scholarly journals Copy number gain of 11q13.3 genes associates with pathological stage in hypopharyngeal squamous cell carcinoma

2016 ◽  
Vol 56 (3) ◽  
pp. 185-198 ◽  
Author(s):  
Samuel B. Pattle ◽  
Natasa Utjesanovic ◽  
Athena Togo ◽  
Lucy Wells ◽  
Brendan Conn ◽  
...  
2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Endi Xia ◽  
Sotaro Kanematsu ◽  
Yusuke Suenaga ◽  
Asmaa Elzawahry ◽  
Hitomi Kondo ◽  
...  

2010 ◽  
Vol 49 (1) ◽  
pp. 9-16 ◽  
Author(s):  
Kolja Freier ◽  
Karl Knoepfle ◽  
Christa Flechtenmacher ◽  
Susanne Pungs ◽  
Frauke Devens ◽  
...  

2016 ◽  
Vol 468 (5) ◽  
pp. 579-587 ◽  
Author(s):  
Diána Brauswetter ◽  
Kornél Dános ◽  
Bianka Gurbi ◽  
Éva Fruzsina Félegyházi ◽  
Ede Birtalan ◽  
...  

2009 ◽  
Vol 125 (3) ◽  
pp. 603-611 ◽  
Author(s):  
Mauting Lin ◽  
Carl D. Morrison ◽  
Susie Jones ◽  
Nehad Mohamed ◽  
Jason Bacher ◽  
...  

Oncotarget ◽  
2017 ◽  
Vol 8 (50) ◽  
pp. 87699-87709 ◽  
Author(s):  
Chen Xu ◽  
Yalan Liu ◽  
Jie Huang ◽  
Hao Wang ◽  
Lijie Tan ◽  
...  

2021 ◽  
Vol 22 (6) ◽  
pp. 2831
Author(s):  
Ryan Bensen ◽  
John Brognard

Squamous cell carcinomas of the lung, head and neck, esophagus, and cervix account for more than two million cases of cancer per year worldwide with very few targetable therapies available and minimal clinical improvement in the past three decades. Although these carcinomas are differentiated anatomically, their genetic landscape shares numerous common genetic alterations. Amplification of the third chromosome’s distal portion (3q) is a distinguishing genetic alteration in most of these carcinomas and leads to copy-number gain and amplification of numerous oncogenic proteins. This area of the chromosome harbors known oncogenes involved in squamous cell fate decisions and differentiation, including TP63, SOX2, ECT2, and PIK3CA. Furthermore, novel targetable oncogenic kinases within this amplicon include PRKCI, PAK2, MAP3K13, and TNIK. TCGA analysis of these genes identified amplification in more than 20% of clinical squamous cell carcinoma samples, correlating with a significant decrease in overall patient survival. Alteration of these genes frequently co-occurs and is dependent on 3q-chromosome amplification. The dependency of cancer cells on these amplified kinases provides a route toward personalized medicine in squamous cell carcinoma patients through development of small-molecules targeting these kinases.


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