Reduced expression of the Tslc1 gene and its aberrant DNA methylation in rat lung tumors

2006 ◽  
Vol 347 (1) ◽  
pp. 358-362 ◽  
Author(s):  
Kyoko Shimizu ◽  
Yumi Itsuzaki ◽  
Mariko Onishi ◽  
Hiromasa Fujii ◽  
Kanya Honoki ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Lung Tumors ◽  
Rat Lung ◽  
Aberrant Dna Methylation ◽  
Tslc1 Gene

Reduced expression of the Connexin26 gene and its aberrant DNA methylation in rat lung adenocarcinomas induced by N-nitrosobis(2-Hydroxypropyl)amine

2006 ◽  
Vol 45 (9) ◽  
pp. 710-714 ◽  
Author(s):  
Kyoko Shimizu ◽  
Yozo Shimoichi ◽  
Daisei Hinotsume ◽  
Yumi Itsuzaki ◽  
Hiromasa Fujii ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Rat Lung ◽  
Aberrant Dna Methylation ◽  
Lung Adenocarcinomas

Aberrant DNA methylation ofE-cadherin andp16 genes in rat lung adenocarcinomas induced by N-nitrosobis(2-hydroxypropyl)amine

2006 ◽  
Vol 45 (2) ◽  
pp. 106-111 ◽  
Author(s):  
Ayumi Kato ◽  
Kyoko Shimizu ◽  
Yozo Shimoichi ◽  
Hiromasa Fujii ◽  
Kanya Honoki ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Rat Lung ◽  
Aberrant Dna Methylation ◽  
Lung Adenocarcinomas

Aberrant DNA methylation of the 5′ upstream region of Tslc1 gene in hamster pancreatic tumors

2007 ◽  
Vol 353 (2) ◽  
pp. 522-526 ◽  
Author(s):  
Kyoko Shimizu ◽  
Mariko Onishi ◽  
Eriko Sugata ◽  
Hiromasa Fujii ◽  
Kanya Honoki ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Pancreatic Tumors ◽  
Upstream Region ◽  
Aberrant Dna Methylation ◽  
Tslc1 Gene

Aberrant DNA Methylation Is Associated with Reduced Response to SRC Inhibition in Primary Human Vestibular Schwannoma Cells

2019 ◽  
Author(s):  
Christine Dinh ◽  
Juan Young ◽  
Olena Bracho ◽  
Rahul Mittal ◽  
Denise Yan ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Vestibular Schwannoma ◽  
Aberrant Dna Methylation

245-LB: Aberrant DNA Methylation as a Contributor to Obesity-Associated Vascular Dysfunction

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 245-LB
Author(s):  
MOHAMED M. ALI ◽  
CHANDRA HASSAN ◽  
MARIO MASRUR ◽  
FRANCESCO BIANCO ◽  
SHANE A. PHILLIPS ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Vascular Dysfunction ◽  
Aberrant Dna Methylation

scholarly journals Neuroblastoma and the epigenome

2021 ◽  
Author(s):  
Irfete S. Fetahu ◽  
Sabine Taschner-Mandl
Keyword(s):  
Dna Methylation ◽  
Histone Modifications ◽  
Disease Diagnosis ◽  
Dna Methyltransferases ◽  
Epigenetic Alterations ◽  
Aberrant Expression ◽  
Tet Proteins ◽  
Relative Paucity ◽  
Underlying Causes ◽  
Aberrant Dna Methylation

AbstractNeuroblastoma (NB) is a pediatric cancer of the sympathetic nervous system and one of the most common solid tumors in infancy. Amplification of MYCN, copy number alterations, numerical and segmental chromosomal aberrations, mutations, and rearrangements on a handful of genes, such as ALK, ATRX, TP53, RAS/MAPK pathway genes, and TERT, are attributed as underlying causes that give rise to NB. However, the heterogeneous nature of the disease—along with the relative paucity of recurrent somatic mutations—reinforces the need to understand the interplay of genetic factors and epigenetic alterations in the context of NB. Epigenetic mechanisms tightly control gene expression, embryogenesis, imprinting, chromosomal stability, and tumorigenesis, thereby playing a pivotal role in physio- and pathological settings. The main epigenetic alterations include aberrant DNA methylation, disrupted patterns of posttranslational histone modifications, alterations in chromatin composition and/or architecture, and aberrant expression of non-coding RNAs. DNA methylation and demethylation are mediated by DNA methyltransferases (DNMTs) and ten-eleven translocation (TET) proteins, respectively, while histone modifications are coordinated by histone acetyltransferases and deacetylases (HATs, HDACs), and histone methyltransferases and demethylases (HMTs, HDMs). This article focuses predominately on the crosstalk between the epigenome and NB, and the implications it has on disease diagnosis and treatment.

scholarly journals Hypermethylation of mismatch repair gene hMSH2 associates with platinum-resistant disease in epithelial ovarian cancer

2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Hua Tian ◽  
Li Yan ◽  
Li Xiao-fei ◽  
Sun Hai-yan ◽  
Chen Juan ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Ovarian Cancer ◽  
Dna Methylation ◽  
Epithelial Ovarian Cancer ◽  
Upstream Region ◽  
Platinum Resistance ◽  
Maldi Tof Mass Spectrometry ◽  
Platinum Resistant ◽  
Aberrant Dna Methylation ◽  
Low Expression

Abstract Purpose One major reason of the high mortality of epithelial ovarian cancer (EOC) is due to platinum-based chemotherapy resistance. Aberrant DNA methylation may be a potential mechanism underlying the development of platinum resistance in EOC. The purpose of this study is to discover potential aberrant DNA methylation that contributes to drug resistance. Methods By initially screening of 16 platinum-sensitive/resistant samples from EOC patients with reduced representation bisulfite sequencing (RRBS), the upstream region of the hMSH2 gene was discovered hypermethylated in the platinum-resistant group. The effect of hMSH2 methylation on the cellular response to cisplatin was explored by demethylation and knockdown assays in ovarian cancer cell line A2780. Matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) mass spectrometry was employed to examine the methylation levels of hMSH2 upstream region in additional 40 EOC patient samples. RT-qPCR and IHC assay was used to detect the hMSH2 mRNA and protein expression in extended 150 patients. Results RRBS assay discovered an upstream region from − 1193 to − 1125 of hMSH2 was significant hypermethylated in resistant EOC patients (P = 1.06 × 10−14). In vitro analysis demonstrated that global demethylation increased cisplatin sensitivity along with a higher expression of the hMSH2 mRNA and protein. Knockdown hMSH2 reduced the cell sensitivity to cisplatin. MALDI-TOF mass spectrometry assay validated the strong association of hypermethylation of hMSH2 upstream region with platinum resistance. Spearman’s correlation analysis revealed a significantly negative connection between methylation level of hMSH2 upstream region and its expression. The Kaplan-Meier analyses showed the high methylation of hMSH2 promoter region, and its low expressions are associated with worse survival. In multivariable models, hMSH2 low expression was an independent factor predicting poor outcome (P = 0.03, HR = 1.91, 95%CI = 1.85–2.31). Conclusion The hypermethylation of hMSH2 upstream region is associated with platinum resistant in EOC, and low expression of hMSH2 may be an index for the poor prognosis.

Reply to: “Development of an MSI-positive colon tumor with aberrant DNA methylation in a PPAP patient”

2019 ◽  
Vol 65 (6) ◽  
pp. 513-514 ◽  
Author(s):  
Pilar Mur ◽  
Claire Palles ◽  
Ian Tomlinson ◽  
Laura Valle
Keyword(s):  
Dna Methylation ◽  
Colon Tumor ◽  
Aberrant Dna Methylation
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