February 8th, 2006. Peculiar features of mesothelioma occurrence as related to exposure patterns and circumstances in the Lombard Region, Italy
Conclusions: The high proportion of cases with unknown exposure underlines the need to explore new tools and sources to ascertain asbestos exposure. An ad hoc survey in textile industries showed exposure to asbestos to be widely spread in this industry.
To foster discussion among investigators working in this field, and to exchange different viewpoints concerning the newest advances in MMe pathogenesis and treatment, the VII International Mesothelioma Interest Group (IMIG) meeting was held in Brescia (Italy) between 24 and 26 June 2004 in cooperation with the Italian Group for the Study and Therapy of MMe (GIMe). The aim of this report is to summarize the most significant advances in the different disciplines applied to MMe presented and discussed during the IMIG meeting and how these advances will be changing the perspective of patients with MMe.
February 8th, 2006. Proteasome inhibitor PSI induces apoptosis in human mesothelioma cells
PSI seemed to decrease mesothelioma viability by inducing apoptosis, as verified by cell morphology, Western blotting analysis of caspase 3 cleavage, and flow-cytometric analysis. In conclusion, PSI, a representative agent that reduces viability and induces apoptosis of mesothelioma cells, might be useful in the treatment of patients with mesothelioma, especially of epithelioid phenotype.
February 8th, 2006. Human neoplastic mesothelial cells express voltage-gated sodium channels involved in cell motility
Interestingly, blockade of VGSCs with TTX decreased mesothelioma cell migration in in vitro motility assays; on the other hand, TTX failed to interfere with cell viability, proliferation, and apoptosis progression triggered by UV exposure. In summary, the results of the present study suggest that VGSCs expression in MPM cells may favor the increased motility of the neoplastic cells, a phenotypic feature often associated with the malignant phenotype.
February 6th, 2006. Survival from rare cancer in adults: a population-based study
Interpretation: Because effective treatments are available for several of the rare cancers we assessed, further research is needed to ascertain why survival is lower in some European countries than in others, particularly in older patients. Audit of best practice for rare cancers with treatment protocols would be useful.
February 6th, 2006. Soluble Mesothelin-related Protein in the Diagnosis of Malignant Pleural Mesothelioma
Interpretation: We show that SMRP may be a promising marker for mesothelioma diagnosis when measured either in serum or pleural fluid. The diagnostic value of SMRP was similar in both types of samples, but pleural fluid SMRP may better discriminate mesothelioma from pleural metastasis.
Conclusions: CRS + IPHP presented acceptable morbidity, toxicity, and mortality rates, all of which support prospective Phase III clinical trials.
February 6th, 2006. Statins revert doxorubicin resistance via nitric oxide in malignant mesothelioma
Both the Rho kinase inhibitor Y27632 and the RhoA inhibitor toxin B (from Clostridium difficile) mimicked the statins' effects, enhancing doxorubicin accumulation, NO synthesis and IKK phosphorylation and decreasing the amount of IkB in HMM cells. Simvastatin, Y27632 and toxin B elicited tyrosine nitration in the P-glycoprotein, thus providing a likely mechanism by which NO reverts the doxorubicin resistance in HMM cells.
February 6th, 2006. Adenosine deaminase 2 in the diagnosis of tuberculous pleuritis
Conclusion: Pleural ADA2 is useful in the diagnosis of tuberculous pleuritis, which has similar sensitivity and a little better specificity compared with pleural ADA.
Conclusions: Completeness of cytoreduction, performance status, and MC seem to be the best determinants of outcome. These data warrant confirmation by a further prospective formal trial. No biological markers presented a significant correlation with the outcome. The overexpression of epidermal growth factor receptor, matrix metalloproteinase 2, and matrix metalloproteinase 9 and absent or reduced expression of p16 might be related to the underlining tumor kinetics of DMPM and warrant further investigation with other methods.
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