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1. Bonde JP: [Occupational medicine--origins and perspectives]. Ugeskr Laeger; 2009 Feb 9;171(7):529-31
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  • [Title] [Occupational medicine--origins and perspectives].
  • Technological innovation and preventive measures have had a major impact on the occurrence of occupational disease in Denmark over the past 50 years, although some diseases such as asbestos-related cancer are still being diagnosed.
  • The main challenges for modern occupational medicine is to unravel if low-level exposure in critical, narrow time windows during development have consequences for later chronic conditions like infertility, allergy and cardiovascular disease, to develop strategies to counteract premature expulsion from work because of musculoskeletal disorders and to learn when and how psychosocial workplace factors are detrimental to health.
  • [MeSH-major] Occupational Diseases. Occupational Medicine

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  • (PMID = 19210938.001).
  • [ISSN] 1603-6824
  • [Journal-full-title] Ugeskrift for laeger
  • [ISO-abbreviation] Ugeskr. Laeg.
  • [Language] dan
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Denmark
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2. Adiseshaiah P, Lindner DJ, Kalvakolanu DV, Reddy SP: FRA-1 proto-oncogene induces lung epithelial cell invasion and anchorage-independent growth in vitro, but is insufficient to promote tumor growth in vivo. Cancer Res; 2007 Jul 1;67(13):6204-11
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  • We and others have shown a high level of persistent induction of FRA-1 by lung carcinogens, such as cigarette smoke and asbestos, in pulmonary epithelial cells.
  • To examine this aspect, we have stably overexpressed FRA-1 in human type-II-like alveolar malignant cell line (A549) and a nonmalignant bronchial epithelial cell line (BEAS-2B).
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lung Neoplasms / metabolism. Proto-Oncogene Proteins c-fos / metabolism. Proto-Oncogene Proteins c-fos / physiology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Collagen / chemistry. Drug Combinations. Epithelial Cells. Humans. In Vitro Techniques. Laminin / chemistry. Male. Metaplasia / pathology. Mice. Mice, Nude. Neoplasm Invasiveness. Neoplasm Transplantation. Proteoglycans / chemistry

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  • (PMID = 17616677.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA095020; United States / NCI NIH HHS / CA / CA105005; United States / NCI NIH HHS / CA / CA78282; United States / NIEHS NIH HHS / ES / ES11863; United States / NHLBI NIH HHS / HL / HL66109
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Laminin; 0 / Proteoglycans; 0 / Proto-Oncogene Proteins c-fos; 0 / fos-related antigen 1; 119978-18-6 / matrigel; 9007-34-5 / Collagen
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3. 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.
  • 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-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


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4. Wilson R, McConnell EE, Ross M, Axten CW, Nolan RP: Risk assessment due to environmental exposures to fibrous particulates associated with taconite ore. Regul Toxicol Pharmacol; 2008 Oct;52(1 Suppl):S232-45
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  • In the early 1970s, it became a concern that exposure to the mineral fibers associated taconite ore processed in Silver Bay, Minnesota would cause asbestos-related disease including gastrointestinal cancer.
  • To further our understanding of the types of airborne fibers in Silver Bay we undertook a geological survey of their source the Peter Mitchell Pit, and found that there are no primary asbestos minerals at a detectable level.
  • However we identified two non-asbestos types of fibrous minerals in very limited geological locales.
  • Air sampling useful for risk assessment was done to determine the type, concentrations and size distribution of the population of airborne fibers around Silver Bay.
  • We calculate the risk of asbestos-related mesothelioma and lung cancer using a variety of different pessimistic assumptions. (i) that all the non-asbestos fibers are as potent as asbestos fibers used in the EPA-IRIS listing for asbestos; with a calculated risk of asbestos-related cancer for environmental exposure at Silver Bay of 1 excess cancer in 28,500 lifetimes (or 35 excess cancers per 1,000,000 lifetimes) and secondly that taconite associated fibers are as potent as chrysotile the least potent form of asbestos.
  • The calculated risk is less than 0.77 excess cancer case in 1,000,000 lifetimes.
  • Finally, we briefly review the epidemiology studies of grunerite asbestos (amosite) focusing on the exposure conditions associated with increased risk of human mesothelioma.
  • [MeSH-minor] Air / analysis. Dose-Response Relationship, Drug. Environmental Monitoring. Epidemiological Monitoring. Humans. Inhalation Exposure. Mineral Fibers / adverse effects. Mineral Fibers / analysis. Mineral Fibers / classification. Minnesota / epidemiology. Models, Biological. Odds Ratio. Risk Assessment

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  • (PMID = 18207296.001).
  • [ISSN] 1096-0295
  • [Journal-full-title] Regulatory toxicology and pharmacology : RTP
  • [ISO-abbreviation] Regul. Toxicol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Air Pollutants, Occupational; 0 / Mineral Fibers; 0 / Particulate Matter; 0 / Silicates; 12249-26-2 / taconite; E1UOL152H7 / Iron
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5. 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.


7. 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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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-minor] Humans. Neoplasm Staging. Prognosis


9. 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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10. 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.
  • We discovered a close relation between gene profile and resistance towards topoisomerase poisons, alkylating agents, antitubulines, antifolates, platinum compounds and radiation therapy.
  • 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.
  • [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


11. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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.
  • 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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12. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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-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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