scholarly journals p16INK4Aand p14ARFGene Promoter Hypermethylation as Prognostic Biomarker in Oral and Oropharyngeal Squamous Cell Carcinoma: A Review

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
A. Al-Kaabi ◽  
L. W. van Bockel ◽  
A. J. Pothen ◽  
S. M. Willems

Head and neck squamous cell carcinoma is a heterogeneous group of tumors with each subtype having a distinct histopathological and molecular profile. Most tumors share, to some extent, the same multistep carcinogenic pathways, which include a wide variety of genetic and epigenetic changes. Epigenetic alterations represent all changes in gene expression patterns that do not alter the actual DNA sequence. Recently, it has become clear that silencing of cancer related genes is not exclusively a result of genetic changes such as mutations or deletions, but it can also be regulated on epigenetic level, mostly by means of gene promoter hypermethylation. Results from recent studies have demonstrated that DNA methylation patterns contain tumor-type-specific signatures, which could serve as biomarkers for clinical outcome in the near future. The topic of this review discusses gene promoter hypermethylation in oral and oropharyngeal squamous cell carcinoma (OSCC). The main objective is to analyse the available data on gene promoter hypermethylation of the cell cycle regulatory proteinsp16INK4Aandp14ARFand to investigate their clinical significance as novel biomarkers in OSCC. Hypermethylation of both genes seems to possess predictive properties for several clinicopathological outcomes. We conclude that the methylation status ofp16INK4Ais definitely a promising candidate biomarker for predicting clinical outcome of OSCC, especially for recurrence-free survival.

Author(s):  
Aida Mirza Aghasi ◽  
Saied Ghorbian

Introduction: The changes in the level of SEPT9 gene promoter methylation can contribute to the formation of esophageal squamous cell carcinoma. The aim of this study was to evaluate the level of changes in the level of SEPT9 gene promoter methylation in the esophageal squamous cell carcinoma. Methods: In the present case-control study, we collected 75 paraffin blocks of esophageal cancer tissues and 75 paraffin blocks healthy tissues, which were referred to the Noor-E-Nejat and Tabriz International Hospitals during 2013-2017. After DNA extraction and treatment with sodium metabisulfite, the changes of SEPT9 gene promoter methylation assessed using high resolution melting (HRM) technique. The data were analyzed by SPSS 22 and Chi-square test. Results: Our findings did not show a statistically significant difference between the changes of SEPT9 gene promoter methylation in cancer tissues compared to the healthy tissues (P=0.106). Conclusion: This study shows that SEPT9 gene promoter methylation cannot contribute to the esophageal squamous cell carcinoma cancerogenesis.  


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Ana Carolina de Carvalho ◽  
Sandra Perdomo ◽  
Wellington dos Santos ◽  
Gabriela Carvalho Fernandes ◽  
Lais Machado de Jesus ◽  
...  

Toukeibu Gan ◽  
2011 ◽  
Vol 37 (3) ◽  
pp. 405-410
Author(s):  
Koji Ebisumoto ◽  
Kenji Okami ◽  
Akihiro Sakai ◽  
Taku Atsumi ◽  
Daisuke Maki ◽  
...  

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e77025 ◽  
Author(s):  
Anders Näsman ◽  
Emilia Andersson ◽  
Linda Marklund ◽  
Nikolaos Tertipis ◽  
Lalle Hammarstedt-Nordenvall ◽  
...  

2001 ◽  
Vol 27 (1) ◽  
pp. 85-90 ◽  
Author(s):  
Yasukazu MIKAMI ◽  
Mamoru TSUKUDA ◽  
Izumi MOCHIMATSU ◽  
Yasuhiro ARAI ◽  
Satoshi KAWAI ◽  
...  

2014 ◽  
Vol 3 (5) ◽  
pp. 1185-1196 ◽  
Author(s):  
Pauline M. W. Kempen ◽  
Liselotte Bockel ◽  
Weibel W. Braunius ◽  
Cathy B. Moelans ◽  
Marina Olst ◽  
...  

Cancers ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 584 ◽  
Author(s):  
Chao Rong ◽  
Marie Muller ◽  
Christa Flechtenmacher ◽  
Dana Holzinger ◽  
Gerhard Dyckhoff ◽  
...  

Human papillomavirus (HPV)-related oropharyngeal squamous cell carcinoma (OPSCC) forms a distinct tumor entity with better survival clinical outcome. Numerous underlying molecular mechanisms have been postulated for differences in treatment response, but the impact of MEK/ERK signaling, a main driver of carcinogenesis in various cancers including OPSCC and key player mediating therapy resistance remains elusive. In a retrospective experimental cohort study, primary tumor samples from OPSCC patients (n = 124) were available on tissue microarrays (TMAs) and expression levels of phosphorylated ERK1/2 (pERK1/2) were detected by immunohistochemical staining. Correlations of pERK1/2 expression patterns with clinicopathological features and clinical outcome were evaluated by statistical analysis. A low pERK1/2 expression was strongly associated with HPV-related OPSCC, while primary tumors with high pERK1/2 staining showed a distinctly worse survival outcome and were associated with higher cellular differentiation. Co-activation of both ERK1/2 and AKT was a common event and was associated with unfavorable prognosis in our cohort. However, the combinatorial analysis of pAKT (Ser473) and pERK1/2 did not strengthen the predictive power of pERK1/2, suggesting that pERK1/2 plays a more significant function in OPSCC. In summary, our data provide a compelling experimental and statistical evidence that low levels of tumor cell intrinsic ERK1/2 activation contribute at least in part to the favorable outcome of HPV-related OPSCC. On the other hand, presented findings indicate that non-HPV-related OPSCC with elevated ERK phosphorylation are at high risk for treatment failure and might benefit from targeted therapy of MEK/ERK signaling.


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