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Promoter Methylation of CDKN2A, RARβ, and RASSF1A in Non-Small Cell Lung Carcinoma: Quantitative Evaluation Using Pyrosequencing.

Lee JU, Sul HJ, Son JW - Tuberc Respir Dis (Seoul) (2012)

Bottom Line: Hyperrmethylation of CDKN2A was significantly associated with p16(INK4A) immunoexpression loss (p=0.045).With regard to the clinicopathological characteristics of NSCLC, certain histopathological subtypes were found to be strongly associated with the loss of p16(INK4A) immunoexpression (p=0.016).We showed a significant correlation between CDKN2A hypermethylation and p16(INK4A) immunoexpression loss.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, St. Mary's Hospital, The Catholic University of Korea School of Medicine, Daejeon, Korea.

ABSTRACT

Background: While qualitative analysis of methylation has been reviewed, the quantitative analysis of methylation has rarely been studied. We evaluated the methylation status of CDKN2A, RARβ, and RASSF1A promoter regions in non-small cell lung carcinomas (NSCLCs) by using pyrosequencing. Then, we evaluated the association between methylation at the promoter regions of these tumor suppressor genes and the clinicopathological parameters of the NSCLCs.

Methods: We collected tumor tissues from a total of 53 patients with NSCLCs and analyzed the methylation level of the CDKN2A, RARβ, and RASSF1A promoter regions by using pyrosequencing. In addition, we investigated the correlation between the hypermethylation of CDKN2A and the loss of p16(INK4A) immunoexpression.

Results: Hypermethylation of CDKN2A, RARβ, and RASSF1A promoter regions were 16 (30.2%), 22 (41.5%), and 21 tumors (39.6%), respectively. The incidence of hypermethylation at the CDKN2A promoter in the tumors was higher in undifferentiated large cell carcinomas than in other subtypes (p=0.002). Hyperrmethylation of CDKN2A was significantly associated with p16(INK4A) immunoexpression loss (p=0.045). With regard to the clinicopathological characteristics of NSCLC, certain histopathological subtypes were found to be strongly associated with the loss of p16(INK4A) immunoexpression (p=0.016). Squamous cell carcinoma and undifferentiated large cell carcinoma showed p16(INK4A) immunoexpression loss more frequently. The Kaplan-Meier survival curves analysis showed that methylation level and patient survival were barely related to one another.

Conclusion: We quantitatively analyzed the promoter methylation status by using pyrosequencing. We showed a significant correlation between CDKN2A hypermethylation and p16(INK4A) immunoexpression loss.

No MeSH data available.


Related in: MedlinePlus

Survival analysis in CDKN2A (A), RARβ (B), RASSF1A (C) promoter with hypermethylation and unmethylation in non-small cell lung cancer.
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Figure 2: Survival analysis in CDKN2A (A), RARβ (B), RASSF1A (C) promoter with hypermethylation and unmethylation in non-small cell lung cancer.

Mentions: The incidence of hypermethylation at the CDKN2A promoter in the tumors was higher in the samples of undifferentiated LCC than in the samples of other subtypes (p=0.002) (Table 5). However, the number of LCC samples studied was too small to obtain meaningful results. The RARβ or RASSF1A gene promoters were not correlated with any clinicopathological parameters of NSCLC. We analyzed the effect of CDKN2A, RARβ or RASSF1A methylation on patient survival. Kaplan-Meier survival curves analysis showed that methylation level and patient survival were barely related (Figure 2).


Promoter Methylation of CDKN2A, RARβ, and RASSF1A in Non-Small Cell Lung Carcinoma: Quantitative Evaluation Using Pyrosequencing.

Lee JU, Sul HJ, Son JW - Tuberc Respir Dis (Seoul) (2012)

Survival analysis in CDKN2A (A), RARβ (B), RASSF1A (C) promoter with hypermethylation and unmethylation in non-small cell lung cancer.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC3475475&req=5

Figure 2: Survival analysis in CDKN2A (A), RARβ (B), RASSF1A (C) promoter with hypermethylation and unmethylation in non-small cell lung cancer.
Mentions: The incidence of hypermethylation at the CDKN2A promoter in the tumors was higher in the samples of undifferentiated LCC than in the samples of other subtypes (p=0.002) (Table 5). However, the number of LCC samples studied was too small to obtain meaningful results. The RARβ or RASSF1A gene promoters were not correlated with any clinicopathological parameters of NSCLC. We analyzed the effect of CDKN2A, RARβ or RASSF1A methylation on patient survival. Kaplan-Meier survival curves analysis showed that methylation level and patient survival were barely related (Figure 2).

Bottom Line: Hyperrmethylation of CDKN2A was significantly associated with p16(INK4A) immunoexpression loss (p=0.045).With regard to the clinicopathological characteristics of NSCLC, certain histopathological subtypes were found to be strongly associated with the loss of p16(INK4A) immunoexpression (p=0.016).We showed a significant correlation between CDKN2A hypermethylation and p16(INK4A) immunoexpression loss.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, St. Mary's Hospital, The Catholic University of Korea School of Medicine, Daejeon, Korea.

ABSTRACT

Background: While qualitative analysis of methylation has been reviewed, the quantitative analysis of methylation has rarely been studied. We evaluated the methylation status of CDKN2A, RARβ, and RASSF1A promoter regions in non-small cell lung carcinomas (NSCLCs) by using pyrosequencing. Then, we evaluated the association between methylation at the promoter regions of these tumor suppressor genes and the clinicopathological parameters of the NSCLCs.

Methods: We collected tumor tissues from a total of 53 patients with NSCLCs and analyzed the methylation level of the CDKN2A, RARβ, and RASSF1A promoter regions by using pyrosequencing. In addition, we investigated the correlation between the hypermethylation of CDKN2A and the loss of p16(INK4A) immunoexpression.

Results: Hypermethylation of CDKN2A, RARβ, and RASSF1A promoter regions were 16 (30.2%), 22 (41.5%), and 21 tumors (39.6%), respectively. The incidence of hypermethylation at the CDKN2A promoter in the tumors was higher in undifferentiated large cell carcinomas than in other subtypes (p=0.002). Hyperrmethylation of CDKN2A was significantly associated with p16(INK4A) immunoexpression loss (p=0.045). With regard to the clinicopathological characteristics of NSCLC, certain histopathological subtypes were found to be strongly associated with the loss of p16(INK4A) immunoexpression (p=0.016). Squamous cell carcinoma and undifferentiated large cell carcinoma showed p16(INK4A) immunoexpression loss more frequently. The Kaplan-Meier survival curves analysis showed that methylation level and patient survival were barely related to one another.

Conclusion: We quantitatively analyzed the promoter methylation status by using pyrosequencing. We showed a significant correlation between CDKN2A hypermethylation and p16(INK4A) immunoexpression loss.

No MeSH data available.


Related in: MedlinePlus