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      Elevated Foxp3/CD8 Ratio in Lung Adenocarcinoma Metastatic Lymph Nodes Resected by Transcervical Extended Mediastinal Lymphadenectomy

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          Abstract

          A balance between tumor invasion and immune defence system is widely investigated. Objective. The aim of this study was to evaluate lymphocyte phenotype in lymph nodes (LNs) of patients with lung cancer in relation to the presence of metastases. Methods. We investigated 364 LNs resected by transcervical extended mediastinal lymphadenectomy (TEMLA) of 49 patients with squamous cell carcinoma (SCC) or adenocarcinoma (AD) with (A) and without metastases (B). Expression of CD4, CD8, CD25, CTLA-4, and Foxp3 was assessed by immunohistochemical staining. Results. We observed a strong nuclear staining for Foxp3 in lymphocytes and cancer cells and strong membranous/cytoplasmatic reaction for CD4 and CD8, but low for CD25 and CTLA-4. There were significantly higher proportions of CD8+ cells in AD (B) versus AD (A) LNs (80% versus 52.5%, p < 0.05). The Foxp3/CD8 ratio was higher in AD (A) versus AD (B) LNs (0.4 versus 0.25, p < 0.05). No significant differences in the cell markers expression in SCC LNs were found. Conclusion. Significant differences in lymphocyte phenotype in AD may indicate an exceptional biology of this type of lung cancer. TEMLA resected LNs may serve as valuable samples for evaluation of immune status in lung cancer patients.

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          CANCER IMMUNOLOGY. The "cancer immunogram".

          C U Blank, J. Haanen, Á. Ribas … (2016)
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            Epidemiology of lung cancer: Diagnosis and management of lung cancer, 3rd ed: American College of Chest Physicians evidence-based clinical practice guidelines.

            Anthony J Alberg, Malcolm Brock, Jean Ford … (2013)
            Ever since a lung cancer epidemic emerged in the mid-1900 s, the epidemiology of lung cancer has been intensively investigated to characterize its causes and patterns of occurrence. This report summarizes the key findings of this research. A detailed literature search provided the basis for a narrative review, identifying and summarizing key reports on population patterns and factors that affect lung cancer risk. Established environmental risk factors for lung cancer include smoking cigarettes and other tobacco products and exposure to secondhand tobacco smoke, occupational lung carcinogens, radiation, and indoor and outdoor air pollution. Cigarette smoking is the predominant cause of lung cancer and the leading worldwide cause of cancer death. Smoking prevalence in developing nations has increased, starting new lung cancer epidemics in these nations. A positive family history and acquired lung disease are examples of host factors that are clinically useful risk indicators. Risk prediction models based on lung cancer risk factors have been developed, but further refinement is needed to provide clinically useful risk stratification. Promising biomarkers of lung cancer risk and early detection have been identified, but none are ready for broad clinical application. Almost all lung cancer deaths are caused by cigarette smoking, underscoring the need for ongoing efforts at tobacco control throughout the world. Further research is needed into the reasons underlying lung cancer disparities, the causes of lung cancer in never smokers, the potential role of HIV in lung carcinogenesis, and the development of biomarkers.
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              Tumor-induced perturbations of cytokines and immune cell networks.

              Brett Burkholder, Ren-Yu Huang, Rob Burgess … (2014)
              Until recently, the intrinsically high level of cross-talk between immune cells, the complexity of immune cell development, and the pleiotropic nature of cytokine signaling have hampered progress in understanding the mechanisms of immunosuppression by which tumor cells circumvent native and adaptive immune responses. One technology that has helped to shed light on this complex signaling network is the cytokine antibody array, which facilitates simultaneous screening of dozens to hundreds of secreted signal proteins in complex biological samples. The combined applications of traditional methods of molecular and cell biology with the high-content, high-throughput screening capabilities of cytokine antibody arrays and other multiplexed immunoassays have revealed a complex mechanism that involves multiple cytokine signals contributed not just by tumor cells but by stromal cells and a wide spectrum of immune cell types. This review will summarize the interactions among cancerous and immune cell types, as well as the key cytokine signals that are required for tumors to survive immunoediting in a dormant state or to grow and spread by escaping it. Additionally, it will present examples of how probing secreted cell-cell signal networks in the tumor microenvironment (TME) with cytokine screens have contributed to our current understanding of these processes and discuss the implications of this understanding to antitumor therapies.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Biomed Res Int
                Journal ID (iso-abbrev): Biomed Res Int
                Journal ID (publisher-id): BMRI
                Title: BioMed Research International
                Publisher: Hindawi
                ISSN (Print): 2314-6133
                ISSN (Electronic): 2314-6141
                Publication date (Print): 2017
                Publication date (Electronic): 2 August 2017
                Volume: 2017
                Electronic Location Identifier: 5185034
                Affiliations
                1Department of Internal Medicine, Pulmonology and Allergology, Medical University of Warsaw, Warsaw, Poland
                2Laboratory of Flow Cytometry and Hematology, Department of Internal Medicine and Hematology, Military Medical Institute, Warsaw, Poland
                3Department of Pathology, Pulmonary Hospital, Zakopane, Poland
                4Department of Pathology, Medical University of Warsaw, Warsaw, Poland
                5Department of Thoracic Surgery, Pulmonary Hospital, Zakopane, Poland
                Author notes
                *Joanna Domagala-Kulawik: domagalakulawik@ 123456gmail.com

                Academic Editor: Torsten Goldmann

                Author information
                http://orcid.org/0000-0002-2260-3676
                Article
                DOI: 10.1155/2017/5185034
                PMC ID: 5558641
                PubMed ID: 28831395
                SO-VID: 4c5a8bbe-93a8-4c4b-b7e9-5501ad4a277f
                Copyright © Copyright © 2017 Joanna Domagala-Kulawik et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 7 March 2017
                Date revision received : 20 June 2017
                Date accepted : 5 July 2017
                Categories
                Subject: Research Article

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