ArticleCancer immunology, immunotherapy : CII1994
Patho- and immunobiology of malignant mesothelioma: characterisation of tumour infiltrating leucocytes and cytokine production in a murine model.
Article in Cancer immunology, immunotherapy : CII, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 55 citations in OpenAlex.
- PD-1 Blockade Mitigates Surgery-Induced Immunosuppression and Increases the Efficacy of Photodynamic Therapy for Pleural Mesothelioma.Cancer research communications · 2025Article
- How Our Continuing Studies of the Pre-clinical Inbred Mouse Models of Mesothelioma Have Influenced the Development of New Therapies.Frontiers in pharmacology · 2022Review
- The Synthetic Lignan Secoisolariciresinol Diglucoside Prevents Asbestos-Induced NLRP3 Inflammasome Activation in Murine Macrophages.Oxidative medicine and cellular longevity · 2017Article
- The Potential Protective Effects of Polyphenols in Asbestos-Mediated Inflammation and Carcinogenesis of Mesothelium.Nutrients · 2016Review
- Inflammation-Related IL1β/IL1R Signaling Promotes the Development of Asbestos-Induced Malignant Mesothelioma.Cancer prevention research (Philadelphia, Pa.) · 2016Article
- Asbestos Induces Oxidative Stress and Activation of Nrf2 Signaling in Murine Macrophages: Chemopreventive Role of the Synthetic Lignan Secoisolariciresinol Diglucoside (LGM2605).International journal of molecular sciences · 2016Article
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- A multifunctional mesothelin antibody-tagged microparticle targets human mesotheliomas.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2012Article
- Inflammation precedes the development of human malignant mesotheliomas in a SCID mouse xenograft model.Annals of the New York Academy of Sciences · 2010Article
- Expression of cancer-associated molecules in malignant mesothelioma.Biomarker insights · 2007Article
- Establishment of permanent cell lines purified from human mesothelioma: morphological aspects, new marker expression and karyotypic analysis.Histochemistry and cell biology · 2004Article
- Regression of AK7 malignant mesothelioma established in immunocompetent mice following intratumoral gene transfer of interferon gamma.Cancer gene therapy · 2003Article
- Malignant mesothelioma: new insights into tumour biology and immunology as a basis for new treatment approaches.Thorax · 1995Review
- Interleukin-6 involvement in mesothelioma pathobiology: inhibition by interferon alpha immunotherapy.Cancer immunology, immunotherapy : CII · 1995Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malignant mesothelioma (MM) is an aggressive, uniformly fatal serosal tumour, usually associated with asbestos exposure, for which there currently is no effective treatment. In order to gain insight into the mechanism(s) whereby MM might escape immune surveillance, a murine model for MM was used (a) to characterise the tumour-infiltrating lymphocytes (TIL) and macrophages (TIM) phenotypically, (b) to examine systemic immune recognition of MM, and (c) to examine the possible influence of tumour-derived cytokines on systemic and local pathobiological manifestations of MM. A profound down-regulation of lymphocyte surface markers, known to be involved in T cell activation, was found in TIL. Likewise, although TIM were present in large numbers, their expression of MHC class II antigen and integrins was weak or absent, suggestive of altered functional activity. Significant amounts of cytokines, in particular transforming growth factor beta, interleukin-6 (IL-6), IL-1 and tumour necrosis factor were produced during the course of MM tumour development-directly by the MM cells and/or indirectly in response to tumour growth. These factors may contribute both to derangement of antitumour effector mechanisms and to the clinical and pathological manifestations of the disease.
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