Over-expression of tumour suppressor gene p53 in laryngeal squamous cell carcinomas and its prognostic significance

1995 ◽  
Vol 20 (1) ◽  
pp. 49-52 ◽  
Author(s):  
M. A. SALAM ◽  
J. CROCKER ◽  
A. MORRIS
Keyword(s):  
Squamous Cell ◽  
Prognostic Significance ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Squamous Cell Carcinomas ◽  
Tumour Suppressor ◽  
Over Expression

scholarly journals Prognostic significance of downregulated expression of the candidate tumour suppressor gene SASH1 in colon cancer

2006 ◽  
Vol 95 (10) ◽  
pp. 1419-1423 ◽  
Author(s):  
C Rimkus ◽  
M Martini ◽  
J Friederichs ◽  
R Rosenberg ◽  
D Doll ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Prognostic Significance ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor ◽  
Candidate Tumour Suppressor

SGK1 mutations in DLBCL generate hyperstable protein neoisoforms that promote AKT independence.

Blood ◽  
2021 ◽  
Author(s):  
Jie Gao ◽  
Eirini Sidiropoulou ◽  
Ieuan Walker ◽  
Joanna Alicja Krupka ◽  
Karol Mizielinski ◽  
...  
Keyword(s):  
Therapeutic Strategy ◽  
B Cell Lymphoma ◽  
Suppressor Gene ◽  
Kinase Domain ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor ◽  
Protein Isoforms ◽  
Loss Of Function ◽  
Over Expression ◽  
Frequent Finding

Serum and Glucocorticoid-regulated Kinase-1 (SGK1) is one of the most frequently mutated genes in Diffuse Large B Cell Lymphoma (DLBCL). However, little is known about its function or the consequence of its mutation. The frequent finding of truncating mutations has led to the widespread assumption that these represent loss-of-function variants and accordingly, that SGK1 must act as a tumour suppressor. Here we show that instead, the most common SGK1 mutations lead to production of aberrantly spliced mRNA neoisoforms in which translation is initiated from downstream methionines. The resulting N-terminal truncated protein isoforms show increased expression due to the exclusion of an N-terminal degradation domain. However, they retain a functional kinase domain, the over-expression of which renders cells resistant to AKT inhibition in part due to increased phosphorylation of GSK3B. These findings challenge the prevailing assumption that SGK1 is a tumour suppressor gene in DLBCL and provide the impetus to explore further the pharmacological inhibition of SGK1 as a therapeutic strategy for DLBCL.

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