scholarly journals Expression Rate and PAX5 Gene Methylation in the Blood of People Suffering from Gastric Cancer

2018 ◽  
Vol 6 (9) ◽  
pp. 1571-1576 ◽  
Author(s):  
Mozhdeh Khajeh Haghverdi ◽  
Elham Moslemi
Keyword(s):  
Gastric Cancer ◽  
Promoter Methylation ◽  
Methylation Status ◽  
Gene Promoter ◽  
Gene Promoters ◽  
Health Issues ◽  
Blood Samples ◽  
Important Health ◽  
Expression Rate ◽  
Pax5 Gene

BACKGROUND: Gastric cancer is one of the most important health issues in the world. Considering the lack of plenty of pre-awarenesses, the survival of gastric cancer is still quite disappointing. Methylation of PAX5 gene promoter is observed in most cancer cells of a human. A study has shown that PAX5 is a new tumoral suppressor in gastric cancer and methylation of the PAX5 promoter is associated with the survival rate of gastric cancer. AIM: The present research seeks to study the expression rate and methylation of the PAX5 gene in the blood of patients who have gastric cancer to be used as a biomarker in this type of cancer. MATERIAL AND METHODS: Real-time PCR technique was used to assess expression of PAX5 gene, while the methylation status of PAX5 gene promoter in the blood samples of people who have gastric cancer versus blood samples obtained from normal Iranian population was studied using MS PCR technique. RESULTS: The final results pointed to the fact that expression of PAX5 in blood samples obtained from those who have gastric cancer is much less than what is observed in normal blood samples. A significant correlation was also observed between expression of this gene and age and promoter methylation rate. The results of methylation also indicated that 28% of PAX5 gene promoters among patients were methylated, while all normal samples were non-methylated. CONCLUSION: Studying the decrease observed in PAX5 gene expression and the rise in promoter methylation can be utilised as a biomarker to enhance pre-awareness of gastric cancer.

scholarly journals Studying the expression rate and methylation of Reprimo gene in the blood of patients suffering from gastric cancer

2018 ◽  
Vol 28 (2) ◽  
Author(s):  
Amin Abbasi ◽  
Sahar Heydari
Keyword(s):  
Gastric Cancer ◽  
Early Diagnosis ◽  
Cancer Patients ◽  
Methylation Status ◽  
Blood Samples ◽  
Specific Pcr ◽  
Expression Rate ◽  
And Performance ◽  
Gastric Cancer Patients ◽  
Gene Age

As gastric cancer has no exclusive signals in its initial phases, it is usually diagnosed in advanced phases. Although many researches have been conducted on methylation and diagnosis of cancer’s markers, the methylation and expression of Reprimo gene and its correlation with gastric cancer has not been thoroughly studied. Methylation of Reprimo promoter is a repetitive procedure exclusive to cancer which nullifies its expression and performance. The present research seeks to study the expression and methylation of Reprimo among people suffering with gastric cancer so that it may be used as a biomarker for early diagnosis. Fifty blood samples taken from healthy people (normal samples) and 50 blood samples obtained from gastric cancer patients were analyzed using Real-Time PCR. The methylation status of the promoter of Reprimo was studied using Methylation Specific PCR technique in normal samples and in gastric cancer Iranian patients. We observed reduction in expression rate of Reprimo in the blood samples of patients suffering with gastric cancer in comparison to normal blood samples. A significant correlation was also observed between the expression rate of this gene, age and methylation of its promoter among patients suffering with gastric cancer and various analysis points to a correlation between reduced expressions of Reprimo gene in gastric cancer patients. In conclusion, reduced expression of Reprimo gene and greater levels of methylation of its promoter seems to be promising biomarkers for early diagnosis of gastric cancer.

scholarly journals Genome-wide analysis identifies critical DNA methylations within NTRKs genes in colorectal cancer

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Zijian Chen ◽  
Zenghong Huang ◽  
Yanxin Luo ◽  
Qi Zou ◽  
Liangliang Bai ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dna Methylation ◽  
Promoter Methylation ◽  
Expression Profiles ◽  
Methylation Status ◽  
Gene Promoter ◽  
Normal Mucosa ◽  
Suppressor Gene ◽  
Survival Outcome ◽  
Prognostic Models

Abstract Background Neurotrophic tropomyosin receptor kinases (NTRKs) are a gene family function as oncogene or tumor suppressor gene in distinct cancers. We aimed to investigate the methylation and expression profiles and prognostic value of NTRKs gene in colorectal cancer (CRC). Methods An analysis of DNA methylation and expression profiles in CRC patients was performed to explore the critical methylations within NTRKs genes. The methylation marker was validated in a retrospectively collected cohort of 229 CRC patients and tested in other tumor types from TCGA. DNA methylation status was determined by quantitative methylation-specific PCR (QMSP). Results The profiles in six CRC cohorts showed that NTRKs gene promoter was more frequently methylated in CRC compared to normal mucosa, which was associated with suppressed gene expression. We identified a specific methylated region within NTRK3 promoter targeted by cg27034819 and cg11525479 that best predicted survival outcome in CRC. NTRK3 promoter methylation showed independently predictive value for survival outcome in the validation cohort (P = 0.004, HR 2.688, 95% CI [1.355, 5.333]). Based on this, a nomogram predicting survival outcome was developed with a C-index of 0.705. Furthermore, the addition of NTRK3 promoter methylation improved the performance of currently-used prognostic model (AIC: 516.49 vs 513.91; LR: 39.06 vs 43.64, P = 0.032). Finally, NTRK3 promoter methylation also predicted survival in other tumors, including pancreatic cancer, glioblastoma and stomach adenocarcinoma. Conclusions This study highlights the essential value of NTRK3 methylation in prognostic evaluation and the potential to improve current prognostic models in CRC and other tumors.

Association Between Cyclin D1 Polymorphism with CpG Island Promoter Methylation Status of Tumor Suppressor Genes in Gastric Cancer

2010 ◽  
Vol 55 (12) ◽  
pp. 3449-3457 ◽  
Author(s):  
Tomomitsu Tahara ◽  
Tomoyuki Shibata ◽  
Masakatsu Nakamura ◽  
Hiromi Yamashita ◽  
Daisuke Yoshioka ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Suppressor ◽  
Cyclin D1 ◽  
Promoter Methylation ◽  
Tumor Suppressor Genes ◽  
Cpg Island ◽  
Methylation Status ◽  
Suppressor Genes ◽  
Promoter Methylation Status

scholarly journals Analysis of smad4 gene promoter methylation in pancreatic and endometrial cancers

2017 ◽  
Vol 23 (2) ◽  
pp. 17-19
Author(s):  
Aleksandra Nikolic ◽  
Filip Opincal ◽  
Momcilo Ristanovic ◽  
Jovanka Trifunovic ◽  
Srbislav Knezevic ◽  
...  
Keyword(s):  
Promoter Methylation ◽  
Methylation Status ◽  
Gene Promoter ◽  
Promoter Hypermethylation ◽  
Surgical Removal ◽  
Smad4 Gene ◽  
Frequent Event ◽  
Cancer Types ◽  
Endometrial Cancers ◽  
Tumor Types

Background. Promoter hypermethylation of the SMAD4 gene has been registered in some cancer types, but in general doesn?t appear to be a frequent event in carcinogenesis. However, only a few published studies deal with this topic and not many cancer types have been analyzed. The aim of this study was to establish SMAD4 gene promoter methylation status in pancreatic and endometrial cancers. Methods. Patients included in the study (62 subjects) were diagnosed and surgically treated at the University of Belgrade, Clinical Center of Serbia. Patients with pancreatic carcinoma (17 subjects) underwent surgical removal of the pancreatic adenocarcinoma at the First Surgical Clinic, while the patients with endometrial carcinoma (45 subjects) underwent hysterectomy with adnexectomy at the Institute for Gynecology and Obstetrics. Extraction of DNA from fresh tissue samples was performed and the methylation status of the SMAD4 gene promoter was studied by a previously designed PCR-based HpaII and MspI restriction enzyme assay. The resulting PCR products were analyzed by electrophoresis in 2% agarose gels. Results. Neither of the analyzed samples was found to be hypermethylated. Conclusion. This is the first report on SMAD4 methylation status in pancreatic and endometrial tumor specimens, and supports the viewpoint that SMAD4 hypermethylation is not a common event in malignant tumors. Nevertheless, promoter hypermethylation remains a candidate mechanism for SMAD4 inactivation in malignant tissue as a potential cause of decreased or lost SMAD4 expression in certain tumor types, and should be further investigated in different tumor types and larger cohorts of patients.

scholarly journals Analysis of SEPT9 Gene Promoter Methylation Status in Esophageal Squamous Cell Carcinoma

2020 ◽  
Author(s):  
Aida Mirza Aghasi ◽  
Saied Ghorbian
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Promoter Methylation ◽  
Methylation Status ◽  
Gene Promoter ◽  
Sodium Metabisulfite ◽  
Significant Difference ◽  
Cancer Tissues

Introduction: The changes in the level of SEPT9 gene promoter methylation can contribute to the formation of esophageal squamous cell carcinoma. The aim of this study was to evaluate the level of changes in the level of SEPT9 gene promoter methylation in the esophageal squamous cell carcinoma. Methods: In the present case-control study, we collected 75 paraffin blocks of esophageal cancer tissues and 75 paraffin blocks healthy tissues, which were referred to the Noor-E-Nejat and Tabriz International Hospitals during 2013-2017. After DNA extraction and treatment with sodium metabisulfite, the changes of SEPT9 gene promoter methylation assessed using high resolution melting (HRM) technique. The data were analyzed by SPSS 22 and Chi-square test. Results: Our findings did not show a statistically significant difference between the changes of SEPT9 gene promoter methylation in cancer tissues compared to the healthy tissues (P=0.106). Conclusion: This study shows that SEPT9 gene promoter methylation cannot contribute to the esophageal squamous cell carcinoma cancerogenesis.  

scholarly journals Bisphenol a Exposure, DNA Methylation, and Asthma in Children

2020 ◽  
Vol 17 (1) ◽  
pp. 298 ◽  
Author(s):  
Chia-Feng Yang ◽  
Wilfried J. J. Karmaus ◽  
Chen-Chang Yang ◽  
Mei-Lien Chen ◽  
I-Jen Wang
Keyword(s):  
Dna Methylation ◽  
Bisphenol A ◽  
Candidate Genes ◽  
Promoter Methylation ◽  
Childhood Asthma ◽  
Methylation Status ◽  
Differential Methylation ◽  
Study Cohort ◽  
Blood Samples ◽  
Asthma In Children

Epidemiological studies have reported the relationship between bisphenol A (BPA) exposure and increased prevalence of asthma, but the mechanisms remain unclear. Here, we investigated whether BPA exposure and DNA methylation related to asthma in children. We collected urinary and blood samples from 228 children (Childhood Environment and Allergic Diseases Study cohort) aged 3 years. Thirty-three candidate genes potentially interacting with BPA exposure were selected from a toxicogenomics database. DNA methylation was measured in 22 blood samples with top-high and bottom-low exposures of BPA. Candidate genes with differential methylation levels were validated by qPCR and promoter associated CpG islands have been investigated. Correlations between the methylation percentage and BPA exposure and asthma were analyzed. According to our findings, MAPK1 showed differential methylation and was further investigated in 228 children. Adjusting for confounders, urinary BPA glucuronide (BPAG) level inversely correlated with MAPK1 promoter methylation (β = −0.539, p = 0.010). For the logistic regression analysis, MAPK1 methylation status was dichotomized into higher methylated and lower methylated groups with cut off continuous variable of median of promoter methylation percentage (50%) while performing the analysis. MAPK1 methylation was lower in children with asthma than in children without asthma (mean ± SD; 69.82 ± 5.88% vs. 79.82 ± 5.56%) (p = 0.001). Mediation analysis suggested that MAPK1 methylation acts as a mediation variable between BPA exposure and asthma. The mechanism of BPA exposure on childhood asthma might, therefore, be through the alteration of MAPK1 methylation. The mechanism of BPA exposure on childhood asthma might, therefore, be through the alteration of MAPK1 methylation.

scholarly journals Potential utility of HOP homeobox gene promoter methylation as a marker of tumor aggressiveness in gastric cancer

Oncogene ◽  
2010 ◽  
Vol 29 (22) ◽  
pp. 3263-3275 ◽  
Author(s):  
A Ooki ◽  
K Yamashita ◽  
S Kikuchi ◽  
S Sakuramoto ◽  
N Katada ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Promoter Methylation ◽  
Homeobox Gene ◽  
Gene Promoter ◽  
Potential Utility ◽  
Tumor Aggressiveness

scholarly journals Predictive value of the serum RASSF10 promoter methylation status in gastric cancer

2019 ◽  
Vol 47 (7) ◽  
pp. 2890-2900 ◽  
Author(s):  
Yilin Hu ◽  
Peng Ma ◽  
Ying Feng ◽  
Peng Li ◽  
Hua Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Promoter Methylation ◽  
Cox Regression ◽  
Methylation Status ◽  
Disease Free Survival ◽  
Prognostic Indicator ◽  
Chronic Atrophic Gastritis ◽  
Survival Times ◽  
Cox Regression Analysis ◽  
Specific Pcr

Background This study aimed to investigate whether the detection of methylation in the promoter of the Ras association domain family 10 gene ( RASSF10) in the serum of patients with gastric cancer (GC) by methylation-specific PCR (MSP) can be used as a diagnostic and prognostic indicator of GC. Methods We used MSP to examine RASSF10 methylation levels in the serum and/or tumor samples from 100 GC patients, 50 patients with chronic atrophic gastritis (CAG), and 45 healthy controls (HC). We also analyzed clinicopathological and follow-up data. Results Our results showed that the rate of serum RASFF10 promoter methylation among patients with GC (49/100) was higher than in those with CAG (1/50) or HC (0/45). Moreover, the RASSF10 methylation status was consistent between serum and tumor tissues. GC patients with serum RASSF10 promoter methylation had significantly shorter overall survival and disease-free survival times than GC patients without serum RASSF10 promoter methylation. Multivariable Cox regression analysis showed that serum RASSF10 promoter methylation and lymph node metastasis both correlated with reduced survival in GC patients. Conclusions Detection of the serum RASSF10 methylation status by MSP is feasible as a diagnostic and prognostic indicator of GC.

scholarly journals Altered expression of PTCH and HHIP in gastric cancer through their gene promoter methylation: Novel targets for gastric cancer

2013 ◽  
Vol 7 (4) ◽  
pp. 1159-1168 ◽  
Author(s):  
YU SONG ◽  
YE TIAN ◽  
YUN ZUO ◽  
JIAN-CHENG TU ◽  
YU-FANG FENG ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Promoter Methylation ◽  
Gene Promoter ◽  
Altered Expression ◽  
Novel Targets

scholarly journals Methylation in p14ARF is Frequently Observed in Colorectal Cancer with Low-level Microsatellite Instability

2009 ◽  
Vol 37 (4) ◽  
pp. 1038-1045 ◽  
Author(s):  
K Kominami ◽  
T Nagasaka ◽  
HM Cullings ◽  
N Hoshizima ◽  
H Sasamoto ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Microsatellite Instability ◽  
Promoter Methylation ◽  
Dna Methyltransferase ◽  
Methylation Status ◽  
Gene Promoters ◽  
Braf Mutations ◽  
Low Level ◽  
Methylguanine Dna Methyltransferase ◽  
High Level

Colorectal cancer (CRC) can be classified as high-level microsatellite instability (MSI-H), low-level MSI (MSI-L) and microsatellite stable (MSS) depending on levels of MSI. MSI-H CRC relies on a distinct molecular pathway due to the mismatch repair (MMR) deficiency and shows methylation in multiple gene promoters. The genetic pathway leading to MSI-L is unknown, although higher levels of promoter methylation are observed in this group compared with MSS CRCs. This study explored how promoter methylation affects MSI phenotype, by analysing the methylation status of eight CRC-related promoters, MSI phenotype and KRAS/BRAF mutations in a series of 234 CRCs. Promoter methylation of p14ARF was significantly related to MSI-L CRC with KRAS mutation. The MSI-H phenotype was related to methylation of MLH1 as expected, while the MSS phenotype was related to methylation of p16INK4a and O6-methylguanine-DNA methyltransferase, although this was not statistically significant. Thus, promoter methylation of p14ARF could be a significant alteration leading to CRC with MSI-L.

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