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| Malignant Pleural Mesothelioma |
Malignant Pleural Mesothelioma is showing low survival rate regardless of tumor stage at diagnosis. Malignant Mesothelioma does not respond to treatments and new protocols are badly needed there. The localized nature, the potential availability and the relative lack of distant metastases of malignant mesothelioma is a particularly attractive candidate for somatic gene therapy.
A common goal for the treatment of cancer, the p53 tumor suppressor protein. P53 does not appear to be mutated or deleted in malignant mesothelioma, but it can bind to other proteins, such as inactivated MDM2 and SV40 large T antigen
It tested the effect of a replication-deficient adenoviral vector, the cDNA of wild-type p53 in human cells, malignant mesothelioma. Our results indicate that over 95% of malignant mesothelioma cells efficiently with 25 multiplicity of infection (MOI) of infected vector.
P53 wild type was actually expressed> 80% inhibition of cell proliferation in malignant mesothelioma cells. AdCMV.p53 infection-induced apoptosis, whereas controls showed no obvious morphological change.
Ex vivo gene transfer, p53 inhibited tumor growth in nude mice. Arrested in vivo by direct intratumoral injection AdCMV.p53 of tumor growth and prolonged survival time of treated mice. These results strongly indicate that p53 gene therapy to be used for clinical trials of patients with malignant mesothelioma. By Monty Wrobleski.
A common goal for the treatment of cancer, the p53 tumor suppressor protein. P53 does not appear to be mutated or deleted in malignant mesothelioma, but it can bind to other proteins, such as inactivated MDM2 and SV40 large T antigen
It tested the effect of a replication-deficient adenoviral vector, the cDNA of wild-type p53 in human cells, malignant mesothelioma. Our results indicate that over 95% of malignant mesothelioma cells efficiently with 25 multiplicity of infection (MOI) of infected vector.
P53 wild type was actually expressed> 80% inhibition of cell proliferation in malignant mesothelioma cells. AdCMV.p53 infection-induced apoptosis, whereas controls showed no obvious morphological change.
Ex vivo gene transfer, p53 inhibited tumor growth in nude mice. Arrested in vivo by direct intratumoral injection AdCMV.p53 of tumor growth and prolonged survival time of treated mice. These results strongly indicate that p53 gene therapy to be used for clinical trials of patients with malignant mesothelioma. By Monty Wrobleski.
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