Archive for the 'SV40' Category
Simian Virius 40 polio vaccine.
December 17th, 2008. Simian virus 40 sequences in blood specimens from healthy individuals of Casale Monferrato, an industrial town with a history of asbestos pollution
Conclusions: SV40 sequences are present in blood samples of healthy donors from Casale Monferrato with a prevalence similar to that reported in previous investigations of healthy donors from asbestos-free areas. Altogether these data suggest that SV40 is circulating in the human population.
September 13th, 2008. Pathogenesis of malignant pleural mesothelioma and the role of environmental and genetic factors
Conclusion: Many risk factors for MPM development have been recognized including environmental exposures, genetic susceptibility, viral contamination, and radiation. In this review, we discuss the current molecular and genetic contributors to MPM pathogenesis and the risk factors associated with these carcinogenic processes.
September 2nd, 2008. The role of polio-vaccine in pleural mesothelioma–an epidemiological observation
This is the opposite to what would be expected if potential SV40 contamination of polio vaccine used had a causative role in the development of the tumour. On the other hand, shorter latency period reflected by very high percentage of 45-year-old or younger mesothelioma patients in vaccinated group (15 out of 58), with all of them having a history of occupational asbestos exposure, raises a question for a possible enhancing effect of the vaccine used to asbestos exposure, if it was contaminated with SV40.
August 19th, 2008. Mesothelioma Epidemiology, Carcinogenesis, and Pathogenesis
An exciting new development comes from the discovery that genetic susceptibility to mineral fiber carcinogenesis plays a critical role in the incidence of this cancer in certain families. It is hoped that the identification of this putative mesothelioma gene will lead to novel mechanistically driven preventive and therapeutic approaches.
June 15th, 2008. SV40 large T antigen-specific human T cell memory responses
Peptide-stimulated T cells also killed SV40 Tag-transfected target cells. This article demonstrates the presence, and provides a detailed analysis, of SV40-specific T cell memory in man.
June 4th, 2008. Malignant mesothelioma 2008
Novel therapies including intrapleural chemotherapy, photodynamic therapy and hyperthermic perfusion have also been used with some success. Finally there are several attempts at immunomodulating and targeted treatments, which are in phase I/II trials.
Posted in Causation, Chemotherapy, Determining Efficacy, Diagnosis & Differentiation, Full Archive, General, Immune-based Therapies, New & Novel, Occupational Asbestos Exposure, Photodynamic Therapy (PDT), Radiation, SV40, Serum Marker/Blood Test, Survival, Treatment, Type of Assessment: | No Comments »
June 4th, 2008. The relationship between simian virus 40 and mesothelioma
Epidemiological data possibly linking simian virus 40 and malignant mesothelioma is lacking owing to unattainable identification of infected from noninfected cohorts. Summary: Available evidence appears sufficient to link simian virus 40 either alone or in conjunction with asbestos in causing malignant mesotheliomas; however, it is still insufficient to speculate about the contribution of simian virus 40 to the overall incidence of malignant mesotheliomas.
June 4th, 2008. Mesothelioma due to environmental exposure to erionite in Turkey
It has also been confirmed that a genetic predisposition to erionite carcinogenesis is the cause of the mesothelioma epidemic in Cappadocia. Summary: The data obtained recently on the epidemiology, etiology, and pathogenesis of the mesothelioma due to erionite exposure in Turkey are described.
April 4th, 2008. Establishment of three novel human malignant pleural mesothelioma cell lines: morphological and cytogenetical studies and EGFR mutation status
Conclusion: FACS analysis is more sensitive for evaluating mesothelin expression than immunohistochemistry of cut specimens. Irrespective of the expression of EGFR on FACS analysis, no EGFR mutation was detected. These three cell lines may be useful for studying cellular, molecular and genetic aspects of mesothelioma.
March 8th, 2008. Advances in the molecular biology of malignant mesothelioma
Although the causative role of asbestos is well-known in MM, much less information is available for MM than for other malignant tumors regarding the molecular alterations that occur in the disease. In terms of future tasks, it will be necessary to apply the knowledge that is learned about molecular alterations to clinical practice and to further elucidate the pathogenesis of MM with extensive research.
January 30th, 2008. No detection of SV40 DNA in mesothelioma tissues from a high incidence area in Sweden
Eighteen tumors were amplifiable, but none contained SV40 DNA. The results do not support an association between mesothelioma and SV40.
December 22nd, 2007. Fra-1 governs cell migration via modulation of CD44 expression in human mesotheliomas
Lastly, in contrast to normal lung tissue, tissue microarrays revealed that Fra-1 was expressed in 33 of 34 human MMs, and that all CD44+ tumors were SV40-. These results suggest that Fra-1 is associated with cell migration in human MMs and that Fra-1 modulation of CD44 may govern migration of selected MMs.
November 24th, 2007. Peritoneal malignant mesothelioma: case report
Different pathogenic mechanisms for the pathogenesis of a peritoneal diffuse malignant mesothelioma in this patient can be hypothesized, for example, SV40 infection and genetic susceptibility; a minimal domestic exposure to asbestos can be not excluded. Therefore, further studies in a more large number of subjects are necessary to determine whether one or all of these hypothetic pathogenic mechanisms are more significant for the develop of malignant mesothelioma.
September 19th, 2007. SV40 Multiple Tissue Infection and Asbestos Exposure in a Hyperendemic Area for Malignant Mesothelioma
045). This survey shows that SV40 sustains infections in multiple tissues in malignant mesothelioma patients from a geographic area affected with asbestos-related mesothelioma.
August 7th, 2007. Simian virus 40 and mesothelioma in Great Britain
Conclusion: Although the results for females show a reduction in the mesothelioma mortality rate coinciding with the introduction of the SV40-free Sabin polio vaccine, the absence of a similar result in males and of a priori biological evidence of a sex-specific SV40 effect, makes chance the most plausible interpretation of these findings.
July 6th, 2007. Evaluation of simian virus-40 as a biological prognostic factor in Egyptian patients with malignant pleural mesothelioma
SV40 and asbestos exposure are common in Egyptian MPM, denoting a possible etiological role and a synergistic effect for both agents. Combined positivity for SV40 and asbestos exposure is an independent prognostic factor in MPM, having a detrimental effect on OS.
May 22nd, 2007. Low prevalence of SV40 in Swiss mesothelioma patients after elimination of false-positive PCR results
SV40 DNA and protein were found at low prevalence (5%) in plasma and tumour tissue, respectively. This suggests that SV40 does not appear to play a major role in the development of mesothelioma.
May 15th, 2007. Eighth International Mesothelioma Interest Group
Here, experts in different disciplines critically review some of the most exciting presentations of the IMIG meeting. The result is a comprehensive review of the research field of asbestos carcinogenesis and mesothelioma, and of the progress that has been made in recent years in both basic and clinical sciences.
April 19th, 2007. SV40 oncoproteins enhance asbestos-induced DNA double-strand breaks and abrogate senescence in murine mesothelial cells
These studies suggest that exposure to DNA-damaging agents can induce senescence in both murine and human mesothelioma cell lines and suggest a major, although not exclusive, role for p53 in this response. SV40 virus may contribute to mesothelioma progression by impairing stress-induced senescence, in part through p53 inactivation, thereby favoring survival and proliferation of mesothelial cells that have sustained DNA damage.
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