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From Single Level Analysis to Multi-Omics Integrative Approaches: A Powerful Strategy towards the Precision Oncology
Published in Shaker A. Mousa, Raj Bawa, Gerald F. Audette, The Road from Nanomedicine to Precision Medicine, 2020
Maria Eugenia Gallo Cantafio, Katia Grillone, Daniele Caracciolo, Francesca Scionti, Mariamena Arbitrio, Vito Barbieri, Licia Pensabene, Pietro Hiram Guzzi, Maria Teresa Di Martino
Among these datasets, TCGA is the most extensive, and includes multi-omics data deposited from many centers involved in the TCGA research network, as well as patient’s clinical metadata prospectively collected. TCGA data currently refers to 33 cancer types from more than 11,000 patients that have been obtained through different high-throughput technologies such as DNA-seq, SNP-based platforms, array-based DNA methylation-seq, microRNA-seq, RNA-seq, and RPPA by providing a comprehensive view of the human cancer molecular bases. Each platform produces data that are informative about DNA mutational status, SNP, methylation, loss of heterozygosity (LOH), copy number variation, miRNA expression, gene expression, and protein expression.
From Single Level Analysis to Multi-Omics Integrative Approaches: A Powerful Strategy towards the Precision Oncology
Published in Shaker A. Mousa, Raj Bawa, Gerald F. Audette, The Road from Nanomedicine to Precision Medicine, 2019
Maria Eugenia Gallo Cantafio, Katia Grillone, Daniele Caracciolo, Francesca Scionti, Mariamena Arbitrio, Vito Barbieri, Licia Pensabene, Pietro Hiram Guzzi, Maria Teresa Di Martino
Among these datasets, TCGA is the most extensive, and includes multi-omics data deposited from many centers involved in the TCGA research network, as well as patient’s clinical metadata prospectively collected. TCGA data currently refers to 33 cancer types from more than 11,000 patients that have been obtained through different high-throughput technologies such as DNA-seq, SNP-based platforms, array-based DNA methylation-seq, microRNA-seq, RNA-seq, and RPPA by providing a comprehensive view of the human cancer molecular bases. Each platform produces data that are informative about DNA mutational status, SNP, methylation, loss of heterozygosity (LOH), copy number variation, miRNA expression, gene expression, and protein expression.
Asbestos, the Carcinogen, and Its Bioremediation
Published in Tanmoy Chakraborty, Lalita Ledwani, Research Methodology in Chemical Sciences, 2017
Shabori Bhattacharya, Lalita Ledwani, P. J. John
Studies carried out for diffuse malignant mesothelioma have brought to the forefront a number of results related to chromosomal changes. A major event associated with diffuse malignant mesothelioma is deletion or hypermethylation at CDKN2A/ARF locus on chromosome 9p21, which carries three important tumor suppressor genes p15, p16INK4A, and p14ARF.113 Reports state that RASSFIA and GPC3 tumor suppressor genes are silenced, while another tumor suppressor gene NF2 is inactivated in diffuse malignant mesothelioma.122,123 Point mutations in p53 tumor suppressor gene and loss of heterozygosity were described in lung carcinoma of asbestos-exposed workers.98
Influence of quartz exposure on lung cancer types in cases of lymph node–only silicosis and lung silicosis in German uranium miners
Published in Archives of Environmental & Occupational Health, 2018
Stefan Mielke, Dirk Taeger, Kerstin Weitmann, Thomas Brüning, Wolfgang Hoffmann
All tumor types share the leading genetic principles on the way from a normal cell to an invasive carcinoma. These include “allelic losses (LOH), chromosomal instability and imbalance, mutations in oncogenes and tumor suppressor genes, epigenetic gene silencing through promoter hypermethylation and aberrant expressions of genes involved in the control of cell proliferation.”81 The dynamic interplay between these effects in the course of carcinogenesis is likely different between tumor types. For example, mutations in the most important tumor suppression gene, TP53, are more frequent in SCLC (70%) than in SqLC or AC (50%).87 Furthermore, the activation of the important tumor suppression gene Retinoblastoma (Rb) 1 differs between SCLC and the other histological types. ACs have more mutations in k-RAS, a proto-oncogene.81 There are no major differences between the cancer cells of the same histological tumor type in different tumor patients, but there are differences between the cells of different tumor types.