Mesothelioma And Cancer Gene Therapy

One particular intriguing study is called, Adenovirus-mediated wild-sort p53 overexpression reverts tumourigenicity of human mesothelioma cells. By Giuliano M, Catalano A, Strizzi L, Vianale G, Capogrossi M, Procopio A. Int J Mol Med. 2000 Jun5(6):591-6. Department of Oncology and Neuroscience, Clinical Pathology Section, Gabriele D’Annunzio University, 66013 Chieti, Italy. Right here is an excerpt: Abstract – Pleural malignant mesothelioma (MM) shows poor survival, regardless of tumour stage at diagnosis. MM is unresponsive to present therapy regimens and new protocols are desperately needed. The localised nature, the potential accessibility, and the relative lack of distant metastases make MM a particularly appealing candidate for somatic gene therapy. A typical target for cancer gene therapy is the tumour suppressor protein p53. p53 does not seem to be mutated or deleted in MM, but it can be inactivated by binding to other proteins, like mdm2 and SV40 significant T antigen. We tested the effects of a replication-deficient adenoviral vector carrying wild-variety p53 cDNA in human MM cells. Our results show that &gt95% of MM cells had been efficiently infected with 25 multiplicity of infection (MOI) of vector. Wild-sort p53 was efficiently expressed resulting in &gt80% inhibition of proliferation in MM cells. AdCMV.p53 infection induced apoptosis even though controls did not show any evident morphological alterations. Ex vivo p53 gene transfer experiments inhibited tumourigenesis in nude mice. In vivo, direct intratumour injection of AdCMV.p53 arrested tumour growth and prolonged survival of treated mice. These outcomes indicate that p53-gene therapy really should be strongly exploited for clinical trials in MM patients.

Yet another study is named, Congenital polycystic tumor of the atrioventricular node (endodermal heterotopia, mesothelioma): A histogenetic appraisal with evidence for its endodermal origin – Human Pathology Volume 18, Problem 8, August 1987, Pages 791-795 by MD Gerald Fine and MD Usha Raju. Here is an excerpt: The modest, variously designated, principal atrioventricular node tumor has been thought of to be of endothelial, endodermal, or mesothelial origin. To determine its derivation, we studied seven tumors making use of silver staining and immunocytochemical labeling with a range of antibodies. Cytoplasmic argyrophil granules but not argentaffin granules were identified in isolated cells amongst the a lot more numerous bubule-lining cells in 4 tumors. Serotonin and calcitonin had been demonstrable in seven and six tumors, respectively, in a related distribution to that of the argyrophil cells. A good reaction of diverse distribution from that of the argyrophil cells was noted in a varying number of tubule-lining cells for carcinoembryonic antigen, epithelial membrane antigen, and blood group antigen in seven, four, and seven tumors, respectively. No activity was noted in the tumor cells for factor VIII-connected antigen or a number of peptides. An endodermal rather than mesothelial or epithelial origin for the tumor is substantiated by the presence of neuroendocrine cells in the midst of the a lot more quite a few carcinoembryonic-antigen-good lining cells of the tumor tubules.

Another study is called, SV40 expression in human neoplastic and non-neoplastic tissues: perspectives on diagnosis, prognosis and therapy of human malignant mesothelioma. By Procopio A, Marinacci R, Marinetti MR, Strizzi L, Paludi D, Iezzi T, Tassi G, Casalini A, Modesti A. Dev Biol Stand. 199894:361-7. Department of Oncology and Neuroscience, Gabriele D’Annunzio University, Chieti, Italy. Here is an excerpt: Abstract – We have recently demonstrated the association of SV40 and human pleural malignant mesothelioma. Right here, we have investigated whether or not SV40 viral sequences might be associated with other human tumours or other non-neoplastic pathology and whether or not SV40 DNA or protein expression may be of diagnostic, prognostic or therapeutic relevance. DNA was extracted from paraffin embedded tissues. SV40, JC and BK viral sequences were detected by the polymerase chain reaction and molecular hybridization with specific probes. The screening with three distinct sets of SV40-connected primers demonstrated that 7/18 (38.8%) mesothelioma specimens had been SV40 constructive as nicely as five/18 (27.7%) tubercular pleural lesions. None of the 18 lung cancers, nor the 20 pleural non-precise inflammatory specimens tested had been good. Twenty-five blood samples and 18 urinary sediments from MM patients had been also negative. We have also found that SV40 Tag proteins are present in mesothelioma cells and tumours. Tag proteins could interfere with tumour suppressor gene goods, such as p53. Preliminary final results suggest that wild type p53 transgene expression, obtained following infection with recombinant adenovirus (AdCMV.p53), inhibited in vitro and in vivo proliferation, inducing apoptosis of mesothelioma cells. Infections with control viruses had been ineffective. As a result, SV40 DNA and Tag expression in mesothelioma tumour cells, although most likely not pertinent for diagnostic or prognostic purposes, may possibly be vital for innovative gene therapy methods.

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