Journal Articles on Mesothelioma: 'Gene Therapy' Category
August 8th, 2008. Novel Functional View of the Crocidolite Asbestos-Treated A549 Human Lung Epithelial Transcriptome Reveals an Intricate Network of Pathways with Opposing Functions
Conclusions: Our analyses demonstrate the power of combining a statistically robust, comprehensive dataset and a functional network genomics approach to 1) identify and explore relationships between genes of known importance 2) identify novel candidate genes, and 3) observe the complex interplay between genes/gene products that function in seemingly different processes. This study represents the first function-based global approach toward understanding the response of human lung epithelial cells to the carcinogen crocidolite. Importantly, our investigation paints a much broader landscape for the crocidolite response than was previously appreciated and reveals novel paths to study. Our graphical representations of the function-based global network will be a valuable resource to model new research findings.
May 14th, 2008. Molecular targets and targeted therapies for malignant mesothelioma
Alternative approaches are based on inhibitors of the ubiquitin-proteasome pathway and of histone deacetylases which, notwithstanding the functional divergence of the corresponding targets, share the ability to determine a wide modulation of the cancer cell phenotype that can lead to cell cycle arrest, apoptosis and sensitization to different antineoplastic treatments. A recombinant immunotoxin targeted to the membrane antigen mesothelin is an additional agent whose activity is being evaluated in mesothelioma patients.
May 6th, 2008. Overexpression and altered glycosylation of MUC1 in malignant mesothelioma
CA15-3 in effusions could differentiate malignant from benign effusions but were not specific for mesothelioma. Thus, as in other cancers, alterations in MUC1 biology occur in mesothelioma and these results suggest that specific MUC1 characteristics may be useful for mesothelioma diagnosis and should also be investigated as a potential therapeutic target.
April 21st, 2008. Genetic susceptibility to malignant pleural mesothelioma and other asbestos-associated diseases
Major limitations in the study design, including the small size of study groups, affected the reliability of these studies. Technical improvements such as the use of high-throughput techniques will help to identify molecular pathways regulated by candidate genes.
April 9th, 2008. Frequent p16 inactivation by homozygous deletion or methylation is associated with a poor prognosis in Japanese patients with pleural mesothelioma
Our study showed that P16 inactivation by homozygous deletions or methylation is a frequent event in Japanese patients with MPMs, relating to poor prognosis. Homozygous deletion is the major cause of P16 inactivation, but methylation also lead to the inactivation of P16 when the P16 alleles are retained.
April 4th, 2008. Inhibition of both mesothelioma cell growth and Cdk4 activity following treatment with a TATp16INK4a peptide
Conclusion: Therapeutic strategies which introduce either TATp16INK4a peptide, or small molecule mimetic, could be an effective strategy for mesothelioma treatment.
March 28th, 2008. Cell-cycle molecules in mesothelioma: an overview
Several studies report the importance of cell cycle regulator proteins in the pathogenesis and the prognosis of mesothelioma. This article will review the most recent data from the literature about the expression and the diagnostic and prognostic significance of cell cycle molecules in mesothelioma.
March 7th, 2008. Characterization of Human Mesothelioma Cell Lines as Tumor Models for Suicide Gene Therapy
Conclusion: The characterized cell lines described here may serve as a model for in vitro and in vivo preclinical gene therapy for the treatment of MPM using rAAV2 suicide vectors.
March 4th, 2008. Asbestos exposure predicts cell cycle control gene promoter methylation in pleural mesothelioma
05) after controlling for age, gender, and tumor histology. These data suggest a novel tumorigenic mechanism of action of asbestos, and may contribute to the understanding of precisely how asbestos exposure influences the etiology and clinical course of malignant mesothelioma.
February 28th, 2008. Transcriptome sequencing of malignant pleural mesothelioma tumors
Of the seven point mutations, three were observed in at least one tumor from 49 other MPM patients. The mutations were in genes that could be causally related to cancer and included XRCC6, PDZK1IP1, ACTR1A, and AVEN.
February 8th, 2008. Ensemble methods for classification of patients for personalized medicine with high-dimensional data
Conclusion: The statistical classification method for individualized treatment of diseases developed in this study is expected to play a critical role in developing safer and more effective therapies that replace one-size-fits-all drugs with treatments that focus on specific patient needs.
February 7th, 2008. PTEN expression is a strong predictor of survival in mesothelioma patients
Conclusion: PTEN is an independent prognostic biomarker in mesothelioma patients. The frequent loss of expression of the tumour suppressor gene PTEN suggests involvement of the PI3K-AKT/protein kinase B (PKB) pathway in MPMs, which may be relevant for future mesothelioma treatment.
January 30th, 2008. Targeting the Wnt signaling pathway with dishevelled and cisplatin synergistically suppresses mesothelioma cell growth
Conclusion: Our data suggest that inhibition of Wnt signaling leads to significant antitumor effects.
January 29th, 2008. Imatinib mesylate enhances therapeutic effects of gemcitabine in human malignant mesothelioma xenografts
Conclusions: Imatinib mesylate enhances the therapeutic response to gemcitabine, in accordance with our previous in vitro data. These in vivo results validate imatinib mesylate and gemcitabine as a combination treatment of malignant mesothelioma, also in view of its known positive effects on tumor drug uptake. These evidences provide the rationale for the currently ongoing clinical trials.
November 28th, 2007. Molecular genetics and mechanisms of apoptosis in carcinomas of the lung and pleura: Therapeutic targets
Stem cell therapy and gene replacement offer the prospect of novel approaches that are likely in the near future to play a definitive role in the treatment of advanced lung cancer. Furthermore, with their apparent minimal toxicity to normal tissues, the newer molecular targets represent attractive investigational directions for innovative cancer therapies.
November 27th, 2007. Role of fragile histidine triad protein expression in pathogenesis of malignant pleural mesothelioma
Conclusion: The results support the role of FHIT as a tumour suppressor gene in asbestos induced MPM. There is no significant correlation between FHIT and cell proliferation marker expressions in malignant pleural mesothelioma. Therefore, it can be concluded that loss of FHIT does not interfere with tumour proliferation. This can be accepted as evidence for an early role of FHIT loss in carcinogenesis; however, it needs to be strengthened by further studies.
October 24th, 2007. Receptor EphA2 activation with ephrinA1 suppresses growth of malignant mesothelioma (MM)
Ligand activated and ephrinA1 vector (pcDNA/EFNA1) transfected MMC demonstrated decreased clonal growth in 3-D matrigels when compared to resting MMC. These studies suggest that EphA2 activation by its ligand ephrinA1 transmits intracellular signals from cell membrane to nucleus via ERK1/2 signaling cascade and inhibits MM growth.
October 17th, 2007. Malignant mesothelioma cells are rapidly sensitized to TRAIL-induced apoptosis by low-dose anisomycin via Bim
Overall, our data indicate that the rapid and selective sensitization by anisomycin in mesothelioma cells is mediated by posttranslational potentiation of Bim, which primes the cells for apoptosis via the death receptor pathway. Such subtoxic approaches to sensitization may enhance the value of TRAIL in cancer therapy.
October 5th, 2007. A microaliquoting technique for precise histological annotation and optimization of cell content in frozen tissue specimens
High yield and quality RNA was extracted from precision annotated, tumor-enriched subsamples prepared by combining individual microaliquots with the highest tumor cellularity estimates. Microaliquoting provides accurate cell content annotation and permits genomic analysis of enriched subpopulations of cells without fixation or amplification.
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