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Original Articles
- The Overexpression of Histone Deacetylase 1 and Its Relationship with p16INK4a Gene Hypermethylation in Pulmonary Squamous Cell Carcinoma and Adenocarcinoma.
- Jong Hyeok Park, Young Seoub Hong, Phil Jo Choi, Na Young Kim, Kyung Eun Lee, Mee Sook Roh
- Korean J Pathol. 2009;43(2):107-112.
- DOI: https://doi.org/10.4132/KoreanJPathol.2009.43.2.107
- 3,493 View
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- 4 Crossref
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Abstract
PDF - BACKGROUND
DNA methylation and histone modification are dynamically linked in the epigenetic control of gene silencing and they play an important role in tumorigenesis.
METHODS
To evaluate the role of histone deacetylase 1 (HDAC1) in the development of lung cancer and the relationship between a HDAC1 overexpression and p16INK4a hypermethylation, we performed immunohistochemical staining for HDAC1 in 76 lung cancer specimens (39 squamous cell carcinomas and 37 adenocarcinomas) that had been previously evaluated for their p16INK4a methylation status by real-time quantitative polymerase chain reaction.
RESULTS
A HDAC1 overexpression (>50% of HDAC1 immunoreactive cells) was detected in 65 (85.5%) out of the 76 cases and it was more frequently seen in the squamous cell carcinomas (97.4%) than in the adenocarcinomas (73.0%) (p=0.002). The incidence of HDAC1 overexpression tended to be higher in the heavy smokers with more than 20 pack-years (p=0.067). Although there was no statistical significance, the frequency of p16INK4a hypermethylation in the cases with a HDAC1 overexpression (27.7%) tended to be higher than that in the cases without a HDAC1 overexpression (9.0%) (p=0.175).
CONCLUSIONS
A HDAC1 overexpression might be involved in lung carcinogenesis, and especially in a subgroup of smoking and squamous cell carcinoma patients, and a HDAC1 overexpression may be associated with p16INK4a hypermethylation. -
Citations
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- Deciphering the Mysterious Relationship between the Cross-Pathogenetic Mechanisms of Neurodegenerative and Oncological Diseases
Yulia Aleksandrova, Margarita Neganova
International Journal of Molecular Sciences.2023; 24(19): 14766. CrossRef - Microbiome dysbiosis and epigenetic modulations in lung cancer: From pathogenesis to therapy
Faizan Haider Khan, Basharat Ahmad Bhat, Bashir Ahmad Sheikh, Lubna Tariq, Roshan Padmanabhan, Jay Prakash Verma, Amritesh Chandra Shukla, Afshin Dowlati, Ata Abbas
Seminars in Cancer Biology.2022; 86: 732. CrossRef - Histone deacetylase HDAC1 expression correlates with the progression and prognosis of lung cancer
Lin-Lin Cao, Xiaoxu Song, Lin Pei, Lianhua Liu, Hui Wang, Mei Jia
Medicine.2017; 96(31): e7663. CrossRef - The synthesis and evaluation of N1-(4-(2-[18F]-fluoroethyl)phenyl)-N8-hydroxyoctanediamide ([18F]-FESAHA), A PET radiotracer designed for the delineation of histone deacetylase expression in cancer
Brian M. Zeglis, NagaVaraKishore Pillarsetty, Vadim Divilov, Ronald A. Blasberg, Jason S. Lewis
Nuclear Medicine and Biology.2011; 38(5): 683. CrossRef
- Deciphering the Mysterious Relationship between the Cross-Pathogenetic Mechanisms of Neurodegenerative and Oncological Diseases
- Inactivation of TPEF Gene by Aberrant Methylation in Hepatocellular Carcinoma.
- Woon Bok Chung, Soon Young Kim, So Young Chun, Ku Seong Kang, Hae Ahm Lee, Joung Ok Kim, Ji Young Park, Yoon Kyung Sohn, Jung Wan Kim
- Korean J Pathol. 2008;42(1):9-15.
- 1,757 View
- 19 Download
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Abstract
PDF
- BACKGROUND
Abnormalities of genomic methylation patterns have been shown to play a role in the development of carcinoma, and the silencing of tumor suppressor genes is related to local de novo methylation.
METHODS
Using methylation specific arbitrarily primed-Polymerase Chain Reaction (Ms AP-PCR), we identified a 322 bp sequence that contained a 5' un-translated and exon1 regions of the TPEF gene. To evaluate the inactivation of the TPEF gene through hypermethylation in hepatocellular carcinoma (HCC), we investigated the correlation between methylation patterns and TPEF expression in tumor tissues of human HCC and cell lines via a Combined Bisulfite Restriction Assay (CoBRA) and RT-PCR.
RESULTS
A dense methylation pattern of the TPEF was detected in most cell lines, as well as in 10 of the 14 (71.4%) HCC tissues. In addition, loss of heterozygosity (LOH) from the TPEF gene was observed in 5 of the 14 (36%) HCC tissues. Furthermore, RT-PCR analysis revealed TPEF expression in 5 of 8 (62.5%) cell lines. Finally, treatment with a demethylating agent, 5-Aza- 2'-deoxycitidine (5-AzaC), increased the expression of TPEF mRNA.
CONCLUSION
These results indicate that inactivation of the TPEF gene through hypermethylation may be a mechanism by which tumorigenesis occurs in HCC.
- Loss of PTEN Expression in Breast Cancers.
- Sun Hee Chang, Shi Nae Lee, Min Sun Cho, Heasoo Koo, Woon Sup Han, Seock Ah Im, Byung In Moon, Hyun Suk Suh, Hye Young Choi, Sun Hee Sung
- Korean J Pathol. 2005;39(4):236-241.
- 2,008 View
- 27 Download
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Abstract
PDF
- Background
: PTEN, located on chromosome 10q23.31, is a novel tumor suppressor gene. In the sporadic breast cancers, the incidence of the loss of heterozygosity of PTEN is approximately 10% to 40%, but the incidence of intragenic mutation of PTEN is less than 1%. To as- sess the role of the PTEN in the invasive ductal breast cancer, we studied the frequency of the loss of PTEN expression, its correlation with the commonly used prognostic factors of the breast cancer and with PTEN promoter hypermethylation status. Methods : Immunohistochemical staining with an anti-PTEN protein antibody was performed on the paraffin-embedded breast tissues from 129 women with a diagnosis of invasive ductal carcinoma. Methylation specific PCR was performed to detect hypermethylation in the PTEN gene on the 28 cases with the loss of PTEN expression.
Results
: Sixty-two (48%) of 129 breast tumors had the loss of PTEN expression. The loss of PTEN expression was correlated with lymph node metastasis and stage, and there was a near-significant correlation with the tumor size. PTEN promoter hypermethylation was found in five (18%) out of 28 patients. Conclusion : These results suggest that the loss of PTEN expression might play a role in the progression of the breast cancer and that the aberrant promoter methylation is one of the silencing mechanisms of PTEN.
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