DNA hypermethylation: when tumour suppressor genes go silent

2002 ◽  
Vol 111 (2) ◽  
pp. 115-127 ◽  
Author(s):  
George A. Garinis ◽  
George P. Patrinos ◽  
Nick E. Spanakis ◽  
Panayiotis G. Menounos
Keyword(s):  
Tumour Suppressor ◽  
Tumour Suppressor Genes ◽  
Dna Hypermethylation ◽  
Suppressor Genes

scholarly journals Hypermethylation involved in DNA profiles of lung cancer specific tumour suppressor genes and epigenetic modification caused by an ultra-highly diluted homeopathic drug, Condurango 30C, in vitro and in vivo

2021 ◽  
Vol 13 (47) ◽  
pp. 99-99
Author(s):  
Anisur Rahman Khuda-Bukhsh ◽  
Sourav Sidkar
Keyword(s):  
Lung Cancer ◽  
Dna Methylation ◽  
Epigenetic Modification ◽  
Tumour Suppressor ◽  
Tumour Suppressor Genes ◽  
Dna Hypermethylation ◽  
Suppressor Genes ◽  
Homeopathic Drug

Background and objectives: DNA hyper-methylation is an important aspect involved in carcinogenesis and cancer progression, which affects mainly CpG islands of DNA and causes inactivation of tumour suppressor genes. Therefore DNA hypermethylation status of the genomic DNA in both the transformed cancerous cell lines and in carcinogen-induced lung cancer was ascertained by analysis of expressions of certain major lung cancer specific tumour suppressor genes. The other objective was to examine if ultra highly diluted homeopathic drug, Condurango 30C, had ability to modulate DNA methylation. Methods: DNA methylation activity, if any, has been ascertained in H460-NSCLC cells in vitro and in BaP-induced lung cancer of rats in vivo, in respect of tumour suppressor genes like p15, p16, p18 and p53 by using PCR-SSCP analyses. The ability of modulation of DNA methylation, if any, by Condurango 30C was also verified against placebo control in a blinded manner. Results: Condurango 30C-treated DNA showed significant decrease in band-intensity of p15 and p53 genes especially in methylated condition, in vitro, at the IC50 dose (2.43µl/100µl). SSCP analysis of p15 and p53 genes in Condurango 30C-treated DNA also supported ability of Condurango 30C to modulate methylation state, in vitro. Inhibition of p15 hypermethylation was observed after post cancer treatment of rat with Condurango 30C. SSCP results gave a better indication of differences in band-position and single strand separation of p15 and p53 in Condurango 30C treated samples. Conclusion: Condurango 30C could trigger epigenetic modification in lung cancer via modulation of DNA hypermethylation but placebos could not.

scholarly journals Exclusion of BBC1 and CMAR as candidate breast tumour-suppressor genes

1997 ◽  
Vol 76 (12) ◽  
pp. 1550-1553 ◽  
Author(s):  
E Moerland ◽  
MH Breuning ◽  
CJ Cornelisse ◽  
AM Cleton-Jansen
Keyword(s):  
Breast Tumour ◽  
Tumour Suppressor ◽  
Tumour Suppressor Genes ◽  
Suppressor Genes

Infrequent loss of heterozygosity of the major tumour suppressor genes in Indian oral cancers

2002 ◽  
Vol 31 (4) ◽  
pp. 414-418 ◽  
Author(s):  
S. Kannan ◽  
H. Yokozaki ◽  
K. Jayasree ◽  
P. Sebastian ◽  
A. Mathews ◽  
...  
Keyword(s):  
Loss Of Heterozygosity ◽  
Tumour Suppressor ◽  
Tumour Suppressor Genes ◽  
Suppressor Genes ◽  
Oral Cancers

Tumour Suppressor Genes in Hodgkin’s Disease

1995 ◽  
pp. 209-222
Author(s):  
Miguel A. Piris ◽  
Juan C. Martinez ◽  
Margarita Sanchez-Beato ◽  
Juan F. Garcia ◽  
Carmen Bellas ◽  
...  
Keyword(s):  
Hodgkin's Disease ◽  
Hodgkin’S Disease ◽  
Tumour Suppressor ◽  
Tumour Suppressor Genes ◽  
Suppressor Genes

scholarly journals Pan-cancer characterisation of microRNA with hallmarks of cancer reveals role of microRNA-mediated downregulation of tumour suppressor genes

2017 ◽  
Author(s):  
Andrew Dhawan ◽  
Jacob G. Scott ◽  
Adrian L. Harris ◽  
Francesca M. Buffa
Keyword(s):  
Penalized Regression ◽  
Tumour Suppressor ◽  
The Cancer Genome Atlas ◽  
Clinical Samples ◽  
Tumour Suppressor Genes ◽  
Alternative Mechanism ◽  
Mirna Regulation ◽  
Hallmarks Of Cancer ◽  
Suppressor Genes ◽  
Copy Number Changes

microRNA are key regulators of the human transcriptome across a number of diverse biological processes, such as development, aging, and cancer, where particular miRNA have been identified as tumour suppressive and oncogenic. In this work, we sought to elucidate, in a comprehensive manner, across 15 epithelial cancer types comprising 7,316 clinical samples from the Cancer Genome Atlas, the association of miRNA expression and target regulation with the pheno-typic hallmarks of cancer. Utilising penalized regression techniques to integrate transcriptomic, methylation and mutation data, we find evidence for a complex map of interactions underlying the relationship of miRNA regulation and the hallmarks of cancer. This highlighted high redundancy for the oncomiR-1 cluster of oncogenic miRNAs, in particular hsa-miR-17-5p. In addition, we reveal extensive miRNA regulation of tumour suppressor genes such as PTEN, FAT4, and CDK12, uncovering an alternative mechanism of repression in the absence of mutation, methylation or copy number changes.

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