Adverse pathologic features in early oral squamous cell carcinoma and the role of postoperative radiotherapy—a review

2017 ◽  
Vol 124 (1) ◽  
pp. 24-31 ◽  
Author(s):  
Narayana Subramaniam ◽  
Deepak Balasubramanian ◽  
Samskruthi Murthy ◽  
Shashikant Limbachiya ◽  
Krishnakumar Thankappan ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Postoperative Radiotherapy ◽  
Pathologic Features

Rediscussing the Role of Traditional Risk Factors in Young Adults With Oral Squamous Cell Carcinoma

2020 ◽  
Vol 40 (12) ◽  
pp. 6987-6995
Author(s):  
NORBERT NECKEL ◽  
MARCO MICHAEL ◽  
DANIEL TROELTZSCH ◽  
JONAS WÜSTER ◽  
STEFFEN KOERDT ◽  
...  
Keyword(s):  
Risk Factors ◽  
Squamous Cell Carcinoma ◽  
Young Adults ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Traditional Risk Factors

scholarly journals Role of viruses in oral squamous cell carcinoma

2012 ◽  
Vol 6 (2) ◽  
pp. 21 ◽  
Author(s):  
Rashmi Metgud ◽  
Madhusudan Astekar ◽  
Meenal Verma ◽  
Ashish Sharma
Keyword(s):  
Risk Factors ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Genetic Susceptibility ◽  
Squamous Cell ◽  
Oncogenic Viruses ◽  
Exact Role ◽  
Carcinogenic Effects

The etiology of oral squamous cell carcinoma (OSCC) is complex and involves many factors. The most clearly defined risk factors are smoking and alcohol, which substantially increase the risk of oral SCC. However, despite this clear association, a substantial proportion of patients develop OSCC without exposure to them, emphasizing the role of other risk factors such as genetic susceptibility and oncogenic viruses. Some viruses are strongly associated with OSCC while the association of others is less frequent and may depend on co-factors for their carcinogenic effects. Therefore, the exact role of viruses must be evaluated with care in order to improve the diagnosis and treatment of OSCC.

Role of theMIR146Apolymorphism in the origin and progression of oral squamous cell carcinoma

2014 ◽  
Vol 122 (3) ◽  
pp. 198-201 ◽  
Author(s):  
Annalisa Palmieri ◽  
Francesco Carinci ◽  
Marcella Martinelli ◽  
Furio Pezzetti ◽  
Ambra Girardi ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell

scholarly journals METTL3 Intensifies the Progress of Oral Squamous Cell Carcinoma via Modulating the m6A Amount of PRMT5 and PD-L1

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Yilong Ai ◽  
Shiwei Liu ◽  
Hailing Luo ◽  
Siyuan Wu ◽  
Haigang Wei ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Mrna Translation ◽  
Qrt Pcr ◽  
Methylation Assay ◽  
Eukaryotic Mrnas ◽  
M6a Rna Methylation

N6-Methyladenosine (m6A) modification is one of the commonest chemical modifications in eukaryotic mRNAs, which has essential effects on mRNA translation, splicing, and stability. Currently, there is a rising concern on the regulatory role of m6A in tumorigenesis. As a known component in the m6A methyltransferase complex, METTL3 (methyltransferase-like 3) plays an essential role in m6A methylation. Till now, the functions of METTL3 in oral squamous cell carcinoma (OSCC) and its relative mechanism remain to be explored. In this research, through the GEPIA database, we found that high METTL3 expression has a correlation with poor prognosis of squamous cell carcinoma of head and neck. qRT-PCR displayed that METTL3 was highly expressed in OSCC cells. Functionally, METTL3 knockdown reduced the invasion, migration, and proliferation competence of OSCC cells and attenuated the activation of CD8+ T cells. In contrast, METTL3 overexpression resulted in opposite results. GEPIA, UALCAN, and SRAMP databases, PCR, western blot, and m6A RNA methylation assay confirmed the m6A modification of PRMT5 and PD-L1 mediated by METTL3. In conclusion, our results displayed that METTL3 intensified the metastasis and proliferation of OSCC by modulating the m6A amounts of PRMT5 and PD-L1, suggesting that METTL3 may be a therapeutic target for OSCC patients.

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