scholarly journals Putative tumour suppressor gene necdin is hypermethylated and mutated in human cancer

2013 ◽  
Vol 108 (6) ◽  
pp. 1368-1377 ◽  
Author(s):  
L E De Faveri ◽  
C D Hurst ◽  
F M Platt ◽  
C F Taylor ◽  
J-A Roulson ◽  
...  
Keyword(s):  
Human Cancer ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor

scholarly journals Characterising Mutational Spectra of Carcinogens in the Tumour Suppressor Gene TP53 Using Human TP53 Knock-in (Hupki) Mouse Embryo Fibroblasts

2019 ◽  
Vol 2 (4) ◽  
pp. 85 ◽  
Author(s):  
Hölzl-Armstrong ◽  
Kucab ◽  
Korenjak ◽  
Luijten ◽  
Phillips ◽  
...  
Keyword(s):  
Tp53 Mutation ◽  
Human Cancer ◽  
Atmospheric Oxygen ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor ◽  
International Agency ◽  
Human Tumours ◽  
Clonal Cell Lines ◽  
Gene Tp53

DNA in dividing cells is prone to mutagenesis, with mutations making key contributions to human disease including cancer. The tumour suppressor gene TP53 is the most frequently mutated gene in human tumours. Here, we present a robust protocol for studying TP53 mutagenesis utilising human TP53 knock-in (Hupki) mouse embryonic fibroblasts (HUFs). In the HUF immortalisation assay (HIMA), primary HUFs are treated with known or suspected carcinogens at 3% oxygen and then transferred to 20% atmospheric oxygen to induce senescence. Cells containing mutations (e.g., in TP53) that allow bypassing of senescence eventually emerge as immortalised clonal cell lines after 2–3 months of serial passaging. As not all immortalised HUF cells contain TP53 mutations, we developed a Nutlin-3a counter-screen to select for TP53-mutated clones prior to sequencing. TP53 mutation spectra generated can be compared with those of human tumours recorded in the International Agency for Research on Cancer TP53 mutation database. Environmental mutagens that have demonstrated and validated the utility of the HIMA include ultraviolet radiation, aristolochic acid, and benzo[a]pyrene. The TP53 mutation patterns induced by these mutagens in the HIMA corresponded to those found in human tumours from patients exposed to these mutagens. The approach presented helps to deepen our understanding of human cancer aetiology.

Molecular analysis of different allelic variants of wild-type human p53

1992 ◽  
Vol 70 (10-11) ◽  
pp. 1014-1019 ◽  
Author(s):  
France Moreau ◽  
Greg Matlashewski
Keyword(s):  
Cultured Cells ◽  
Human Cancer ◽  
P53 Protein ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor ◽  
Allelic Variant ◽  
Wild Type ◽  
Allelic Variants ◽  
Wild Type P53

The p53 tumour suppressor gene is intensively studied because mutations in this gene are the most common genetic alteration so far identified in human cancer. Considerable emphasis has thus been placed on characterizing the biological differences between mutant and wild-type p53 protein. This has led to the realization that in cultured cells, mutant p53 behaves like an oncogene, whereas wild-type p53 is a tumour suppressor gene. The p53 protein is also a target for the tumour virus oncogene products SV40 large T, adenovirus E1B, and human papillomavirus type 16 E6, which are all capable of forming complexes to the p53 protein. Although p53 represents an extremely important cellular regulatory molecule which is well conserved, there exists two allelic variants of wild-type human p53 that differ both in primary and confirmational structure. One variant contains an arginine at amino acid 72 (p53Arg), whereas the other form contains a proline at this residue (p53Pro). The possible implications for more than one allelic variant of wild-type human p53 in the general population is unknown. The present study was undertaken to compare some of the biological features of the different wild-type p53 variants. We present data demonstrating that there was a post-transcriptional selection against accumulation of both variants of wild-type human p53 in 3T3-A31 cells, arguing that both forms are proliferation inhibitory in these cells. Both variants of human p53 were stabilized by SV40 large T, but did not displace mouse p53 from SV40 large T. Neither allelic variant of human p53 was able to reduce significantly SV40-mediated anchorage-independent growth of 3T3-A31 cells. Taken together, these data suggest that although there are structurally different variants of wild-type human p53, there is no difference in the biological activity of these molecules at the level of the biological assays performed here.Key words: human p53, large T, transformation, oncogenes, tumour suppressor.

scholarly journals The Antiapoptotic RBM5/LUCA-15/H37 Gene and Its Role in Apoptosis and Human Cancer: Research Update

2006 ◽  
Vol 6 ◽  
pp. 1705-1712 ◽  
Author(s):  
Mirna M Maarabouni ◽  
Gwyn T Williams
Keyword(s):  
Gene Locus ◽  
Human Cancer ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor ◽  
Suppressor Activity ◽  
Major Significance ◽  
Tumour Suppressor Activity ◽  
Alternatively Spliced ◽  
Candidate Tumour Suppressor

The candidate tumour-suppressor gene, LUCA-15/RBM5/H37, maps to the lung cancer tumour-suppressor locus 3p21.3. The LUCA-15 gene locus encodes at least four alternatively spliced transcripts that have been shown to function as regulators of apoptosis, a fact which may have major significance in tumour regulation. This review highlights recent evidence that further implicates the LUCA-15 locus in the control of apoptosis and cell proliferation, and focuses on the observations that confirm the tumour-suppressor activity of this gene.

Up-regulated miR-17 promotes cell proliferation, tumour growth and cell cycle progression by targeting the RND3 tumour suppressor gene in colorectal carcinoma

2012 ◽  
Vol 442 (2) ◽  
pp. 311-321 ◽  
Author(s):  
Hesan Luo ◽  
Jinjin Zou ◽  
Zhongyi Dong ◽  
Qin Zeng ◽  
Dehua Wu ◽  
...  
Keyword(s):  
Colorectal Carcinoma ◽  
Tumour Growth ◽  
Human Cancer ◽  
Xenograft Model ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor ◽  
G1 Arrest ◽  
Normal Tissues ◽  
Mouse Xenograft Model

Emerging evidence indicates that the miR-17 family may have a causal role in human cancer tumorigenesis, but their specific effects on the occurrence of CRC (colorectal carcinoma) are still poorly understood. In the present study, we profiled CRC tissue samples by miRNA (microRNA) microarray and found that four members of the miR-17 family had higher expression in CRC tissues than in normal tissues. This finding was further validated by qRT-PCR (quantitative reverse transcription PCR). Transfecting CRC cells with an inhibitor of miR-17 lowered their ability to proliferate and induced G0/G1 arrest. We also confirmed that miR-17 exerted this function by directly targeting RND3 in vitro, and that the expression of miR-17 was negatively correlated with that of RND3 in CRC tissues and CRC cells. Moreover, miR-17 inhibition led to tumour growth suppression and up-regulation of RND3 expression in a nude mouse xenograft model. RND3 expression was found to be significantly lower in CRC tissues than in normal tissues and adenomas, indicating that RND3 may act as a tumour suppressor gene in CRC. In conclusion, the present study suggests that miR-17 plays an important role in CRC carcinogenesis by targeting RND3 and may be a therapeutic agent for CRC.

tumour suppressor gene and the tobacco industry

The Lancet ◽  
2005 ◽  
Vol 365 (9464) ◽  
pp. 1026-1027
Author(s):  
A BITTON ◽  
M NEUMAN ◽  
J BARNOYA ◽  
S GLANTZ
Keyword(s):  
Tobacco Industry ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor

FOXL2 in adult‐type granulosa cell tumour of the ovary: oncogene or tumour suppressor gene?

2021 ◽  
Author(s):  
Jessica A. Pilsworth ◽  
Anne‐Laure Todeschini ◽  
Samantha J. Neilson ◽  
Dawn R. Cochrane ◽  
Daniel Lai ◽  
...  
Keyword(s):  
Granulosa Cell ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor ◽  
Cell Tumour ◽  
Granulosa Cell Tumour ◽  
Adult Type
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