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      Prognostic value of soluble major histocompatibility complex class I polypeptide-related sequence A in non-small-cell lung cancer – significance and development

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          Abstract

          Soluble major histocompatibility complex class I polypeptide-related sequence A (sMICA) is a useful marker in surveillance of lung cancer. High serum sMICA level in patients with non-small-cell lung cancer (NSCLC) seems to be a poor prognostic factor being correlated with poor differentiation and advanced stage. However, the low specificity limits its role as a single prognostic marker of NSCLC, but its evaluation, in addition to standard serum markers, could improve the staging of NSCLC. Despite promising, all current studies are insufficient to assess the real efficiency of sMICA as a prognostic marker of NSCLC, and hence, future studies are required to validate it.

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          Most cited references54

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          Activation of NK cells and T cells by NKG2D, a receptor for stress-inducible MICA.

          Stress-inducible MICA, a distant homolog of major histocompatibility complex (MHC) class I, functions as an antigen for gammadelta T cells and is frequently expressed in epithelial tumors. A receptor for MICA was detected on most gammadelta T cells, CD8+ alphabeta T cells, and natural killer (NK) cells and was identified as NKG2D. Effector cells from all these subsets could be stimulated by ligation of NKG2D. Engagement of NKG2D activated cytolytic responses of gammadelta T cells and NK cells against transfectants and epithelial tumor cells expressing MICA. These results define an activating immunoreceptor-MHC ligand interaction that may promote antitumor NK and T cell responses.
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            The International Epidemiology of Lung Cancer: geographical distribution and secular trends.

            This review presents the latest available international data for lung cancer incidence, mortality and survival, emphasizing the established causal relationship between smoking and lung cancer. In 2002, it was estimated that 1.35 million people throughout the world were diagnosed with lung cancer, and 1.18 million died of lung cancer-more than for any other type of cancer. There are some key differences in the epidemiology of lung cancer between more developed and less developed countries. In more developed countries, incidence and mortality rates are generally declining among males and are starting to plateau for females, reflecting previous trends in smoking prevalence. In contrast, there are some populations in less developed countries where increasing lung cancer rates are predicted to continue, due to endemic use of tobacco. A higher proportion of lung cancer cases are attributable to nonsmoking causes within less developed countries, particularly among women. Worldwide, the majority of lung cancer patients are diagnosed after the disease has progressed to a more advanced stage. Despite advances in chemotherapy, prognosis for lung cancer patients remains poor, with 5-year relative survival less than 14% among males and less than 18% among females in most countries. Given the increasing incidence of lung cancer in less developed countries and the current lack of effective treatment for advanced lung cancers, these results highlight the need for ongoing global tobacco reform to reduce the international burden of lung cancer.
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              Defective expression and function of natural killer cell-triggering receptors in patients with acute myeloid leukemia.

              The cytolytic function of natural killer (NK) cells is induced by the engagement of a series of activating receptors and coreceptors some of which have recently been identified and collectively termed natural cytotoxicity receptors (NCRs). Here, we analyzed the cytolytic function of NK cells obtained from patients with acute myeloid leukemia (AML). In sharp contrast with healthy donors, in most (16 of 18) patients with AML the majority of NK cells displayed low NCR surface density (NCR(dull)). This phenotype correlated with a weak cytolytic activity against autologous leukemic cells that could not be reversed by the monoclonal antibody-mediated disruption of HLA class I/killer immunoglobulinlike receptor interaction. The remaining 2 patients were characterized by NK cells having an NCR(bright) phenotype. Surprisingly, although displaying NCR-mediated cytolytic activity, these NCR(bright) NK cells were unable to kill autologous leukemic blasts. Importantly, the leukemic blasts from these 2 patients were also resistant to lysis mediated by normal NCR(bright) allogeneic NK cells. Our study suggests that in most instances the inability of NK cells to kill autologous leukemic blasts is consequent to low NCR surface expression. In few cases, however, this failure appears to involve a mechanism of tumor escape based on down-regulation of ligands relevant for NCR-mediated target cell recognition.
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                Author and article information

                Journal
                Lung Cancer (Auckl)
                Lung Cancer (Auckl)
                Lung Cancer: Targets and Therapy
                Lung Cancer: Targets and Therapy
                Dove Medical Press
                1179-2728
                2017
                10 October 2017
                : 8
                : 161-167
                Affiliations
                Thoracic Surgery Unit, Università degli Studi della Campania “Luigi Vanvitelli”, Naples, Italy
                Author notes
                Correspondence: Alfonso Fiorelli, Thoracic Surgery Unit, Università degli Studi della Campania “Luigi Vanvitelli”, Piazza Miraglia, 2, I-80138 Naples, Italy, Tel +39 81 566 5228, Fax +39 81 566 5230, Email alfonso.fiorelli@ 123456unicampania.it
                Article
                lctt-8-161
                10.2147/LCTT.S105623
                5644548
                57fe1873-4709-4b2f-8854-c30dcc7a1507
                © 2017 Cascone 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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                nsclc,mica,micb,prognostic factor
                nsclc, mica, micb, prognostic factor

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