scholarly journals High-risk Human Papillomavirus E7 Oncoprotein Detection in Cervical Squamous Cell Carcinoma

2007 ◽  
Vol 13 (23) ◽  
pp. 7067-7072 ◽  
Author(s):  
Sigrun Ressler ◽  
René Scheiden ◽  
Kerstin Dreier ◽  
Andreas Laich ◽  
Elisabeth Müller-Holzner ◽  
...  
2011 ◽  
Vol 64 (5) ◽  
pp. 981-985 ◽  
Author(s):  
Rachel H. Gormley ◽  
Caroline M. Groft ◽  
Christopher J. Miller ◽  
Carrie L. Kovarik

2009 ◽  
Vol 133 (11) ◽  
pp. 1798-1803
Author(s):  
Jonathan B. McHugh

Abstract Human papillomavirus is an established cause of oropharyngeal squamous cell carcinoma. Similar to cervical cancer, these cancers are usually caused by high-risk human papillomavirus types 16 and 18 and are associated with high-risk sexual behaviors. Human papillomavirus–associated oropharyngeal squamous cell carcinoma typically affects the palatine and lingual tonsils and frequently results in cystic neck metastases. The histopathology of this subset of head and neck squamous cell carcinoma is unique and typically characterized by poorly differentiated, nonkeratinizing morphology with a basaloid appearance. These tumors occur in younger patients and are more often seen in nonsmokers compared with conventional oral cavity and oropharyngeal squamous cell carcinomas. The incidence of human papillomavirus–associated squamous cell carcinoma is increasing. Recognition of this unique clinicopathologic subset of head and neck carcinoma is important because these patients typically respond more favorably to organ-sparing treatment modalities and have an improved prognosis.


2019 ◽  
Vol 39 (8) ◽  
Author(s):  
Yunyong Liu ◽  
Mengdan Li ◽  
Huihui Yu ◽  
Haozhe Piao

Abstract LncRNA SRA1 plays important roles in several types of human diseases. The present study aimed to explore the role of SRA1 in cervical squamous cell carcinoma (CSCC). In the present study, we showed that plasma SRA1 was down-regulated in human papillomavirus (HPV)-negative CSCC patients but not in HPV-positive CSCC patients compared with healthy females. Down-regulated SRA1 distinguished HPV-negative CSCC patients from HPV-positive CSCC patients and healthy females. In HPV-negative CSCC patients, miR-9 was up-regulated and inversely correlated with SRA1. In HPV-negative CSCC cells, SRA1 overexpression caused the down-regulated miR-9, while miR-9 overexpression failed to affect SRA1. Moreover, SRA1 overexpression caused decreased, while miR-9 overexpression caused increased proliferation, migration and invasion rates of cancer cells. In addition, miR-9 overexpression attenuated the effects of SRA1 overexpression. Therefore, SRA1 is down-regulated in HPV-negative CSCC and regulates cancer cell behaviors possibly by down-regulating miR-9.


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