CDKN2B, SLC19A3 and DLEC1 promoter methylation alterations in the bone marrow of patients with acute myeloid leukemia during chemotherapy

Hong, Qingxiao; Li, Yirun; Chen, Xiaoying; Ye, Huadan; Tang, Linlin; Zhou, Ang; Hu, Yan; Gao, Yuting; Chen, Rongrong; Xia, Yongming; Duan, Shiwei

doi:10.3892/etm.2016.3092

Cited by 3 publications

(2 citation statements)

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“…DNA methylation was determined after treatment by primers specific for the methylated and unmethylated alleles of each gene, and the methylation status of CDH1, DLEC1 and SFRP5 was evaluated. The primer sequences are summarized in Supplementary Table 1 [21,[23][24][25][26][27][28][29][30][31][32][33][34].…”

Section: Methylation-specific Pcr and Capillary Electrophoresismentioning

confidence: 99%

CDH1 , DLEC1 and SFRP5 Methylation Panel As a Prognostic Marker for Advanced Epithelial Ovarian Cancer

Lin

Chang

et al. 2018

Epigenomics

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To investigate the CDH1, DLEC1 and SFRP5 gene methylation panel for advanced epithelial ovarian carcinoma (EOC). Materials & methods: One hundred and seventy-seven advanced EOC specimens were evaluated by methylation-specific PCR. We also used The Cancer Genome Atlas dataset to evaluate the panel. Results: The presence of two or more methylated genes was significant in recurrence (hazard ratio [HR]: 1.91 [1.33-2.76]; p = 0.002) and death (HR: 1.96 [1.26-3.06]; p = 0.006) in our cohort. In The Cancer Genome Atlas dataset, the presence of two or three methylated genes was significant in death (HR: 1.59 [1.15-2.18]; p = 0.0047) and close to the significance level in recurrence (HR: 1.37 [0.99-1.88]; p = 0.058). Conclusion:The CDH1, DLEC1 and SFRP5 methylation panel is a potential prognostic biomarker for advanced EOC.

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Section: Methylation-specific Pcr and Capillary Electrophoresismentioning

confidence: 99%

CDH1 , DLEC1 and SFRP5 Methylation Panel As a Prognostic Marker for Advanced Epithelial Ovarian Cancer

Lin

Chang

et al. 2018

Epigenomics

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“…Promoter hypermethylation of the tumor suppressor genes has been recognized as an important factor in inducing oncogenesis (6). For example, SRY-box 17 (SOX17) methylation was found in 60.2% of primary lung cancer samples, and promoter methylation of SOX17 silenced gene expression, leading to the elimination of cell proliferation suppression in lung cancer (7).…”

Section: Introductionmentioning

confidence: 99%

AGTR1 promoter hypermethylation in lung squamous cell carcinoma but not in lung adenocarcinoma

et al. 2017

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Abstract. Aberrant DNA methylation is associated with non-small cell lung cancer (NSCLC), suggesting that gene promoter methylation may be a potential biomarker for the detection or risk prediction of NSCLC. The present study aimed to evaluate the potential usage of angiotensin II receptor type 1 (AGTR1) methylation in two major pathologic subtypes: Lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). Quantitative methylation-specific polymerase chain reaction was used to investigate the effect of AGTR1 promoter methylation in the tumor and the paired adjacent non-tumor tissue samples from 42 patients with LUSC, and 69 with LUAD. The percentage of methylated reference was calculated and presented as the median (interquartile range 25th-75th percentile). The results of the current study revealed that there was significantly increased AGTR1 promoter methylation in the tumor tissues compared with the paired adjacent non-tumor tissue [97.4 (57.22-130.5) vs. 85 (48.25-123); P=0.024]. Furthermore, higher AGTR1 promoter methylation was observed in patients with LUSC compared with LUAD (odds ratio=2.483; 95% confidence interval=1.125-5.480; P=0.023). Significant differences were identified in AGTR1 methylation between non-tumor and the tumor tissues in LUSC [113.5 (68.33-148.73) vs. 93.04 (45.94-140); P=0.008]. In addition, the Cancer Genome Atlas data of 378 patients with LUSC and 477 with LUAD revealed an inverse correlation between gene expression and the methylation status of AGTR1 promoter.. These data suggest that AGTR1 hypermethylation is a promising biomarker to assist in LUSC detection and diagnosis. IntroductionLung cancer is a kind of malignancy that arises from epithelial cells. It is the leading cause of cancer-related death worldwide (1). There were nearly 1.8 million new patients and caused 159 million deaths in 2012, of which China accounted for more than one third (2). According to the size and appearance of the malignant cells, lung cancer is categorized as non small cell lung cancer (NSCLC) and small cell lung cancer (3). NSCLC represents approximately 85% of lung cancer (4), and it can be further subdivided into large cell carcinoma, lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). There are a lot of differences in molecular profiling, characteristics and therapeutic methods between LUAD and LUSC (5).Promoter hypermethylation of the tumor suppressor genes has been recognized as an important factor in inducing oncogenesis (6). For example, SRY-box 17 (SOX17) methylation was found in 60.2% of primary lung cancer samples, and promoter methylation of SOX17 silenced gene expression, leading to the elimination of cell proliferation suppression in lung cancer (7). Identification of specific gene hypermethylation may explain the genomic instability and complexity of NSCLC and provide a basis for targeted therapy or risk prediction. AGTR1 promoter hypermethylation in lung squamouscell carcinoma but not in lung adenocarcinoma

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Advances in molecular characterization of myeloid proliferations associated with Down syndrome

Kalev‐Zylinska

2022

Front. Genet.

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Myeloid leukemia associated with Down syndrome (ML-DS) has a unique molecular landscape that differs from other subtypes of acute myeloid leukemia. ML-DS is often preceded by a myeloproliferative neoplastic condition called transient abnormal myelopoiesis (TAM) that disrupts megakaryocytic and erythroid differentiation. Over the last two decades, many genetic and epigenetic changes in TAM and ML-DS have been elucidated. These include overexpression of molecules and micro-RNAs located on chromosome 21, GATA1 mutations, and a range of other somatic mutations and chromosomal alterations. In this review, we summarize molecular changes reported in TAM and ML-DS and provide a comprehensive discussion of these findings. Recent advances in the development of CRISPR/Cas9-modified induced pluripotent stem cell-based disease models are also highlighted. However, despite significant progress in this area, we still do not fully understand the pathogenesis of ML-DS, and there are no targeted therapies. Initial diagnosis of ML-DS has a favorable prognosis, but refractory and relapsed disease can be difficult to treat; therapeutic options are limited in Down syndrome children by their stronger sensitivity to the toxic effects of chemotherapy. Because of the rarity of TAM and ML-DS, large-scale multi-center studies would be helpful to advance molecular characterization of these diseases at different stages of development and progression.

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CDKN2B, SLC19A3 and DLEC1 promoter methylation alterations in the bone marrow of patients with acute myeloid leukemia during chemotherapy

Cited by 3 publications

References 36 publications

CDH1 , DLEC1 and SFRP5 Methylation Panel As a Prognostic Marker for Advanced Epithelial Ovarian Cancer

CDH1 , DLEC1 and SFRP5 Methylation Panel As a Prognostic Marker for Advanced Epithelial Ovarian Cancer

AGTR1 promoter hypermethylation in lung squamous cell carcinoma but not in lung adenocarcinoma

Advances in molecular characterization of myeloid proliferations associated with Down syndrome

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