Retinoblastoma and Wilms' tumour genes — paradigms for tumour suppressor genes

1991 ◽  
Vol 252 (2) ◽  
pp. 170
Author(s):  
N. Hastie
Keyword(s):  
Tumour Suppressor ◽  
Tumour Suppressor Genes ◽  
Wilms Tumour ◽  
Suppressor Genes

The molecular biology of Wilms' tumour

2001 ◽  
Vol 3 (13) ◽  
pp. 1-16 ◽  
Author(s):  
Keith W. Brown ◽  
Karim T.A. Malik
Keyword(s):  
Kidney Development ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor ◽  
Kidney Neoplasm ◽  
Tumour Suppressor Genes ◽  
Loss Of Function ◽  
Wilms Tumour ◽  
Suppressor Genes ◽  
Renal Stem Cells

Wilms' tumour (WT; nephroblastoma), a kidney neoplasm, is one of the most frequently occurring solid tumours of childhood. It arises from the developing kidney by genetic and epigenetic changes that lead to the abnormal proliferation of renal stem cells (metanephric blastema). WT serves as a paradigm for understanding the relationship between loss of developmental control and gain of tumourigenic potential. In particular, loss of function of tumour suppressor genes has been implicated in the development of WT, and the Wilms' tumour suppressor gene WT1 (at chromosome 11p13) was the second tumour suppressor gene to be cloned, after the retinoblastoma gene RB-1. WT1 plays an essential role in kidney development, but is mutated in only approximately 20% of WTs, which suggests that further lesions and genetic loci are involved in Wilms' tumourigenesis. Other chromosomal regions associated with WT include 7p, 11p15, 16q and 17q. Although many of these loci probably contain tumour suppressor genes, imprinted genes (genes showing expression of only one parental allele) and oncogenes have also been implicated in WT. Some loci have been shown to be associated with particular clinical outcomes, suggesting that they might be used to determine prognosis, and especially to identify poor prognostic subgroups that can be targeted for aggressive and/or novel therapies.

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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