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      Investigating the association between allergen-specific immunoglobulin E, cancer risk and survival

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          ABSTRACT

          Prior findings linking allergy and cancer have been inconsistent, which may be driven by diverse assessment methods. We used serum specific immunoglobulin E (IgE) against common inhalant allergens that was assessed prior to cancer diagnosis in studying this association. We selected 8,727 Swedish men and women who had measurements of serum allergen-specific IgE and total IgE between 1992 and 1996. Multivariable Cox regression using age as a timescale was performed to assess the associations of IgE sensitization, defined by any levels of serum specific IgE ≥35 kU/L, with risk of overall and specific cancers. A test for trend was performed by assigning scores derived from allergen-specific IgE levels at baseline as an ordinal scale. Kaplan–Meier curves and log-rank test were used to assess cancer survival by IgE sensitization status. During a mean follow-up of 16 year, 689 persons were diagnosed with cancer. We found an inverse association between IgE sensitization and cancer risk, with a hazard ratio (HR) of 0.83 and 95% confidence intervals (CI) of 0.70–0.99. A similar trend was seen with specific IgE scores overall (P trend = 0.007) and in women (P trend = 0.01). Although IgE sensitization was not associated with risk of common site-specific cancers, serum specific IgE scores were inversely associated with melanoma risk in men and women combined, and with risk of female breast and gynecological cancers combined. No association with survival was observed. The association between circulating IgE levels and incident cancer may point toward a role of T-helper 2 (T H2)-biased response in development of some cancers.

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          Cancer as an overhealing wound: an old hypothesis revisited.

          What is the relationship between the wound-healing process and the development of cancer? Malignant tumours often develop at sites of chronic injury, and tissue injury has an important role in the pathogenesis of malignant disease, with chronic inflammation being the most important risk factor. The development and functional characterization of genetically modified mice that lack or overexpress genes that are involved in repair, combined with gene-expression analysis in wounds and tumours, have highlighted remarkable similarities between wound repair and cancer. However, a few crucial differences were also observed, which could account for the altered metabolism, impaired differentiation capacity and invasive growth of malignant tumours.
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            The regulation of immunoglobulin E class-switch recombination.

            Immunoglobulin E (IgE) isotype antibodies are associated with atopic disease, namely allergic rhinitis, asthma and atopic dermatitis, but are also involved in host immune defence mechanisms against parasitic infection. The commitment of a B cell to isotype class switch to an IgE-producing cell is a tightly regulated process, and our understanding of the regulation of IgE-antibody production is central to the prevention and treatment of atopic disease. Both those that are presently in use and potential future therapies to prevent IgE-mediated disease take advantage of our existing knowledge of the specific mechanisms that are required for IgE class switching.
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              IgG4 subclass antibodies impair antitumor immunity in melanoma.

              Host-induced antibodies and their contributions to cancer inflammation are largely unexplored. IgG4 subclass antibodies are present in IL-10-driven Th2 immune responses in some inflammatory conditions. Since Th2-biased inflammation is a hallmark of tumor microenvironments, we investigated the presence and functional implications of IgG4 in malignant melanoma. Consistent with Th2 inflammation, CD22+ B cells and IgG4(+)-infiltrating cells accumulated in tumors, and IL-10, IL-4, and tumor-reactive IgG4 were expressed in situ. When compared with B cells from patient lymph nodes and blood, tumor-associated B cells were polarized to produce IgG4. Secreted B cells increased VEGF and IgG4, and tumor cells enhanced IL-10 secretion in cocultures. Unlike IgG1, an engineered tumor antigen-specific IgG4 was ineffective in triggering effector cell-mediated tumor killing in vitro. Antigen-specific and nonspecific IgG4 inhibited IgG1-mediated tumoricidal functions. IgG4 blockade was mediated through reduction of FcγRI activation. Additionally, IgG4 significantly impaired the potency of tumoricidal IgG1 in a human melanoma xenograft mouse model. Furthermore, serum IgG4 was inversely correlated with patient survival. These findings suggest that IgG4 promoted by tumor-induced Th2-biased inflammation may restrict effector cell functions against tumors, providing a previously unexplored aspect of tumor-induced immune escape and a basis for biomarker development and patient-specific therapeutic approaches.
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                Author and article information

                Journal
                Oncoimmunology
                Oncoimmunology
                KONI
                Oncoimmunology
                Taylor & Francis
                2162-4011
                2162-402X
                June 2016
                28 March 2016
                28 March 2016
                : 5
                : 6
                : e1154250
                Affiliations
                [a ]Cancer Epidemiology Group, Division of Cancer Studies, King's College London , London, UK
                [b ]Department of Surgical Sciences, Uppsala University Hospital , Uppsala, Sweden
                [c ]Regional Cancer Centre , Uppsala, Sweden
                [d ]St. John's Institute of Dermatology, Division of Genetics and Molecular Medicine, Faculty of Life Sciences and Medicine, King's College London, NIHR Biomedical Research Centre at Guy's and St. Thomas's Hospitals and King's College London , London, UK
                [e ]Center of Allergy Research, Institute of Environmental Medicine, Karolinska Insitutet , Stockholm, Sweden
                [f ]Unit of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet , Stockholm, Sweden
                [g ]Department of Medical Epidemiology and Biostatistics, Karolinska Institutet , Stockholm, Sweden
                [h ]AstraZeneca R&D , Mölndal, Sweden
                [i ]Unit of Cardiovascular Epidemiology, Institute of Environmental Medicine, Karolinska Institutet , Stockholm, Sweden
                [j ]Department of Medicine, Clinical Epidemiological Unit, Karolinska Institutet and CALAB Research , Stockholm, Sweden
                [k ]Richard Dimbleby Department of Cancer Research, Randall Division and Division of Cancer Studies, King's College London , London, UK
                [l ]Division of Hematology/Oncology, Faculty of Medicine, Gadjah Mada University , Yogyakarta, Indonesia
                Author notes
                CONTACT Wahyu Wulaningsih wahyu.wulaningsih@ 123456kcl.ac.uk

                Supplemental data for this article can be accessed on the publisher's website.

                Article
                1154250
                10.1080/2162402X.2016.1154250
                4938379
                27471625
                25583a35-b04b-4a51-bd55-6beab62d59e5
                © 2016 The Author(s). Published with license by Taylor & Francis.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

                History
                : 23 December 2015
                : 29 January 2016
                : 9 February 2016
                Page count
                Figures: 1, Tables: 4, References: 46, Pages: 8
                Categories
                Original Research

                Immunology
                allergy,atopy,cancer,immunoglobulin e,cohort
                Immunology
                allergy, atopy, cancer, immunoglobulin e, cohort

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