scholarly journals ACCELERATED PAPER: Identification of human tumour suppressor genes by monochromosome transfer: rapid growth-arrest response mapped to 9p21 is mediated solely by the cyclin-D-dependent kinase inhibitor gene, CDKN2A(p16INK4A)

1996 ◽  
Vol 17 (8) ◽  
pp. 1567-1575 ◽  
Author(s):  
Nicole L. England ◽  
Andrew P. Cuthbert ◽  
Deborah A. Trott ◽  
Sarah Jezzard ◽  
Tsutomu Nobori ◽  
...  
Keyword(s):  
Rapid Growth ◽  
Kinase Inhibitor ◽  
Growth Arrest ◽  
Tumour Suppressor ◽  
Tumour Suppressor Genes ◽  
Cyclin D ◽  
Human Tumour ◽  
Suppressor Genes ◽  
Inhibitor Gene

scholarly journals Methylation Analysis of Several Tumour Suppressor Genes Shows a Low Frequency of Methylation ofCDKN2AandRARBin Uveal Melanomas

2003 ◽  
Vol 4 (3) ◽  
pp. 329-336 ◽  
Author(s):  
Michael Zeschnigk ◽  
Frank Tschentscher ◽  
Christina Lich ◽  
Birgit Brandt ◽  
Bernhard Horsthemke ◽  
...  
Keyword(s):  
Uveal Melanoma ◽  
Metastatic Disease ◽  
Kinase Inhibitor ◽  
Tumour Suppressor ◽  
Chromosome 3 ◽  
Tumour Suppressor Genes ◽  
Aberrant Methylation ◽  
Causative Role ◽  
Suppressor Genes ◽  
Monosomy 3

We have investigated the frequency of methylation of several tumour suppressor genes in uveal melanoma. As the loss of one copy of chromosome 3 (monosomy 3), which is found in about half of these tumours, is tightly associated with metastatic disease, a special emphasis was laid on genes located on this chromosome, including the fragile histidine triad (FHIT), von Hippel–Lindau (VHL), β-catenin (CTNNB1), activated leukocyte cell adhesion molecule (ALCAM) and retinoic acid receptor-β2 (RARB) genes. In addition, the methylation patterns of the CpG-rich regions 5′ of the E-cadherin (CDH1), p16/cyclin-dependent kinase inhibitor 2 A (CDKN2A) and retinoblastoma (RB1) genes were analysed by bisulphite genomic sequencing or methylation-specific PCR (MSP). Furthermore, the SNRPN andD15S63loci, which are located in the imprinted region of chromosome 15, were included in the study. Aberrant methylation was detected in nine of 40 tumours analysed: The imprintedSNRPNandD15S63loci were hypermethylated in three tumours, all of which retained both copies of chromosome 3. MethylatedRARBalleles were detected in three tumours, whereas in three other tumoursCDKN2Awas found to be methylated. As we did not find RARB and CDKN2A preferentially methylated in tumours with monosomy 3, which is a significant predictor of metastatic disease, we suggest that these genes may play a causative role in the formation of uveal melanoma but not in the development of metastases.

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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