Aberrant CpG island methylation in early-onset sporadic gastric carcinoma

Kim, Hee Cheol; Kim, Jin Cheon; Roh, Sun Ae; Yu, Chang Sik; Yook, Jeong Hwan; Oh, Seok‐Young; Kim, Byung Sik; Park, Kun Choon; Chang, Rin

doi:10.1007/s00432-005-0017-0

Cited by 30 publications

(15 citation statements)

References 29 publications

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“…However, DNA methylation and histone deacetylation of DAPK1 have been found in colorectal and gastric cancers in association with silencing of this gene [22][23][24]. This discrepancy may reflect genetic instability at this site, changes in the balance of apoptosis, or the detected change in copy number may not lead to an increase in expression of the protein.…”

Section: Discussionmentioning

confidence: 84%

Molecular analysis of primary gastric cancer, corresponding xenografts, and 2 novel gastric carcinoma cell lines reveals novel alterations in gastric carcinogenesis

et al. 2007

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Section: Discussionmentioning

confidence: 84%

Molecular analysis of primary gastric cancer, corresponding xenografts, and 2 novel gastric carcinoma cell lines reveals novel alterations in gastric carcinogenesis

et al. 2007

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“…Frequency of promoter methylation in various genes in gastric carcinomaKang et al 2003;Esteller et al 2001a;Kim et al 2005 …”

mentioning

confidence: 99%

Aberrant epigenetic patterns in the etiology of gastrointestinal cancers

2008

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A body of evidence accumulated over the past decade suggests that epigenetic mechanisms play an essential role in maintaining important cellular functions. Changes in epigenetic patterns (mainly DNA hyper- and hypomethylation and, more recently, histone modifications) may contribute to the development of cancer. Aberrant epigenetic events expand thorough tumor progression from the earliest to latest stages, therefore they can serve as convenient markers for detection and prognosis of cancer. The potential reversibility of epigenetic states in the tumor cell is an attractive target for cancer therapy. Much of our current knowledge on epigenetic alternations in cancer comes from studies on gastrointestinal malignancies, mainly on colorectal cancer, which currently serves as a model for epigenetic tumorigenesis. This review summarizes the current knowledge of epigenetic changes in gastrointestinal cancers and how this relates directly to disease progression and prognosis.

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“…The current study found CIMP-H in 22% of GCs using four MINT genes MINT1, MINT2, MINT25 and MINT31 . In other studies, CIMP was de ned by the DNA methylation status of tumor-related genes, rather than MINT genes [18][19][20] -methylguanine DNAmethyltransferase was linked to the responsiveness of brain tumors to alkylating agents. These positive relationships between the DNA methylation of cancer-related genes and therapeutic ef cacy might be implicated in the longer survival time of GC patients with CIMP-H. Our data shows that the survival time of GC patients with CIMP-H is likely to be longer than those with CIMP-L/CIMP-N GCs, but no statistical differences were observed in survival time among patients with different CIMP status.…”

Section: Discussionmentioning

confidence: 99%

CpG Island Methylator Phenotype in Primary Gastric Carcinoma

Tojo

Konishi

Yano

et al. 2013

Showa Univ J Med Sci

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: Gastric cancers GC with methylation of multiple CpG islands have a CpG island methylator phenotype CIMP and they can have different biological features. The aim of this study was to investigate the DNA methylation status of GCs and its association with their clinicopathological features. We evaluated the methylation status of four genes MINT1, MINT2, MINT25 and MINT31 in 105 primary GCs using bisul te-pyrosequencing analysis. We classi ed tumors as CIMPhigh CIMP-H , CIMP-low CIMP-L or CIMP-negative CIMP-N based on the methylation of MINT1, MINT2, MINT25, and MINT31. Overall, the prevalence of CIMP-H, CIMP-L and CIMP-N was 22% 23/105 , 52% 55/105 and 26% 27/105 , respectively. We observed a signi cant difference in tumor stage stages I-II vs. stages III-IV between CIMP-H and CIMP-N tumors P 0.0435 . No significant differences were observed in clinicopathological characteristics gender, age, location and tumor differentiation among the CIMP phenotypes. The prognoses of patients with a CIMP-H tumor is likely to be better than those with CIMP-L or CIMP-N tumors, but these differences are not statistically signi cant P 0.074 and P 0.200 . Our results suggest that CIMP may de ne a subgroup of GCs with distinct biological features.

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Aberrant CpG island methylation in early-onset sporadic gastric carcinoma

Cited by 30 publications

References 29 publications

Molecular analysis of primary gastric cancer, corresponding xenografts, and 2 novel gastric carcinoma cell lines reveals novel alterations in gastric carcinogenesis

Molecular analysis of primary gastric cancer, corresponding xenografts, and 2 novel gastric carcinoma cell lines reveals novel alterations in gastric carcinogenesis

Aberrant epigenetic patterns in the etiology of gastrointestinal cancers

CpG Island Methylator Phenotype in Primary Gastric Carcinoma

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