scholarly journals Aberrant methylation of multiple tumor suppressor genes in aging liver, chronic hepatitis, and hepatocellular carcinoma

Hepatology ◽  
2007 ◽  
Vol 47 (3) ◽  
pp. 908-918 ◽  
Author(s):  
Naoshi Nishida ◽  
Takeshi Nagasaka ◽  
Takafumi Nishimura ◽  
Iwao Ikai ◽  
C. Richard Boland ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Chronic Hepatitis ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Aberrant Methylation ◽  
Suppressor Genes ◽  
Multiple Tumor

scholarly journals Aberrant methylation of multiple tumor suppressor genes in acute myeloid leukemia

2004 ◽  
Vol 77 (3) ◽  
pp. 233-240 ◽  
Author(s):  
Cumhur G. Ekmekci ◽  
Marina I. Gutiérrez ◽  
Abdul K. Siraj ◽  
Ugur Ozbek ◽  
Kishor Bhatia
Keyword(s):  
Acute Myeloid Leukemia ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Myeloid Leukemia ◽  
Aberrant Methylation ◽  
Suppressor Genes ◽  
Multiple Tumor ◽  
Acute Myeloid

scholarly journals Consistent DNA Hypermethylation Patterns in Laryngeal Papillomas

2010 ◽  
Vol 1 (2) ◽  
pp. 69-77 ◽  
Author(s):  
Josena K Stephen ◽  
Kang Mei Chen ◽  
Veena Shah ◽  
Vanessa G Schweitzer ◽  
Glendon Gardner ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Methylation Status ◽  
Promoter Hypermethylation ◽  
Aberrant Methylation ◽  
Dna Hypermethylation ◽  
Suppressor Genes ◽  
Multiple Tumor ◽  
Specific Pcr

Abstract Introduction This study examined the contribution of promoter hypermethylation to the pathogenesis of respiratory papillomatosis (RP), including recurrences (RRP) and progression to squamous cell carcinoma (SSC). Materials and methods A retrospective cohort of 25 laryngeal papilloma cases included 21 RRP, two of which progressed to SCC. Aberrant methylation status was determined using the multigene (22 tumor suppressor genes) methylation-specific multiplex ligationdependent probe amplification assay and confirmed using methylation specific PCR. Results Twenty genes had altered DNA methylation in 22 of 25 cases. Aberrant methylation of CDKN2B and TIMP3 was most frequent. Promoter hypermethylation of BRCA2, APC, CDKN2A and CDKN2B was detected in 2 RRP cases with subsequent progression to SCC. Of the 25 cases, 22 were positive for HPV-6, 2 for HPV-11 and 1 for HPV-16 and 33. Conclusion Consistent aberrant methylation of multiple tumor suppressor genes contributes to the pathogenesis of laryngeal papillomas. Persistent aberrant DNA methylation events in 2 RRP cases that progressed to cancer indicate an epigenetic monoclonal progression continuum to SCC.

Loss of heterozygosity and methylation of multiple tumor suppressor genes on chromosome 3 in hepatocellular carcinoma

2012 ◽  
Vol 48 (1) ◽  
pp. 132-143 ◽  
Author(s):  
Xiaoying Zhang ◽  
Hiu Ming Li ◽  
Zhiyan Liu ◽  
Gengyin Zhou ◽  
Qinghui Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Suppressor ◽  
Loss Of Heterozygosity ◽  
Tumor Suppressor Genes ◽  
Chromosome 3 ◽  
Suppressor Genes ◽  
Multiple Tumor

Aberrant STAT1 methylation as a non-invasive biomarker in blood of HCV induced hepatocellular carcinoma

2021 ◽  
pp. 1-9
Author(s):  
Umaira Zakir ◽  
Nadir Naveed Siddiqui ◽  
Faizan-ul-Hassan Naqvi ◽  
Rizma Khan
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Methylation Status ◽  
Tumor Formation ◽  
Aberrant Methylation ◽  
Suppressor Genes ◽  
Non Invasive ◽  
Specific Pcr

BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common types of cancer in the world and a reason behind different oncogenes activation and tumor suppressor genes inactivation. Hyper-methylation of tumor suppressor genes including RASSF1a, GSTP1, p16, and APC cause gene silencing as well as tumor cell invasion. STAT 1 gene is a part of signaling cascade of JAK/STAT and any dysregulation in signaling has been implicated in tumor formation. OBJECTIVE: The current investigation focus on the methylation role of STAT1 gene as a non-invasive biomarker in the progression and diagnosis of hepatocellular carcinoma. METHODS: STAT1 gene methylation status in 46 HCV induced hepatocellular carcinoma patients and 40 non-HCC controls were examined by methylation specific PCR. STAT1 gene expression was examined by real time PCR and further validated by various bioinformatics tools. RESULTS: STAT1 methylation in HCV-induced HCC (67.4%) was significantly higher compared to the non-HCC controls (p< 0.01). However, mRNA expression of STAT1 gene in methylated groups was significantly lower compared to unmethylated groups (p< 0.05). Furthermore, insilco analysis of STAT1 validated our results and shown expression of STAT1 mRNA was lower in liver cancer with the median 24.3 (p= 0.085). CONCLUSION: After using peripheral blood samples we observed that STAT1 silencing caused by aberrant methylation could be used as potential non-invasive biomarker for the diagnosis of HCV induced hepatocellular carcinoma. We conclude that blood as a sample source could be used instead of biopsy for early detection of HCC.

HELLS Regulates Chromatin Remodeling and Epigenetic Silencing of Multiple Tumor Suppressor Genes in Human Hepatocellular Carcinoma

Hepatology ◽  
2019 ◽  
Vol 69 (5) ◽  
pp. 2013-2030 ◽  
Author(s):  
Cheuk‐Ting Law ◽  
Lai Wei ◽  
Felice Ho‐Ching Tsang ◽  
Cerise Yuen‐Ki Chan ◽  
Iris Ming‐Jing Xu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Suppressor ◽  
Chromatin Remodeling ◽  
Tumor Suppressor Genes ◽  
Human Hepatocellular Carcinoma ◽  
Epigenetic Silencing ◽  
Suppressor Genes ◽  
Multiple Tumor

scholarly journals Modification of Epigenetic Histone Acetylation in Hepatocellular Carcinoma

Cancers ◽  
2018 ◽  
Vol 10 (1) ◽  
pp. 8 ◽  
Author(s):  
Kwei-Yan Liu ◽  
Li-Ting Wang ◽  
Shih-Hsien Hsu
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Chemical Sensor ◽  
Enzyme Level ◽  
Tumor Therapy ◽  
Tumor Formation ◽  
Current Evidence ◽  
Epigenetic Changes ◽  
Suppressor Genes

Cells respond to various environmental factors such as nutrients, food intake, and drugs or toxins by undergoing dynamic epigenetic changes. An imbalance in dynamic epigenetic changes is one of the major causes of disease, oncogenic activities, and immunosuppressive effects. The aryl hydrocarbon receptor (AHR) is a unique cellular chemical sensor present in most organs, and its dysregulation has been demonstrated in multiple stages of tumor progression in humans and experimental models; however, the effects of the pathogenic mechanisms of AHR on epigenetic regulation remain unclear. Apart from proto-oncogene activation, epigenetic repressions of tumor suppressor genes are involved in tumor initiation, procession, and metastasis. Reverse epigenetic repression of the tumor suppressor genes by epigenetic enzyme activity inhibition and epigenetic enzyme level manipulation is a potential path for tumor therapy. Current evidence and our recent work on deacetylation of histones on tumor-suppressive genes suggest that histone deacetylase (HDAC) is involved in tumor formation and progression, and treating hepatocellular carcinoma with HDAC inhibitors can, at least partially, repress tumor proliferation and transformation by recusing the expression of tumor-suppressive genes such as TP53 and RB1.

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