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Mesothelioma Risk modifiers and gene expression

The need for further investment in cancer research can not be overstated. Are diagnosed each year more than 2,000 new cases of mesothelioma. Mesothelioma is a deadly form of cancer caused by inhaling asbestos dust and particles caused. There are some ground-breaking research on risk modifiers and their relationship to mesothelioma. A study on the subject called, "Inherited GSTM1 and NAT2 defects as concurrent risk modifiers in asbestos-related human malignant mesothelioma" by Ari Hirvonen, Katarina Pelin, Lauri Tammilehto, Antti Karjalainen, Karin Mattson and Kaija Linnainmaa - Departments of Industria Hygiene and Toxicology [AH, KP, KL], Epidemiology and Biostatistics [LT] and Uusimaa Regional Institute [AK], Finnish Institute of Occupational Health, FIN-00 250 Helsinki, Finland, and the Department of Internal Medicine, University of Helsinki. Central Hospital, FIN-00290 Helsinki, Finland [KM], in Cancer Research 55, 2981-2983, 15 July 1995 published an excerpt:

"In addition to exposure to asbestos, the sensitivity factors for malignant mesothelioma to set unknown. We, the risk of GSTM1 null genotype and slow acetylation-associated NAT2 genotype for malignant mesothelioma in relation to asbestos. Both the GSTM1 null genotype NAT2 investigated slow acetylator genotype and the individuals at approximately 2-fold increased risk of malignant mesothelioma [odds ratio (OR) = 1.8 placed, 95% confidence interval (CI) = 1.0 to 3.5 and OR = 2.1, 95% CI = 1.1 to 4.1 for GSTM1 and NAT2 genes, respectively]. If the patient based split into low / medium and high exposure groups to their asbestos exposure histories, the effect of at-risk genotypes, especially for the high exposure group (OR = 2.3, 95% CI = 1.0 to 5.6 and OR = 3.7, 95% CI = 1.3 to 10.2, for GSTM1 and NAT2 genes known). People with GSTM1 and NAT2 a combined defects had compared a 4-fold risk of developing malignant mesothelioma to those with the gene GSTM1 and NAT2 rapid acetylator genotype (OR = 3.6, 95% CI = 1.3 to 9.6). In , the risk in subjects exposed to asbestos strongly with the double at-risk genotype more than 7-fold higher compared to those with the lower of the two genotypes of GSTM1 and NAT2 genes (OR = 7.4, 95% CI = 1 , 6 -34.0). "

Another interesting study is called "asbestos caused nuclear factor kappa B (NF-kappa B) DNA-binding activity and NF-kappa B-dependent gene expression in tracheal epithelial cells" by YM Janssen, A Barchowsky, M Treadwell, KE Driscoll, and BT Mossman. Here's an excerpt: "Abstract - nuclear factor kappa B (NF-kappa B) is a transcription factor gene expression internal inflammation and cell proliferation - the properties of asbestos disease in studies here crocidolite-consuming and causes dose-response increase in protein binding. to the nuclear NF-kappa B-binding DNA elements in hamster tracheal epithelial (HTE) cells. This binding was modulated by cellular glutathione levels. Antibodies against p65 and p50 protein members of the NF-kappa B family revealed that proteins in two DNA complexes. transient transfection assays with a construct with six NF-kappa B DNA binding consensus sites linked to a luciferase reporter gene indicated that asbestos-induced transcriptional activation of NF-kappa B-dependent genes, an observation that by Northern blot analysis for c-myc mRNA levels in HTE cells was confirmed. studies suggest that NF-kappa B induction by asbestos is a major event in the regulation of several genes in the pathogenesis of asbestos-related lung cancer. "

If you find one of these fragments using, read the studies in their entirety.

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