Detection of aberrant DNA methylation of tumor suppressor genes in circulating tumor cells from a pancreatic cancer patient

2017 ◽  
Vol 6 ◽  
pp. 31-33
Author(s):  
Hiroaki Kawasaki ◽  
Hiroyuki Abe
Keyword(s):  
Pancreatic Cancer ◽  
Dna Methylation ◽  
Tumor Suppressor ◽  
Cancer Patient ◽  
Tumor Cells ◽  
Circulating Tumor Cells ◽  
Tumor Suppressor Genes ◽  
Pancreatic Cancer Patient ◽  
Suppressor Genes ◽  
Aberrant Dna Methylation

Aberrant DNA methylation of some tumor suppressor genes in lung cancers from workers with chromate exposure

2010 ◽  
Vol 50 (2) ◽  
pp. 89-99 ◽  
Author(s):  
Abdellah H. K. Ali ◽  
Kazuya Kondo ◽  
Toshiaki Namura ◽  
Yoshitaka Senba ◽  
Hiromitsu Takizawa ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Suppressor Genes ◽  
Lung Cancers ◽  
Aberrant Dna Methylation ◽  
Chromate Exposure

Abstract 86: DNA methylation of tumor suppressor and metastasis suppressor genes in circulating tumor cells

2011 ◽  
Author(s):  
Maria Chimonidou ◽  
Areti D. Strati ◽  
Alexandra Tzitzira ◽  
Georgia Sotiropoulou ◽  
Nikos Malamos ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Tumor Suppressor ◽  
Tumor Cells ◽  
Circulating Tumor Cells ◽  
Metastasis Suppressor ◽  
Suppressor Genes ◽  
Metastasis Suppressor Genes

scholarly journals Aberrant DNA Methylation in Cholangiocarcinoma

2017 ◽  
Author(s):  
Toshiaki Nakaoka ◽  
Yoshimasa Saito ◽  
Hidetsugu Saito
Keyword(s):  
Dna Methylation ◽  
Immune Response ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Ampulla Of Vater ◽  
Endogenous Retroviruses ◽  
Epigenetic Therapy ◽  
Suppressor Genes ◽  
Aberrant Dna Methylation ◽  
Dna Methylation Inhibitors

Cholangiocarcinoma is an epithelial malignancy arising in the region between the intrahepatic bile ducts and the ampulla of Vater at the distal end of the common bile duct. The effect of current chemotherapy regimens against cholangiocarcinoma is limited, and the prognosis of patients with cholangiocarcinoma is poor. Aberrant DNA methylation and histone modification induce silencing of tumor suppressor genes and chromosomal instability during carcinogenesis. Studies have shown that the tumor suppressor genes and microRNAs (miRNAs) including MLH1, p14, p16, DAPK, miR-370 and miR-376c are frequently methylated in cholangiocarcinoma. Silencing of these tumor suppressor genes and miRNAs plays critical roles in the initiation and progression of cholangiocarcinoma. In addition, recent studies have demonstrated that DNA methylation inhibitors induce expression of endogenous retroviruses and exert the anti-tumor effect of via an anti-viral immune response. Aberrant DNA methylation of tumor suppressor genes and miRNAs could be a powerful biomarker for diagnosis and treatment of cholangiocarcinoma. Epigenetic therapy with DNA methylation inhibitors hold considerable promise for the treatment of cholangiocarcinoma through re-activation of tumor suppressor genes and miRNAs as well as induction of an anti-viral immune response.

ABERRANT DNA METHYLATION AS A CANCER-INDUCING MECHANISM

2005 ◽  
Vol 45 (1) ◽  
pp. 629-656 ◽  
Author(s):  
Manel Esteller
Keyword(s):  
Dna Methylation ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Cpg Island ◽  
Gene Mutations ◽  
Promoter Hypermethylation ◽  
Dna Methyltransferases ◽  
Tumor Type ◽  
Suppressor Genes ◽  
Aberrant Dna Methylation

Aberrant DNA methylation is the most common molecular lesion of the cancer cell. Neither gene mutations (nucleotide changes, deletions, recombinations) nor cytogenetic abnormalities are as common in human tumors as DNA methylation alterations. The most studied change of DNA methylation in neoplasms is the silencing of tumor suppressor genes by CpG island promoter hypermethylation, which targets genes such as p16INK4a, BRCA1, and hMLH1. There is a profile of CpG island hypermethylation according to the tumor type, and genes silent by methylation represent all cellular pathways. The introduction of bisulfite-PCR methodologies combined with new genomic approaches provides a comprehensive spectrum of the genes undergoing this epigenetic change across all malignancies. However, we still know very little about how this aberrant DNA methylation “invades” the previously unmethylated CpG island and how it is maintained through cell divisions. Furthermore, we should remember that this methylation occurs in the context of a global genomic loss of 5-methylcytosine (5mC). Initial clues to understand this paradox should be revealed from the current studies of DNA methyltransferases and methyl CpG binding proteins. From the translational standpoint, we should make an effort to validate the use of some hypermethylated genes as biomarkers of the disease; for example, it may occur with MGMT and GSTP1 in brain and prostate tumors, respectively. Finally, we must expect the development of new and more specific DNA demethylating agents that awake these methyl-dormant tumor suppressor genes and prove their therapeutic values. The expectations are high.

Development of a novel approach, the epigenome-based outlier approach, to identify tumor-suppressor genes silenced by aberrant DNA methylation

2012 ◽  
Vol 322 (2) ◽  
pp. 204-212 ◽  
Author(s):  
Mizuho Kikuyama ◽  
Hideyuki Takeshima ◽  
Takayuki Kinoshita ◽  
Eriko Okochi-Takada ◽  
Mika Wakabayashi ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Suppressor Genes ◽  
Novel Approach ◽  
Aberrant Dna Methylation

scholarly journals Targeting DNA methylation for treating triple-negative breast cancer

2019 ◽  
Vol 20 (16) ◽  
pp. 1151-1157 ◽  
Author(s):  
Jia Yu ◽  
Jacqueline Zayas ◽  
Bo Qin ◽  
Liewei Wang
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Tumor Suppressor ◽  
Triple Negative Breast Cancer ◽  
Targeted Therapies ◽  
Tumor Suppressor Genes ◽  
Dna Methyltransferase ◽  
Triple Negative ◽  
Suppressor Genes ◽  
Dna Methyltransferase Inhibitors

Triple-negative breast cancer (TNBC) accounts for 15–20% of all invasive breast cancers and tends to have aggressive histological features and poor clinical outcomes. Unlike, estrogen receptor- or HER2-positive diseases, TNBC patients currently lack the US FDA-approved targeted therapies. DNA methylation is a critical mechanism of epigenetic modification. It is well known that aberrant DNA methylation contributes to the malignant transformation of cells by silencing critical tumor suppressor genes. DNA methyltransferase inhibitors reactivate silenced tumor suppressor genes and result in tumor growth arrest, with therapeutic effects observed in patients with hematologic malignancies. The antitumor effect of these DNA methyltransferase inhibitors has also been explored in solid tumors, especially in TNBC that currently lacks targeted therapies.

Abstract A37: SB insertional mutagenesis identifies new metastasis-promoting tumor suppressor genes in pancreatic cancer

2018 ◽  
Author(s):  
Michelle Maurin ◽  
Devin J. Jones ◽  
Mik A. Black ◽  
Justin Y. Newberg ◽  
Nancy A. Jenkins ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Insertional Mutagenesis ◽  
Suppressor Genes

Abstract A15: Exome sequencing identifies candidate tumor suppressor genes in familial pancreatic cancer.

2012 ◽  
Author(s):  
Robert C. Grant ◽  
Timothy Beck ◽  
Lakshmi Muthuswamy ◽  
Ayelet Borgida ◽  
Spring Holter ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Suppressor ◽  
Exome Sequencing ◽  
Tumor Suppressor Genes ◽  
Familial Pancreatic Cancer ◽  
Suppressor Genes ◽  
Candidate Tumor Suppressor
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