adults with and without obstructive lung disease. We studied participants in the First National Health and Nutrition Examination Survey, who had up to 22 years of follow-up. We classified subjects as having moderate or severe obstructive lung disease at baseline if the ratio of forced expiratory volume in 1 second (FEV1) to forced vital capacity (FVC) was less than 70% and the FEV1 was less than 80% of the predicted value. We also determined incident cases of lung cancer during the follow-up period. A total of 113 lung cancers occurred in the 5402 adults in the cohort. In the proportional hazards model adjusted for covariates of age, sex, race, education, smoking status, and duration and intensity of smoking, the presence of moderate or severe obstructive lung disease was associated with a higher risk for incident lung cancer (hazard ratio, 2.8; 95% confidence interval, 1.8-4.4). The presence of moderate or severe obstructive lung disease is a significant predictor of incident lung cancer in long-term follow-up. This finding may be useful clinically and in studies evaluating the utility of new tools for the early detection of lung cancer.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2017
                03 October 2017
                : 12
                : 2841-2847
                Affiliations
                [1 ]Department of Clinical Sciences, Division of Respiratory Medicine & Allergology, Lund University, Lund, Sweden
                [2 ]Department of Respiratory Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden
                [3 ]Department of Respiratory Medicine, Skåne University Hospital, Lund University, Malmö, Sweden
                Author notes
                Correspondence: Hanan A Tanash, Department of Respiratory Medicine, Skåne University Hospital, Lund University, Jan Waldenströms gata 24, plan 4, S-205 02, Malmö, Sweden, Tel +46 40 331 000, Fax +46 40 336 225, Email hanan.tanash@ 123456med.lu.se
                Article
                copd-12-2841
                10.2147/COPD.S147065
                5633308
                © 2017 Ekström et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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                Original Research

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