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1. Montomoli L, Spisso M, Romeo R, Spina D, Ghiribelli C, Sartorelli P: [Work related mesothelioma: analysis of cases discovered at the Section for Occupational Medicine and Toxicology of Siena University during the years 2000-2007]. G Ital Med Lav Ergon; 2007 Jul-Sep;29(3 Suppl):332-3
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  • [Title] [Work related mesothelioma: analysis of cases discovered at the Section for Occupational Medicine and Toxicology of Siena University during the years 2000-2007].
  • This study focuses on the spread of mesothelioma in Siena.
  • The association between malignant masothelioma and exposure to asbestos was deduced by the occupational history.
  • The mesothelioma was noted both in traditional industries and other jobs such as the chain of manifacture, plumbers, electricians, carpenters, installers of asbestos insulation and construction workers.
  • Thus it is possible to find other malignant and nonmalignant asbestos-related diseases more frequently than mesothelioma.
  • [MeSH-major] Mesothelioma / epidemiology. Occupational Diseases / epidemiology. Pleural Neoplasms / epidemiology
  • [MeSH-minor] Aged. Asbestos / adverse effects. Female. Humans. Italy. Male. Universities

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  • (PMID = 18409711.001).
  • [ISSN] 1592-7830
  • [Journal-full-title] Giornale italiano di medicina del lavoro ed ergonomia
  • [ISO-abbreviation] G Ital Med Lav Ergon
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 1332-21-4 / Asbestos
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2. Lee HE, Kim HR: Occupational respiratory cancer in Korea. J Korean Med Sci; 2010 Dec;25(Suppl):S94-8
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  • Malignant mesothelioma and lung cancer are representative examples of occupational cancer.
  • Lung cancer is the leading cause of cancer death, and the incidence of malignant mesothelioma is expected to increase sharply in the near future.
  • The first official case of occupational cancer was malignant mesothelioma caused by asbestos exposure in the asbestos textile industry in 1992.
  • Other main causative agents of occupational lung cancer included asbestos, hexavalent chromium, and crystalline silica.
  • Related jobs included welders, foundry workers, platers, plumbers, and vehicle maintenance workers.
  • Compensated malignant mesotheliomas were associated with asbestos exposure.
  • Epidemiologic studies conducted in Korea have indicated an elevated risk of lung cancer in pneumoconiosis patients, foundry workers, and asbestos textile workers.
  • [MeSH-major] Lung Neoplasms / epidemiology. Lung Neoplasms / etiology. Mesothelioma / etiology. Occupational Diseases / epidemiology. Occupational Exposure / adverse effects
  • [MeSH-minor] Asbestos / toxicity. Carcinogens / toxicity. Chromium / toxicity. Female. Humans. Male. Pneumoconiosis / complications. Republic of Korea / epidemiology. Silicon Dioxide / toxicity. Workers' Compensation

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  • (PMID = 21258597.001).
  • [ISSN] 1598-6357
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Carcinogens; 0R0008Q3JB / Chromium; 1332-21-4 / Asbestos; 18540-29-9 / chromium hexavalent ion; 7631-86-9 / Silicon Dioxide
  • [Other-IDs] NLM/ PMC3023347
  • [Keywords] NOTNLM ; Asbestos / Carcinogenic Substances / Lung Cancer / Mesothelioma / Occupational
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3. Travaglione S, Bruni BM, Falzano L, Filippini P, Fabbri A, Paoletti L, Fiorentini C: Multinucleation and pro-inflammatory cytokine release promoted by fibrous fluoro-edenite in lung epithelial A549 cells. Toxicol In Vitro; 2006 Sep;20(6):841-50
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  • An unusual cluster of malignant mesothelioma was evidenced in Biancavilla, a Sicily village where no inhabitant had been significantly and professionally exposed to asbestos.
  • We previously reported, by using the human lung epithelial A549 cells, that prismatic fluoro-edenite was unable to induce changes that could be somehow related to cellular transformation, and this was in accordance with studies carried out in vivo.
  • This fibrous fluoro-edenite was shown to induce mesothelioma in rats.
  • Hence, in lung epithelial cells, fibrous fluoro-edenite behaved similarly to the unrelated asbestos type crocidolite, whose connection with severe inflammation and cancer of the lung is renowned.
  • [MeSH-major] Asbestos, Amphibole / toxicity. Cytokines / biosynthesis. Inflammation / complications. Lung / drug effects. Mesothelioma / etiology
  • [MeSH-minor] Asbestos, Crocidolite / toxicity. Cell Proliferation / drug effects. Cell Survival / drug effects. Cells, Cultured. Epithelial Cells / drug effects. Humans. Interleukin-6 / biosynthesis. Interleukin-8 / biosynthesis

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  • (PMID = 16480849.001).
  • [ISSN] 0887-2333
  • [Journal-full-title] Toxicology in vitro : an international journal published in association with BIBRA
  • [ISO-abbreviation] Toxicol In Vitro
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Asbestos, Amphibole; 0 / Cytokines; 0 / Interleukin-6; 0 / Interleukin-8; 12001-28-4 / Asbestos, Crocidolite
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4. Watanabe Y, Kojima T, Kagawa S, Uno F, Hashimoto Y, Kyo S, Mizuguchi H, Tanaka N, Kawamura H, Ichimaru D, Urata Y, Fujiwara T: A novel translational approach for human malignant pleural mesothelioma: heparanase-assisted dual virotherapy. Oncogene; 2010 Feb 25;29(8):1145-54
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  • [Title] A novel translational approach for human malignant pleural mesothelioma: heparanase-assisted dual virotherapy.
  • Malignant pleural mesothelioma (MPM) is a highly aggressive tumor that is related to asbestos exposure.
  • In this study, we show that telomerase-specific, replication-selective adenovirus OBP-301 can efficiently infect and kill human mesothelioma cells by viral replication.
  • Intrathoracic administration of virus significantly reduced the number and size of human mesothelioma tumors intrathoracically implanted into nu/nu mice.
  • A high-definition, fluorescence optical imaging system with an ultra-thin, flexible fibered microprobe clearly detected intracellular replication of green fluorescent protein-expressing oncolytic virus in intrathoracically established mesothelioma tumors.
  • As the extracellular matrix (ECM) may contribute to the physiological resistance of a solid tumor by preventing the penetration of therapeutic agents (including oncolytic viruses), we also examined whether the co-expression of heparanase, an endoglucuronidase capable of specifically degrading heparan sulfate, that influences the physiological barrier to macromolecule penetration, can modify the permeability of the ECM, resulting in profound therapeutic efficacy.
  • Our results suggest that intrathoracic dual virotherapy with telomerase-specific oncolytic adenovirus in combination with heparanase-expressing adenovirus may be efficacious in the prevention and treatment of pleural dissemination of human malignant mesothelioma.
  • [MeSH-major] Adenoviridae / genetics. Genetic Therapy. Glucuronidase / genetics. Mesothelioma / therapy. Oncolytic Virotherapy. Pleural Neoplasms / therapy. Transfection / methods
  • [MeSH-minor] Animals. Cell Line, Tumor. Combined Modality Therapy. Gene Expression Regulation, Neoplastic. Gene Transfer Techniques. Humans. Lung Neoplasms / chemically induced. Lung Neoplasms / therapy. Mice. Mice, Nude. Neoplasm Transplantation. Protein Biosynthesis. Virus Replication. Xenograft Model Antitumor Assays


5. Hillegass JM, Shukla A, MacPherson MB, Lathrop SA, Alexeeva V, Perkins TN, van der Vliet A, Vacek PM, Gunter ME, Mossman BT: Mechanisms of oxidative stress and alterations in gene expression by Libby six-mix in human mesothelial cells. Part Fibre Toxicol; 2010 Sep 11;7:26
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  • BACKGROUND: Exposures to an amphibole fiber in Libby, Montana cause increases in malignant mesothelioma (MM), a tumor of the pleural and peritoneal cavities with a poor prognosis.
  • Affymetrix microarray/GeneSifter analysis was used to determine alterations in gene expression of a human mesothelial cell line (LP9/TERT-1) by a non-toxic concentration (15×10(6) μm2/cm2) of unprocessed Libby six-mix and negative (glass beads) and positive (crocidolite asbestos) controls.
  • A dose-related increase in SOD2 activity was observed, although total SOD activity remained unchanged.
  • Both Libby six-mix and crocidolite asbestos at 75×10(6) μm2/cm2 caused transient decreases (p < 0.05) in GSH for up to 24 h and increases in gene expression of heme oxygenase 1 (HO-1) in LP9/TERT-1 and HKNM-2 cells.

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  • (PMID = 20831825.001).
  • [ISSN] 1743-8977
  • [Journal-full-title] Particle and fibre toxicology
  • [ISO-abbreviation] Part Fibre Toxicol
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL085646; United States / NIEHS NIH HHS / ES / T32ES007122
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Asbestos, Amphibole; 0 / Reactive Oxygen Species; 12001-28-4 / Asbestos, Crocidolite; EC 1.14.99.3 / HMOX1 protein, human; EC 1.14.99.3 / Heme Oxygenase-1; EC 1.15.1.1 / Superoxide Dismutase; EC 1.15.1.1 / superoxide dismutase 2; GAN16C9B8O / Glutathione
  • [Other-IDs] NLM/ PMC2945990
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6. Currie AJ, van der Most RG, Broomfield SA, Prosser AC, Tovey MG, Robinson BW: Targeting the effector site with IFN-alphabeta-inducing TLR ligands reactivates tumor-resident CD8 T cell responses to eradicate established solid tumors. J Immunol; 2008 Feb 1;180(3):1535-44
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  • We investigated this response by injecting a range of TLR agonists into established tumors using a mouse model of malignant mesothelioma stably transduced with the hemagglutinin (HA) gene as a marker Ag (AB1-HA).
  • Experiments in athymic nude mice along with CD8 depletion and IFN-alphabeta blocking studies revealed that tumor resolution required both CD8 T cells and type I IFN induction, and was associated with local changes in MHC class I expression.
  • These studies suggest that, once reactivated, pre-existing local CD8 T cell responses are sufficient to resolve established tumors and that in situ type I IFN is a determining factor.
  • [MeSH-major] CD8-Positive T-Lymphocytes / immunology. Immunity, Innate. Interferon-alpha / metabolism. Interferon-beta / metabolism. Mesothelioma / immunology
  • [MeSH-minor] Animals. Antiviral Agents / pharmacology. Cell Line, Tumor. Cell Proliferation / drug effects. Ligands. Lymphocyte Depletion. Mice. Mice, Inbred BALB C. Nucleic Acids / immunology. Poly I-C / pharmacology. RNA, Double-Stranded / pharmacology

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  • (PMID = 18209049.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Interferon-alpha; 0 / Ligands; 0 / Nucleic Acids; 0 / RNA, Double-Stranded; 24939-03-5 / Poly I-C; 77238-31-4 / Interferon-beta
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7. Riva MA, Carnevale F, Sironi VA, De Vito G, Cesana G: Mesothelioma and asbestos, fifty years of evidence: Chris Wagner and the contribution of the Italian occupational medicine community. Med Lav; 2010 Nov-Dec;101(6):409-15
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  • [Title] Mesothelioma and asbestos, fifty years of evidence: Chris Wagner and the contribution of the Italian occupational medicine community.
  • BACKGROUND: One of the first studies that "convincingly" described the relationship between pleural mesothelioma and asbestos was made by Wagner, Sleggs and Marchard in 1960.
  • This article, published fifty years ago, contains much of what we still know to-day about malignant mesothelioma.
  • OBJECTIVES: The aims of this article were to analyze the historical and scientific developments that led to the publication of Wagner's paper, to critically examine its contents and to consider the contribution to the initernational debate on the carcinogenesis of asbestos fibres made by occupational medicine in Italy in that period.
  • METHODS: A thorough analysis ofscientific and historical literature on the relationship between asbestos exposure and tumours was conducted, with special regard to the articles by Italian authors in the 1960's.
  • RESULTS: The decisive role of Wagner's paper in understanding the aetiopathogenetic mechanisms of asbestos-related tumours is inconfutable.
  • Enrico Vigliani, then director of the "Clinica del Lavoro" in Milan, made important contributions to this debate, also through the collection of data regarding mortality among Italian asbestos workers.
  • [MeSH-major] Asbestos / adverse effects. Mesothelioma / history. Occupational Diseases / history. Occupational Medicine. Pleural Neoplasms / history

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  • (PMID = 21141345.001).
  • [ISSN] 0025-7818
  • [Journal-full-title] La Medicina del lavoro
  • [ISO-abbreviation] Med Lav
  • [Language] eng
  • [Publication-type] Biography; Historical Article; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Mineral Fibers; 1332-21-4 / Asbestos
  • [Personal-name-as-subject] Wagner JC
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8. Ray M, Kindler HL: Malignant pleural mesothelioma: an update on biomarkers and treatment. Chest; 2009 Sep;136(3):888-896
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  • [Title] Malignant pleural mesothelioma: an update on biomarkers and treatment.
  • Although the insulating properties of asbestos have been known for millennia, the link between asbestos exposure and mesothelioma was not recognized until 1960, when it was first described in South African asbestos miners.
  • The incidence of mesothelioma parallels asbestos usage with a latency of 20 to 40+ years; thus, patient numbers are declining in the United States but rising in the developing world.
  • Newly described biomarkers, including soluble mesothelin-related peptide, megakaryocyte potentiation factor, and osteopontin, may predict which asbestos-exposed individuals will develop mesothelioma, and may prove useful in assessing response to treatment.
  • This combination improves response, survival, time to progression, pulmonary function, and disease-related symptoms.
  • Other active agents include raltitrexed, gemcitabine, and vinorelbine.
  • Novel agents in clinical trials include inhibitors of the epidermal growth factor receptor, vascular endothelial growth factor, mesothelin, and histone deacetylases.
  • Although disappointing results of early trials did not confirm promising preclinical data, recent studies have suggested that some novel agents may be effective.
  • As we learn more about mesothelioma biology, molecularly targeted agents may become treatment options.
  • [MeSH-major] Biomarkers, Tumor / analysis. Mesothelioma / therapy. Pleural Neoplasms / therapy


9. Belyanskaya LL, Marti TM, Hopkins-Donaldson S, Kurtz S, Felley-Bosco E, Stahel RA: Human agonistic TRAIL receptor antibodies Mapatumumab and Lexatumumab induce apoptosis in malignant mesothelioma and act synergistically with cisplatin. Mol Cancer; 2007;6:66
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  • [Title] Human agonistic TRAIL receptor antibodies Mapatumumab and Lexatumumab induce apoptosis in malignant mesothelioma and act synergistically with cisplatin.
  • BACKGROUND: The incidence of malignant pleural mesothelioma (MPM) is associated with exposure to asbestos, and projections suggest that the yearly number of deaths in Western Europe due to MPM will increase until 2020.
  • Inducing apoptosis by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) or agonistic monoclonal antibodies which target TRAIL-receptor 1 (TRAIL-R1) or TRAIL-R2 has been thought to be a promising cancer therapy.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Apoptosis / drug effects. Cisplatin / pharmacology. Mesothelioma / drug therapy. Receptors, TNF-Related Apoptosis-Inducing Ligand / immunology
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Drug Synergism. Flow Cytometry. Humans. Immunoblotting. Jurkat Cells / drug effects. Jurkat Cells / metabolism. Receptors, Tumor Necrosis Factor / immunology

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  • (PMID = 17953743.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFRSF10A protein, human; 0 / TNFRSF10B protein, human; 0 / lexatumumab; 0 / mapatumumab; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ PMC2134932
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10. Edakuni N, Ikuta K, Yano S, Nakataki E, Muguruma H, Uehara H, Tani M, Yokota J, Aizawa H, Sone S: Restored expression of the MYO18B gene suppresses orthotopic growth and the production of bloody pleural effusion by human malignant pleural mesothelioma cells in SCID mice. Oncol Res; 2006;16(5):235-43
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  • [Title] Restored expression of the MYO18B gene suppresses orthotopic growth and the production of bloody pleural effusion by human malignant pleural mesothelioma cells in SCID mice.
  • Malignant pleural mesothelioma (MPM) is closely related to exposure to asbestos, and a rapid increase in the number of MPM patients is therefore estimated to occur from 2010 to 2040 in Japan.
  • The inactivation of the MYO18B gene plays an important role in several malignant diseases.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / genetics. Lung Neoplasms / genetics. Mesothelioma / genetics. Myosins / genetics. Myosins / pharmacology. Pleural Effusion / genetics. Pleural Neoplasms / genetics. Tumor Suppressor Proteins / genetics. Tumor Suppressor Proteins / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Growth Processes / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Disease Models, Animal. Humans. Male. Mice. Mice, SCID. Neoplasms, Experimental / genetics. Neoplasms, Experimental / metabolism. Neoplasms, Experimental / pathology. Xenograft Model Antitumor Assays

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  • (PMID = 17294804.001).
  • [ISSN] 0965-0407
  • [Journal-full-title] Oncology research
  • [ISO-abbreviation] Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MYO18B protein, human; 0 / Tumor Suppressor Proteins; EC 3.6.4.1 / Myosins
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11. Bianchi C, Ramani L, Bianchi T: Concurrent malignant mesothelioma of the pleura and hepatocellular carcinoma in the same patient: a report of five cases. Ind Health; 2002 Oct;40(4):383-7
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  • [Title] Concurrent malignant mesothelioma of the pleura and hepatocellular carcinoma in the same patient: a report of five cases.
  • Five cases are reported in which malignant mesothelioma of the pleura and hepatocellular carcinoma co-existed in the same patient.
  • All mesotheliomas were asbestos-related.
  • In particular, asbestos could favour liver cancerogenesis by inducing immune impairment.
  • [MeSH-major] Carcinoma, Hepatocellular / complications. Liver Neoplasms / complications. Mesothelioma / complications. Neoplasms, Multiple Primary. Pleural Neoplasms / complications
  • [MeSH-minor] Aged. Asbestos / adverse effects. Female. Humans. Immune System / drug effects. Immune System / physiopathology. Male. Middle Aged

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  • (PMID = 12502242.001).
  • [ISSN] 0019-8366
  • [Journal-full-title] Industrial health
  • [ISO-abbreviation] Ind Health
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 1332-21-4 / Asbestos
  • [Number-of-references] 45
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12. Aceto N, Bertino P, Barbone D, Tassi G, Manzo L, Porta C, Mutti L, Gaudino G: Taurolidine and oxidative stress: a rationale for local treatment of mesothelioma. Eur Respir J; 2009 Dec;34(6):1399-407
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  • [Title] Taurolidine and oxidative stress: a rationale for local treatment of mesothelioma.
  • Malignant mesothelioma is an asbestos-related, aggressive tumour, resistant to most anticancer therapies.
  • Akt is a key mediator of mesothelioma cell survival and chemoresistance.
  • This study aimed to clarify the mechanism by which taurolidine (TN), a known synthetic compound with antimicrobial and antineoplastic properties, leads to mesothelioma cell death.
  • TN induces cell death of mesothelioma cells, but not of non-neoplastic human mesothelial cells.
  • After TN treatment of mesothelioma cells, Akt but not extracellular signal-regulated kinase (Erk) 1/2 activity is inhibited a in time- and dose-dependent manner.
  • Protein phosphatase (PP)1alpha and PP2A are activated several hours after drug addition.
  • TN induces mesothelioma cell death via oxidative stress, accompanied by inhibition of Akt signalling.
  • This provides a promising molecular rationale for TN as local treatment of malignant mesothelioma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology. Mesothelioma / drug therapy. Mesothelioma / pathology. Oxidative Stress. Taurine / analogs & derivatives. Thiadiazines / therapeutic use
  • [MeSH-minor] Apoptosis. Cell Death. Cell Line, Tumor. Cells, Cultured. DNA / metabolism. Fibroblasts / metabolism. Humans. In Situ Nick-End Labeling. Proto-Oncogene Proteins c-akt / metabolism. Time Factors


13. Yang H, Rivera Z, Jube S, Nasu M, Bertino P, Goparaju C, Franzoso G, Lotze MT, Krausz T, Pass HI, Bianchi ME, Carbone M: Programmed necrosis induced by asbestos in human mesothelial cells causes high-mobility group box 1 protein release and resultant inflammation. Proc Natl Acad Sci U S A; 2010 Jul 13;107(28):12611-6
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  • [Title] Programmed necrosis induced by asbestos in human mesothelial cells causes high-mobility group box 1 protein release and resultant inflammation.
  • Asbestos carcinogenesis has been linked to the release of cytokines and mutagenic reactive oxygen species (ROS) from inflammatory cells.
  • Asbestos is cytotoxic to human mesothelial cells (HM), which appears counterintuitive for a carcinogen.
  • We show that asbestos-induced HM cell death is a regulated form of necrosis that links to carcinogenesis.
  • Asbestos-exposed HM activate poly(ADP-ribose) polymerase, secrete H(2)O(2), deplete ATP, and translocate high-mobility group box 1 protein (HMGB1) from the nucleus to the cytoplasm, and into the extracellular space.
  • The release of HMGB1 induces macrophages to secrete TNF-alpha, which protects HM from asbestos-induced cell death and triggers a chronic inflammatory response; both favor HM transformation.
  • In both mice and hamsters injected with asbestos, HMGB1 was specifically detected in the nuclei, cytoplasm, and extracellular space of mesothelial and inflammatory cells around asbestos deposits.
  • HMGB1 levels in asbestos-exposed individuals were significantly higher than in nonexposed controls (P < 0.0001).
  • Our findings identify the release of HMGB1 as a critical initial step in the pathogenesis of asbestos-related disease, and provide mechanistic links between asbestos-induced cell death, chronic inflammation, and carcinogenesis.
  • Chemopreventive approaches aimed at inhibiting the chronic inflammatory response, and especially blocking HMGB1, may decrease the risk of malignant mesothelioma among asbestos-exposed cohorts.
  • [MeSH-minor] Adenosine Diphosphate Ribose / metabolism. Adenosine Diphosphate Ribose / pharmacology. Animals. Asbestos / metabolism. Asbestos / pharmacology. Carcinogens / metabolism. Carcinogens / pharmacology. Cell Death. Cell Nucleus / metabolism. Cells / metabolism. Cricetinae. Cytokines / metabolism. Cytokines / pharmacology. Epithelial Cells / metabolism. Epithelium / drug effects. Epithelium / metabolism. Female. HMGB Proteins / metabolism. HMGB Proteins / pharmacology. Humans. Hydrogen Peroxide / metabolism. Hydrogen Peroxide / pharmacology. Macrophages / metabolism. Mesocricetus. Mesothelioma / metabolism. Mice. Mice, Inbred BALB C. Necrosis / metabolism. Pleural Neoplasms / metabolism. Poly Adenosine Diphosphate Ribose / pharmacology. Poly(ADP-ribose) Polymerases / metabolism. Poly(ADP-ribose) Polymerases / pharmacology. Reactive Oxygen Species / metabolism. Reactive Oxygen Species / pharmacology. Tumor Necrosis Factor-alpha / metabolism. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 20616036.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Cytokines; 0 / HMGB Proteins; 0 / HMGB1 Protein; 0 / Reactive Oxygen Species; 0 / Tumor Necrosis Factor-alpha; 1332-21-4 / Asbestos; 20762-30-5 / Adenosine Diphosphate Ribose; 26656-46-2 / Poly Adenosine Diphosphate Ribose; BBX060AN9V / Hydrogen Peroxide; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases
  • [Other-IDs] NLM/ PMC2906549
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14. Huncharek M: Non-asbestos related diffuse malignant mesothelioma. Tumori; 2002 Jan-Feb;88(1):1-9
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  • [Title] Non-asbestos related diffuse malignant mesothelioma.
  • AIMS: The association between asbestos exposure and the development of malignant mesothelioma is well known.
  • Nonetheless, a proportion of patients suffering from this disease do not appear to have documented exposure to asbestos fibers from any known source.
  • This paper will review existing data related to non-asbestos related mesothelioma and suggest avenues for further research.
  • METHODS AND STUDY DESIGN: A comprehensive electronic MEDLARS search of the literature pertinent to non-asbestos related malignant mesothelioma was performed including the years 1996-2001.
  • (1) radiation associated mesothelioma, (2) familial mesothelioma, (3) dietary factors, (4) childhood mesothelioma and (5) the role or SV40.
  • The interplay of genes and environment require further elucidation in the pathogenesis of mesothelioma.
  • Whether other environmental or infectious agents are involved in mesothelioma development remains speculative.
  • CONCLUSION: The biology of mesothelioma is an enigma.
  • Although this disease appears to occur in the absence of asbestos exposure, the genetic and biological differences between asbestos related and non-asbestos related tumors is unclear.
  • Additional epidemiological and laboratory studies are needed to provide a better understanding of the relationship between environmental and non-environmental causes of mesothelioma.
  • [MeSH-major] Mesothelioma / etiology. Pleural Neoplasms / etiology

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  • (PMID = 12004841.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 73
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15. Orbaugh KK: Nursing considerations for administering pemetrexed (Alimta) in combination with cisplatin for malignant pleural mesothelioma. Clin J Oncol Nurs; 2004 Jun;8(3):242-7
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  • [Title] Nursing considerations for administering pemetrexed (Alimta) in combination with cisplatin for malignant pleural mesothelioma.
  • No known cure exists for malignant pleural mesothelioma (MPM).
  • The prognosis for patients with this relatively rare, asbestos-related malignancy of the pleural lining of the lung is quite poor.
  • The U.S. Food and Drug Administration recently approved pemetrexed with cisplatin for treating MPM.
  • Nurses should become familiar with the proper preparation and administration of pemetrexed, including the necessity of supplementation with folic acid and vitamin B12.
  • As with all drugs, careful attention must be paid to patient selection, laboratory monitoring, contraindications, and appropriate interventions in the event of adverse reactions or overdose.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Guanine / analogs & derivatives. Mesothelioma / drug therapy. Mesothelioma / nursing. Nursing Assessment. Pleural Neoplasms / drug therapy. Pleural Neoplasms / nursing
  • [MeSH-minor] Cisplatin / administration & dosage. Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Glutamates / administration & dosage. Humans. Infusions, Intravenous. Male. Maximum Tolerated Dose. Oncology Nursing. Pemetrexed. Prognosis. Risk Assessment. Treatment Outcome

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  • (PMID = 15208818.001).
  • [ISSN] 1092-1095
  • [Journal-full-title] Clinical journal of oncology nursing
  • [ISO-abbreviation] Clin J Oncol Nurs
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glutamates; 04Q9AIZ7NO / Pemetrexed; 5Z93L87A1R / Guanine; Q20Q21Q62J / Cisplatin
  • [Number-of-references] 15
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16. Fach E, Kristovich R, Long JF, Waldman WJ, Dutta PK, Williams MV: The effect of iron on the biological activities of erionite and mordenite. Environ Int; 2003 Jul;29(4):451-8
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  • [Title] The effect of iron on the biological activities of erionite and mordenite.
  • Epidemiological data has demonstrated that environmental and/or occupational exposure to mineral particulates may result in the development of pulmonary fibrosis, bronchogenic carcinoma and malignant mesothelioma many years following exposure.
  • It has been suggested that the genotoxic effects of fibrous particulates, such as asbestos, is due in part to the generation of reactive oxygen species (ROS) from iron associated with the particulates.
  • The naturally occurring zeolites, erionite and mordenite share several physiochemical properties but they elicit very different biological responses, with erionite, a fibrous particulate, being highly toxic, and mordenite, a nonfibrous particulate, being relatively benign.
  • We are using these natural zeolites as a model system to determine what physicochemical properties of these zeolites are responsible for their biological response(s) and to evaluate the parameters that influence these responses.
  • These results suggest that while the cytotoxicity of mordenite and erionite may be related to the ability of these fibers to transport iron into a cell, the different coordination state of iron associated with the two fiber surfaces is critical for inducing genotoxic damage.
  • [MeSH-minor] Animals. CHO Cells. Cricetinae. Dose-Response Relationship, Drug. Drug Interactions. Mutagenicity Tests

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  • (PMID = 12705942.001).
  • [ISSN] 0160-4120
  • [Journal-full-title] Environment international
  • [ISO-abbreviation] Environ Int
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aluminum Silicates; 12445-20-4 / mordenite; 12510-42-8 / erionite; 1318-02-1 / Zeolites; E1UOL152H7 / Iron
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17. Petazzi A, Gaudiello F, Canti Z, Mensi C: [Cluster cases of malignant pleural mesothelioma in an oil factory]. Med Lav; 2005 Sep-Oct;96(5):440-4
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  • [Title] [Cluster cases of malignant pleural mesothelioma in an oil factory].
  • BACKGROUND: The traditional occupational hazards of the productive cycle of oils are attributable to chemicals (use of solvents, pesticides and other agents), dusts, labour accidents (trauma, ignition, explosion), noise, manual lifting, work organization and hot-wet microclimate.
  • No cases are reported in literature of asbestos related disease in subjects who worked in oil factories.
  • Nevertheless the structure and organization of the workplace, which is similar to that of sugar refineries, where cases of malignant mesothelioma have been described (moreover in workers employed in running and maintenance of the plants), led to the assumption that even in oil factories asbestos for the insulation of pipes and boilers could be present.
  • OBJECTIVES: To describe 3 cases of Malignant Mesothelioma that occurred in workers of the same oil factory.
  • METHODS: Since this occupational sector is not conventionally known for asbestos exposure the Local Health Unit and the Lombardy Mesothelioma Registry decided to investigate this industrial plant.
  • RESULTS: Following examination of the archives of the Local Health Unit and inspection of the plant, an environmental asbestos contamination (pipes and boilers) was found.
  • This underlines the importance of close cooperation with Local Health Units of occupational medicine and the Regional Mesothelioma Registry in the study and acknowledgment of cases which would otherwise not have been recognized, with consequent loss of precious information.
  • [MeSH-major] Air Pollutants, Occupational / adverse effects. Asbestos / adverse effects. Chemical Industry. Mesothelioma / epidemiology. Occupational Diseases / epidemiology. Petroleum. Pleural Neoplasms / epidemiology


18. Riehemann K, Schmitt O, Ehlers EM: The effects of thermochemotherapy using cyclophosphamide plus hyperthermia on the malignant pleural mesothelioma in vivo. Ann Anat; 2005 Jul;187(3):215-23
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  • [Title] The effects of thermochemotherapy using cyclophosphamide plus hyperthermia on the malignant pleural mesothelioma in vivo.
  • The human malignant pleural mesothelioma is related to the use of asbestos in the majority of cases.
  • Though the use of asbestos has been prohibited since the 1990s, the incidence of pleural mesothelioma is still increasing because of a latency period of at least 20 years.
  • This study investigated the benefit of single therapy with cyclophosphamide or hyperthermia or the combination of both on cells of a human pleural mesothelioma cell line, xenotransplanted subcutaneously in the paw of mice.
  • Superior effects could be achieved by performing additional cycles of chemotherapy or adding another drug or radiation for instance.
  • This study shows promising results in the treatment of malignant pleural mesothelioma.
  • [MeSH-major] Cyclophosphamide / therapeutic use. Hyperthermia, Induced. Mesothelioma / therapy. Pleural Neoplasms / therapy
  • [MeSH-minor] Animals. Antineoplastic Agents, Alkylating / therapeutic use. Cell Line, Tumor. Combined Modality Therapy. Female. Humans. Mice. Mice, Nude. Transplantation, Heterologous

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  • (PMID = 16130821.001).
  • [ISSN] 0940-9602
  • [Journal-full-title] Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft
  • [ISO-abbreviation] Ann. Anat.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 8N3DW7272P / Cyclophosphamide
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19. Tomasetti M, Amati M, Santarelli L, Alleva R, Neuzil J: Malignant mesothelioma: biology, diagnosis and therapeutic approaches. Curr Mol Pharmacol; 2009 Jun;2(2):190-206
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  • [Title] Malignant mesothelioma: biology, diagnosis and therapeutic approaches.
  • Malignant mesothelioma (MM) is an aggressive neoplasm of serosal cavities, which is resistant to conventional therapy, with patient survival from presentation of <12 months.
  • Although the main risk factor is asbestos exposure, other factors, Simian virus 40 infection and inheritance of susceptibility genes, likely play a role.
  • Asbestos-related carcinogenic process is primarily based on the interaction between susceptibility (genetic and acquired) and exposure to carcinogenic environmental agents.
  • Asbestos-induced carcinogenesis includes generation of reactive oxygen species, which induce DNA strand breaks and oxidant-induced base modifications to DNA.
  • Several programs have been used to screen asbestos-exposed individuals for lung and pleural disease.
  • [MeSH-major] Mesothelioma / diagnosis
  • [MeSH-minor] Asbestos / toxicity. Carcinogens / toxicity. DNA Damage. Humans. Mitogen-Activated Protein Kinases / metabolism. NF-kappa B / metabolism. Simian virus 40 / physiology. Transcription Factor AP-1 / metabolism

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  • (PMID = 20021458.001).
  • [ISSN] 1874-4702
  • [Journal-full-title] Current molecular pharmacology
  • [ISO-abbreviation] Curr Mol Pharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Carcinogens; 0 / NF-kappa B; 0 / Transcription Factor AP-1; 1332-21-4 / Asbestos; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Number-of-references] 180
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20. Takemura Y, Satoh M, Satoh K, Hamada H, Sekido Y, Kubota S: High dose of ascorbic acid induces cell death in mesothelioma cells. Biochem Biophys Res Commun; 2010 Apr 2;394(2):249-53
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  • [Title] High dose of ascorbic acid induces cell death in mesothelioma cells.
  • Malignant mesothelioma is an asbestos-related fatal disease with no effective cure.
  • We studied whether high dose of ascorbic acid induced cell death of four human mesothelioma cell lines.
  • High dose of ascorbic acid induced cell death of all mesothelioma cell lines in a dose-dependent manner.
  • In vivo experiment, intravenous administration of ascorbic acid significantly decreased the growth rate of mesothelioma tumor inoculated in mice.
  • These data suggest that ascorbic acid may have benefits for patients with mesothelioma.
  • [MeSH-major] Apoptosis. Ascorbic Acid / administration & dosage. Mesothelioma / drug therapy
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Humans. Membrane Potential, Mitochondrial / drug effects. Mice. Mice, SCID. Reactive Oxygen Species / metabolism. Xenograft Model Antitumor Assays

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20171954.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Reactive Oxygen Species; PQ6CK8PD0R / Ascorbic Acid
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21. Bianchi C, Bianchi T: Susceptibility and resistance in the genesis of asbestos-related mesothelioma. Indian J Occup Environ Med; 2008 Aug;12(2):57-60
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  • [Title] Susceptibility and resistance in the genesis of asbestos-related mesothelioma.
  • Asbestos is the principal agent in the etiology of malignant mesothelioma.
  • However, a small proportion of people exposed to asbestos develop mesothelioma.
  • A genetic susceptibility is suggested by the occurrence of more mesothelioma cases among blood-related members of a single family.
  • Such an occurrence reached about 4% in a large mesothelioma series.
  • In some studies, mesothelioma patients showed higher prevalences of additional malignancies when compared with controls.
  • This indicates a particular vulnerability to cancer in people with mesothelioma.
  • Not rarely, very old persons heavily exposed to asbestos remain free from asbestos-related cancer, a fact indicating an absolute resistance to the oncogenic effects of asbestos.
  • A relative resistance may be recognized in people severely exposed to asbestos who develop mesothelioma only after 60 years or more since the onset of the exposure.
  • The long survivals, rarely observed among mesothelioma patients, have been attributed to a high efficiency of immune mechanisms.
  • Mesotheliomas have been reported among people with severe immune impairment, such as acquired immunodeficiency syndrome patients or organ transplant recipients.
  • The natural history of mesothelioma shows that a resistance to the oncogenic effects of asbestos does exist.
  • To strengthen the defence mechanisms may represent a way for preventing mesothelioma among people exposed to asbestos.

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  • (PMID = 20040979.001).
  • [ISSN] 1998-3670
  • [Journal-full-title] Indian journal of occupational and environmental medicine
  • [ISO-abbreviation] Indian J Occup Environ Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2796755
  • [Keywords] NOTNLM ; Asbestos / familial cancer / host factors / immune impairment / mesothelioma / resistance / susceptibility
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22. Nishimura Y, Miura Y, Maeda M, Kumagai N, Murakami S, Hayashi H, Fukuoka K, Nakano T, Otsuki T: Impairment in cytotoxicity and expression of NK cell- activating receptors on human NK cells following exposure to asbestos fibers. Int J Immunopathol Pharmacol; 2009 Jul-Sep;22(3):579-90
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  • [Title] Impairment in cytotoxicity and expression of NK cell- activating receptors on human NK cells following exposure to asbestos fibers.
  • Asbestos is well-known for its tumorigenic activity, but its effect on anti-tumor immunity remains unclear.
  • Therefore, we prepared a sub-line of YT-A1 human NK cells exposed to chrysotile B (CB) asbestos (YT-CB5) as an in vitro model to analyze the effect of asbestos exposure on NK cells, and examined cytotoxicity and expressions of its related molecules.
  • Therefore, peripheral blood NK cells in patients with malignant mesothelioma (MM) were examined and compared with healthy volunteers.
  • To confirm the effect of asbestos exposure on peripheral blood NK cells, PBMCs were cultured under exposure to CB.
  • These results indicate that exposure to asbestos has the potential to impair the cytotoxicity of NK cells and alter the expression of NK cell-activating receptors including NKG2D, 2B4 and NKp46 and intracellular perforin/granzymes.
  • [MeSH-major] Asbestos, Serpentine / toxicity. Cytotoxicity, Immunologic / drug effects. Killer Cells, Natural / drug effects. Mesothelioma / immunology
  • [MeSH-minor] Antigens, CD / metabolism. Case-Control Studies. Cell Degranulation / drug effects. Cell Survival / drug effects. Dose-Response Relationship, Drug. Down-Regulation. Granzymes / metabolism. Humans. K562 Cells. Leukocytes, Mononuclear / drug effects. Leukocytes, Mononuclear / immunology. NK Cell Lectin-Like Receptor Subfamily K / metabolism. Natural Cytotoxicity Triggering Receptor 1 / metabolism. Perforin / metabolism. Receptors, Immunologic / metabolism. Signaling Lymphocytic Activation Molecule Family. Time Factors

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  • (PMID = 19822075.001).
  • [ISSN] 0394-6320
  • [Journal-full-title] International journal of immunopathology and pharmacology
  • [ISO-abbreviation] Int J Immunopathol Pharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Asbestos, Serpentine; 0 / CD244 protein, human; 0 / KLRK1 protein, human; 0 / NCR1 protein, human; 0 / NK Cell Lectin-Like Receptor Subfamily K; 0 / Natural Cytotoxicity Triggering Receptor 1; 0 / Receptors, Immunologic; 0 / Signaling Lymphocytic Activation Molecule Family; 126465-35-8 / Perforin; EC 3.4.21.- / Granzymes; EC 3.4.21.78 / GZMA protein, human
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23. Larson TC, Antao VC, Bove FJ: Vermiculite worker mortality: estimated effects of occupational exposure to Libby amphibole. J Occup Environ Med; 2010 May;52(5):555-60
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  • RESULTS: The Cox models for mesothelioma, asbestosis, lung cancer, and non-malignant respiratory disease were significant with rate ratios that increased monotonically with CFE.
  • CONCLUSIONS: By using a within-cohort comparison, the results demonstrate a clear exposure-response relationship between CFE and mortality from asbestos-related causes.

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  • (PMID = 20431408.001).
  • [ISSN] 1536-5948
  • [Journal-full-title] Journal of occupational and environmental medicine
  • [ISO-abbreviation] J. Occup. Environ. Med.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aluminum Silicates; 0 / Asbestos, Amphibole; 1318-00-9 / vermiculite
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24. Kamp DW: Asbestos-induced lung diseases: an update. Transl Res; 2009 Apr;153(4):143-52
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  • [Title] Asbestos-induced lung diseases: an update.
  • Asbestos causes asbestosis (pulmonary fibrosis caused by asbestos inhalation) and malignancies (bronchogenic carcinoma and mesothelioma) by mechanisms that are not fully elucidated.
  • Despite a dramatic reduction in asbestos use worldwide, asbestos-induced lung diseases remain a substantial health concern primarily because of the vast amounts of fibers that have been mined, processed, and used during the 20th century combined with the long latency period of up to 40 years between exposure and disease presentation.
  • Whereas the development of asbestosis is directly associated with the magnitude and duration of asbestos exposure, the development of a malignant clone of cells can occur in the setting of low-level asbestos exposure.
  • Emphasis is placed on the recent epidemiologic investigations that explore the malignancy risk that occurs from nonoccupational, environmental asbestos exposure.
  • Accumulating studies are shedding light on novel mechanistic pathways by which asbestos damages the lung.
  • The translational significance of these studies is evident in providing the molecular basis for developing novel therapeutic strategies for asbestos-related lung diseases and, importantly, other pulmonary diseases, such as interstitial pulmonary fibrosis and lung cancer.

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  • (PMID = 19304273.001).
  • [ISSN] 1931-5244
  • [Journal-full-title] Translational research : the journal of laboratory and clinical medicine
  • [ISO-abbreviation] Transl Res
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / R01 ES013995; United States / NHLBI NIH HHS / HL / HL035440-21; United States / NHLBI NIH HHS / HL / R01 HL035440-21; United States / NIEHS NIH HHS / ES / ES013995-01A1; United States / NIEHS NIH HHS / ES / R01 ES013995-01A1
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 1332-21-4 / Asbestos
  • [Number-of-references] 106
  • [Other-IDs] NLM/ NIHMS146578; NLM/ PMC3544481
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25. Wang Y, Rishi AK, Puliyappadamba VT, Sharma S, Yang H, Tarca A, Dou QP, Lonardo F, Ruckdeschel JC, Pass HI, Wali A: Targeted proteasome inhibition by Velcade induces apoptosis in human mesothelioma and breast cancer cell lines. Cancer Chemother Pharmacol; 2010 Aug;66(3):455-66
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  • [Title] Targeted proteasome inhibition by Velcade induces apoptosis in human mesothelioma and breast cancer cell lines.
  • Malignant pleural mesothelioma (MPM) is an asbestos-related tumor of the thoracic pleura that lacks effective treatment options.
  • Although proteasome inhibitor Velcade (Bortezomib) has been under clinical investigation for a number of cancers, limited preclinical studies with this agent have thus far been conducted in HBC and MPM malignancies.
  • PURPOSE: To study the biological and molecular responses of MPM and HBC cells to Velcade treatments, and to identify mechanisms involved in transducing growth inhibitory effects of this agent.
  • Pretreatment of mesothelioma cells with Velcade showed synergistic effect with cisplatin combination regimens.
  • High-throughput gene expression profiling among Velcade treated and untreated mesothelioma cell lines resulted in identification of novel transducers of apoptosis such as CARP-1, XAF1, and Troy proteins.
  • This pilot study has paved way for further in-depth analysis of the downstream target molecules associated with presensitization of mesothelioma cells in finding effective therapeutic treatment options for both mesothelioma and recalcitrant breast cancers.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Breast Neoplasms / drug therapy. Mesothelioma / drug therapy. Protease Inhibitors / pharmacology
  • [MeSH-minor] Blotting, Western. Boronic Acids / administration & dosage. Bortezomib. Cell Cycle / drug effects. Cell Line, Tumor. Cisplatin / administration & dosage. Dose-Response Relationship, Drug. Drug Delivery Systems. Drug Synergism. Female. Flow Cytometry. Humans. Pilot Projects. Proteasome Inhibitors. Pyrazines / administration & dosage. Signal Transduction / drug effects. Time Factors


26. Thomas DD, Espey MG, Pociask DA, Ridnour LA, Donzelli S, Wink DA: Asbestos redirects nitric oxide signaling through rapid catalytic conversion to nitrite. Cancer Res; 2006 Dec 15;66(24):11600-4
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  • [Title] Asbestos redirects nitric oxide signaling through rapid catalytic conversion to nitrite.
  • Asbestos exposure is strongly associated with the development of malignant mesothelioma, yet the mechanistic basis of this observation has not been resolved.
  • Carcinogenic transformation or tumor progression mediated by asbestos may be related to the generation of free radical species and perturbation of cell signaling and transcription factors.
  • We report here that exposure of human mesothelioma or lung carcinoma cells to nitric oxide (NO) in the presence of crocidolite asbestos resulted in a marked decrease in intracellular nitrosation and diminished NO-induced posttranslational modifications of tumor-associated proteins (hypoxia-inducible factor-1alpha and p53).
  • Crocidolite also catalyzed the nitration of cellular proteins in the presence of NO(2)(-) and hydrogen peroxide.
  • Nitrated protein adducts are a prominent feature of asbestos-induced lung injury.
  • These data highlight the ability of asbestos to induce phenotypic cellular changes through two processes: (a) by directly reducing bioactive NO levels and preventing its subsequent interaction with target molecules and (b) by increasing oxidative damage and protein modifications through NO(2) production and 3-nitrotyrosine formation.
  • [MeSH-major] Asbestos / pharmacology. Nitric Oxide / physiology. Nitrites / metabolism. Serum Albumin, Bovine / drug effects. Signal Transduction / drug effects
  • [MeSH-minor] Animals. Cattle. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / drug effects. Phosphoserine. Tumor Suppressor Protein p53 / drug effects

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  • (PMID = 17178853.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Nitrites; 0 / Serum Albumin, Bovine; 0 / Tumor Suppressor Protein p53; 1332-21-4 / Asbestos; 17885-08-4 / Phosphoserine; 31C4KY9ESH / Nitric Oxide
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27. Sherwood AL, Mutsaers SE, Peeva VK, Robinson C, DeSilva CJ, Swanson NR, Lake RA: Spontaneously immortalized mouse mesothelial cells display characteristics of malignant transformation. Cell Prolif; 2008 Dec;41(6):894-908
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  • [Title] Spontaneously immortalized mouse mesothelial cells display characteristics of malignant transformation.
  • OBJECTIVES: Mesotheliomas occur in occult serous cavities after chronic exposure of mesothelial cells to asbestos fibres.
  • Comparative gene expression analysis demonstrated that spontaneously transformed cell lines were more closely related to neoplastic cells than to primary cells.
  • [MeSH-minor] Animals. Cell Aging / drug effects. Cell Line, Transformed. Cell Shape / drug effects. DNA / analysis. Down-Regulation / drug effects. Gene Deletion. Gene Expression Profiling. Genes, Tumor Suppressor. Humans. Intercellular Signaling Peptides and Proteins / pharmacology. Mesothelioma / genetics. Mice. Mice, Inbred C57BL

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  • (PMID = 19040568.001).
  • [ISSN] 1365-2184
  • [Journal-full-title] Cell proliferation
  • [ISO-abbreviation] Cell Prolif.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 9007-49-2 / DNA
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28. Røe OD, Anderssen E, Sandeck H, Christensen T, Larsson E, Lundgren S: Malignant pleural mesothelioma: genome-wide expression patterns reflecting general resistance mechanisms and a proposal of novel targets. Lung Cancer; 2010 Jan;67(1):57-68
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  • [Title] Malignant pleural mesothelioma: genome-wide expression patterns reflecting general resistance mechanisms and a proposal of novel targets.
  • Malignant pleural mesothelioma is an asbestos-related multi-resistant tumour with increasing incidence worldwide.
  • Well-characterized snap-frozen normal parietal, visceral pleura and mesothelioma samples were analysed with Affymetrix Human Genome U133 Plus 2.0 GeneChip oligoarray of 38500 genes.
  • We discovered a close relation between gene profile and resistance towards topoisomerase poisons, alkylating agents, antitubulines, antifolates, platinum compounds and radiation therapy.
  • The Fanconi anemia/BRCA2 pathway, responsible for homologous recombination DNA repair appears as a key pathway in both chemo- and radio-resistance of mesothelioma.
  • Gene expression features found in other resistant cancer types related to DNA repair and replication are shared by mesothelioma and could represent general features of tumour resistance.
  • Targeted suppression of some of those key genes and pathways combined with chemotherapy or radiation could improve the outcome of mesothelioma therapy.
  • We propose CHEK1, RAD21, FANCD2 and RAN as new co-targets for mesothelioma treatment.
  • Overexpression of NQO1 may render mesothelioma sensitive to the novel compound beta-Lapachone.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Gene Expression Regulation, Neoplastic. Mesothelioma / genetics. Pleural Neoplasms / genetics. Radiation Tolerance / genetics
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Asbestos / toxicity. Genome-Wide Association Study. Humans


29. Heintz NH, Janssen-Heininger YM, Mossman BT: Asbestos, lung cancers, and mesotheliomas: from molecular approaches to targeting tumor survival pathways. Am J Respir Cell Mol Biol; 2010 Feb;42(2):133-9
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  • [Title] Asbestos, lung cancers, and mesotheliomas: from molecular approaches to targeting tumor survival pathways.
  • Fifteen years have passed since we published findings in the AJRCMB demonstrating that induction of early response fos/jun proto-oncogenes in rodent tracheal and mesothelial cells correlates with fibrous geometry and pathogenicity of asbestos.
  • Our study was the first to suggest that the aberrant induction of signaling responses by crocidolite asbestos and erionite, a fibrous zeolite mineral associated with the development of malignant mesotheliomas (MMs) in areas of Turkey, led to altered gene expression.
  • New data questioned the widely held belief at that time that the carcinogenic effects of asbestos in the development of lung cancer and MM were due to genotoxic or mutagenic effects.
  • Later studies by our group revealed that proto-oncogene expression and several of the signaling pathways activated by asbestos were redox dependent, explaining why antioxidants and antioxidant enzymes were elevated in lung and pleura after exposure to asbestos and how they alleviated many of the phenotypic and functional effects of asbestos in vitro or after inhalation.
  • Since these original studies, our efforts have expanded to understand the interface between asbestos-induced redox-dependent signal transduction cascades, the relationship between these pathways and cell fate, and the role of asbestos and cell interactions in development of asbestos-associated diseases.
  • Of considerable significance is the fact that the signal transduction pathways activated by asbestos are also important in survival and chemoresistance of MMs and lung cancers.
  • An understanding of the pathogenic features of asbestos fibers and dysregulation of signaling pathways allows strategies for the prevention and therapy of asbestos-related diseases.
  • [MeSH-major] Asbestos / toxicity. Lung Neoplasms / etiology. Mesothelioma / etiology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Humans. MAP Kinase Signaling System / drug effects. Models, Biological. NF-kappa B / metabolism. Oxidants / metabolism. Proto-Oncogene Proteins c-fos / metabolism. Proto-Oncogene Proteins c-jun / metabolism. Receptor, Epidermal Growth Factor / metabolism. Receptors, Tumor Necrosis Factor / metabolism. Signal Transduction / drug effects. Transcription Factor AP-1 / metabolism

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  • (PMID = 20068227.001).
  • [ISSN] 1535-4989
  • [Journal-full-title] American journal of respiratory cell and molecular biology
  • [ISO-abbreviation] Am. J. Respir. Cell Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Oxidants; 0 / Proto-Oncogene Proteins c-fos; 0 / Proto-Oncogene Proteins c-jun; 0 / Receptors, Tumor Necrosis Factor; 0 / Transcription Factor AP-1; 1332-21-4 / Asbestos; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 78
  • [Other-IDs] NLM/ PMC2822975
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30. Schneider J, Bernges U: CYP1A1 and CYP1B1 polymorphisms as modifying factors in patients with pneumoconiosis and occupationally related tumours: A pilot study. Mol Med Rep; 2009 Nov-Dec;2(6):1023-8
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  • [Title] CYP1A1 and CYP1B1 polymorphisms as modifying factors in patients with pneumoconiosis and occupationally related tumours: A pilot study.
  • The effect of CYP1A1 and CYP1B1 polymorphisms as genetic modifiers of risk was investigated in individuals with asbestos, silica dust or ionizing radiation-induced occupational tumours compared to exposed non-cancer subjects suffering from pneumoconiosis, particularly in relation to tobacco smoking.
  • CYP1A1 T6235C, CYP1A1 A4889G and CYP1B1 codon 432 polymorphisms were determined by real-time PCR analysis in patients with asbestos-related lung cancer (n=39), patients with diffuse malignant mesotheliomas (n=19), lung cancer in silicosis patients (n=7), uranium miners with lung cancer (UMLC) (n=40), patients with asbestosis (n=181), and silicosis patients (n=204).
  • The results were compared to those from a healthy unexposed control group (n=50) not exposed to carcinogenic (or fibrogenic) agents in the workplace.
  • The risk for patients with the susceptible CYP1A1 A4889G allele was calculated as being between OR=0.39 (95% CI 0.10-1.54) for mesothelioma patients and OR=1.54 (95% CI 0.49-4.89) for UMLC.
  • CYP1B1 Val432Leu polymorphisms were associated with a risk of OR=0.56 (95% CI 0.2-1.55) for UMLC and OR=1.52 (95% CI 0.68-3.39) for asbestos-exposed lung cancer patients.
  • By analyzing the interaction between tobacco smoking, type of exposure to carcinogens and the genotypes, it was determined that smoking and the presence of the susceptible genotypes did not have a combined effect.
  • In this pilot study, the analyzed polymorphism had no consistent modifying effect on pneumoconiosis or occupationally related tumours.

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  • (PMID = 21475938.001).
  • [ISSN] 1791-3004
  • [Journal-full-title] Molecular medicine reports
  • [ISO-abbreviation] Mol Med Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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31. Riganti C, Doublier S, Aldieri E, Orecchia S, Betta PG, Gazzano E, Ghigo D, Bosia A: Asbestos induces doxorubicin resistance in MM98 mesothelioma cells via HIF-1alpha. Eur Respir J; 2008 Aug;32(2):443-51
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  • [Title] Asbestos induces doxorubicin resistance in MM98 mesothelioma cells via HIF-1alpha.
  • Human malignant mesothelioma (HMM), which is strongly related to asbestos exposure, exhibits high resistance to many anticancer drugs.
  • Asbestos fibre deposition in the lung may cause hypoxia and iron chelation at the fibre surface.
  • Hypoxia-inducible factor (HIF)-1alpha, which is upregulated by a decreased availability of oxygen and iron, controls the expression of membrane transporters, such as P-glycoprotein (Pgp), which actively extrude the anticancer drugs.
  • The present study aimed to assess whether asbestos may play a role in the induction of doxorubicin resistance in HMM cells through the activation of HIF-1alpha and an increased expression of Pgp.
  • After 24-h incubation with crocidolite asbestos or with the iron chelator dexrazoxane, or under hypoxia, HMM cells were tested for HIF-1alpha activation, Pgp expression, accumulation of doxorubicin and sensitivity to its toxic effect.
  • Crocidolite, dexrazoxane and hypoxia induce doxorubicin resistance in human malignant mesothelioma cells by increasing hypoxia-inducible factor-1alpha activity, through an iron-sensitive mechanism.
  • [MeSH-major] Asbestos / toxicity. Drug Resistance, Neoplasm. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Lung Neoplasms / drug therapy. Mesothelioma / drug therapy
  • [MeSH-minor] Anoxia. Antineoplastic Agents / pharmacology. Asbestos, Crocidolite / pharmacology. Cell Line, Tumor. Doxorubicin / pharmacology. Humans. Iron / metabolism. Lung / pathology. P-Glycoprotein / metabolism. Razoxane / pharmacology

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  • (PMID = 18385176.001).
  • [ISSN] 1399-3003
  • [Journal-full-title] The European respiratory journal
  • [ISO-abbreviation] Eur. Respir. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / P-Glycoprotein; 12001-28-4 / Asbestos, Crocidolite; 1332-21-4 / Asbestos; 5AR83PR647 / Razoxane; 80168379AG / Doxorubicin; E1UOL152H7 / Iron
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32. Pinton G, Brunelli E, Murer B, Puntoni R, Puntoni M, Fennell DA, Gaudino G, Mutti L, Moro L: Estrogen receptor-beta affects the prognosis of human malignant mesothelioma. Cancer Res; 2009 Jun 1;69(11):4598-604
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  • [Title] Estrogen receptor-beta affects the prognosis of human malignant mesothelioma.
  • Malignant pleural mesothelioma is an asbestos-related neoplasm with poor prognosis, refractory to current therapies, the incidence of which is expected to increase in the next decades.
  • Female gender was identified as a positive prognostic factor among other clinical and biological prognostic markers for malignant mesothelioma, yet a role of estrogen receptors (ERs) has not been studied.
  • Our goal was to investigate ERs expression in malignant mesothelioma and to assess whether their expression correlates with prognosis.
  • Multivariate analysis of 78 malignant mesothelioma patients with pathologic stage, histologic type, therapy, sex, and age at diagnosis indicated that ERbeta expression is an independent prognostic factor of better survival.
  • Moreover, studies in vitro confirmed that treatment with 17beta-estradiol led to an ERbeta-mediated inhibition of malignant mesothelioma cell proliferation as well as p21(CIP1) and p27(KIP1) up-regulation.
  • Our data support the notion that ERbeta acting as a tumor suppressor is of high potential relevance to prediction of disease progression and to therapeutic response of malignant mesothelioma patients.
  • [MeSH-major] Estrogen Receptor beta / metabolism. Estrogen Receptor beta / physiology. Mesothelioma / diagnosis. Pleural Neoplasms / diagnosis


33. Dianzani I, Gibello L, Biava A, Giordano M, Bertolotti M, Betti M, Ferrante D, Guarrera S, Betta GP, Mirabelli D, Matullo G, Magnani C: Polymorphisms in DNA repair genes as risk factors for asbestos-related malignant mesothelioma in a general population study. Mutat Res; 2006 Jul 25;599(1-2):124-34
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  • [Title] Polymorphisms in DNA repair genes as risk factors for asbestos-related malignant mesothelioma in a general population study.
  • Differences in response to carcinogenic agents are due to the allelic variants of the genes that control it.
  • Key genes are those involved in the repair of the DNA damage caused by such agents.
  • This paper describes the results of a case-control epidemiological study designed to determine the genotypes of four of these genes in persons exposed to a single genotoxic factor, i.e. asbestos, who had or had not developed malignant mesothelioma (MM).
  • Our working hypothesis was that an imperfect DNA repair, as revealed by subtle polymorphic variants, could reduce protection against the chronic DNA insult provoked by asbestos and eventually result in mutagenesis and cancer.
  • XRCC1-R399Q-NCBI SNP, XRCC1-R194W, XRCC3-T241M, XRCC3-IVS6-14, XPD-K751Q, XPD-D312N, OGG1-S326C) were investigated in 81 patients and 110 age and sex-matched controls, all residents at Casale Monferrato, a Piedmontese town highly exposed to asbestos pollution.
  • This is the first report of an association between polymorphisms in DNA repair genes and asbestos-associated MM.
  • [MeSH-major] Asbestos / adverse effects. DNA Repair / genetics. Mesothelioma / etiology. Mesothelioma / genetics. Pleural Neoplasms / etiology. Pleural Neoplasms / genetics. Polymorphism, Genetic
  • [MeSH-minor] Aged. Base Sequence. Case-Control Studies. DNA Glycosylases / genetics. DNA Primers / genetics. DNA, Neoplasm / genetics. DNA-Binding Proteins / genetics. Female. Gene Frequency. Haplotypes. Humans. Italy. Male. Middle Aged. Risk Factors. Xeroderma Pigmentosum Group D Protein / genetics

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  • (PMID = 16564556.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / X-ray repair cross complementing protein 1; 0 / X-ray repair cross complementing protein 3; 1332-21-4 / Asbestos; EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / oxoguanine glycosylase 1, human; EC 3.6.4.12 / Xeroderma Pigmentosum Group D Protein; EC 5.99.- / ERCC2 protein, human
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34. Beyer HL, Geschwindt RD, Glover CL, Tran L, Hellstrom I, Hellstrom KE, Miller MC, Verch T, Allard WJ, Pass HI, Sardesai NY: MESOMARK: a potential test for malignant pleural mesothelioma. Clin Chem; 2007 Apr;53(4):666-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MESOMARK: a potential test for malignant pleural mesothelioma.
  • BACKGROUND: Soluble mesothelin-related peptides (SMRP)have been reported to be potential biomarkers for malignant pleural mesothelioma (MPM).
  • No interference was seen from added bilirubin (200 mg/L), hemoglobin (500 mg/L), triglycerides (30 g/L), chemotherapeutic agents, or other tested substances.
  • SMRP was increased in 52% and 5% of MPM patients and asbestos-exposed individuals, respectively.
  • Concentrations in other nonmalignant and malignant conditions were similar to those in healthy controls.
  • CONCLUSIONS: The MESOMARK assay is analytically robust and may be useful for the detection and management of mesothelioma.
  • [MeSH-major] Biomarkers, Tumor / blood. Membrane Glycoproteins / blood. Mesothelioma / diagnosis. Peptides / blood. Pleural Neoplasms / diagnosis
  • [MeSH-minor] Enzyme-Linked Immunosorbent Assay. Female. GPI-Linked Proteins. Humans. Male. ROC Curve. Reference Values. Reproducibility of Results. Sensitivity and Specificity. Solubility

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  • (PMID = 17289801.001).
  • [ISSN] 0009-9147
  • [Journal-full-title] Clinical chemistry
  • [ISO-abbreviation] Clin. Chem.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; 0 / Peptides; 0 / mesothelin
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