705 Genetic alterations of the LKB1 gene in head and neck cancer

2010 ◽  
Vol 8 (5) ◽  
pp. 178
Author(s):  
S. Ekizoglu ◽  
E. Kenanli ◽  
E. Karaman ◽  
O. Enver ◽  
T. Ulutin ◽  
...  
1999 ◽  
Vol 26 (4) ◽  
pp. 254-260 ◽  
Author(s):  
H�l�ne Blons ◽  
J. Pablo Radicella ◽  
Ollivier Laccourreye ◽  
Daniel Brasnu ◽  
Philippe Beaune ◽  
...  

1992 ◽  
Vol 25 (5) ◽  
pp. 1065-1071
Author(s):  
Kenneth D. Somers ◽  
Gary L. Schechter

Oncogene ◽  
1997 ◽  
Vol 15 (14) ◽  
pp. 1699-1704 ◽  
Author(s):  
Pamela Waber ◽  
Sandra Dlugosz ◽  
Qin-Chang Cheng ◽  
John Truelson ◽  
Perry D Nisen

2002 ◽  
Vol 9 (5) ◽  
pp. 369-378 ◽  
Author(s):  
Lyon L. Gleich ◽  
Frank N. Salamone

Background Head and neck cancers have multiple genetic abnormalities that influence tumor behavior and may be useful in developing new treatments. Methods Genetic alterations implicated in head and neck cancer oncogenesis and behavior are reviewed, and molecular techniques for detection and treatment are evaluated. Results The large number of genetic changes present in head and neck cancer cells precludes meaningful use of simple molecular tests and treatments. Detection of abnormalities in multiple genes provides better prognostic information than the detection and assessment of single mutations. Screening tests that rely on amplification of genetic material present in bodily fluids are hindered by the genomic complexity of head and neck cancer. Introduction of genetic material into head and neck cancer cells for gene therapy has shown some efficacy. Conclusions Head and neck cancers comprise a complex genetic disease. Although much has been learned about the molecular genetics of head and neck cancers, continued study of multiple genes is critical for further progress. Gene therapy, although promising, must also overcome this complexity.


Oral Oncology ◽  
2009 ◽  
Vol 45 (4-5) ◽  
pp. 335-339 ◽  
Author(s):  
Patrick K. Ha ◽  
Steven S. Chang ◽  
Chad A. Glazer ◽  
Joseph A. Califano ◽  
David Sidransky

Cells ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 333 ◽  
Author(s):  
Tan ◽  
Bai ◽  
Saintigny ◽  
Darido

The mammalian target of rapamycin (mTOR) signalling pathway is a central regulator of metabolism in all cells. It senses intracellular and extracellular signals and nutrient levels, and coordinates the metabolic requirements for cell growth, survival, and proliferation. Genetic alterations that deregulate mTOR signalling lead to metabolic reprogramming, resulting in the development of several cancers including those of the head and neck. Gain-of-function mutations in EGFR, PIK3CA, and HRAS, or loss-of-function in p53 and PTEN are often associated with mTOR hyperactivation, whereas mutations identified from The Cancer Genome Atlas (TCGA) dataset that potentially lead to aberrant mTOR signalling are found in the EIF4G1, PLD1, RAC1, and SZT2 genes. In this review, we discuss how these mutant genes could affect mTOR signalling and highlight their impact on metabolic processes, as well as suggest potential targets for therapeutic intervention, primarily in head and neck cancer.


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