Prognostic value of p16INK4a and p14ARF gene hypermethylation in human colon cancer

Lee, Minjin; Han, Woon Sup; Kim, Ok Kyoung; Sung, Sun Hee; Cho, Min Sun; Lee, Shi Nae; Koo, Heasoo

doi:10.1016/j.prp.2005.11.011

Cited by 56 publications

(33 citation statements)

References 38 publications

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“…34,36 In contrast, a higher frequency of hypermethylation was found in colorectal carcinomas for APC (750 vs 20% in our study) 34,36 and for CDH13 (65 vs 20% in our study). 37 In addition, frequent hypermethylation of the genes cyclindependent kinase inhibitor 2A (CDKN2A) 38,39 and Ras association domain family 1 (RASSF1A) 40,41 was found in colorectal tumors, in contrast, no hypermethylation was found in our study. Almost no hypermethylation was found in the promotor region of the PAX6 gene in colorectal carcinomas.…”

Section: Discussioncontrasting

confidence: 55%

Chromosomal and methylation alterations in sporadic and familial adenomatous polyposis-related duodenal carcinomas

et al. 2007

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Primary carcinomas of the small intestine are rare and the mechanism of their pathogenesis is poorly understood. Patients with familial adenomatous polyposis (FAP) have a high risk of developing duodenal carcinomas. The aim of this study is to gain more insight into the development of duodenal carcinomas. Therefore, five FAP-related duodenal carcinomas were characterized for chromosomal and methylation alterations, which were compared to those observed in sporadic duodenal carcinomas. Comparative genomic hybridization (CGH) and methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA) was performed in 10 primary sporadic and five primary FAP-related duodenal carcinomas. In the FAP-related carcinomas, frequent gains were observed on chromosomes 8, 17 and 19, whereas in sporadic carcinomas they occurred on chromosomes 8, 12, 13 and 20. In 60% of the sporadic carcinomas, gains in the regions of chromosome 12 were observed which were absent in the FAP-related carcinomas (P ¼ 0.04). Hypermethylation was observed in the immunoglobulin superfamily genes member 4 (IGSF4), TIMP metallopeptidase inhibitor 3 (TIMP3), Estrogen receptor 1 (ESR1), adenomatous polyposis coli (APC), H-cadherin (CDH13) and paired box gene 6 (PAX6) genes. Hypermethylation of PAX6 was only observed in FAP-related carcinomas (3/5) and not in sporadic carcinomas (P ¼ 0.02). In conclusion, in contrast to sporadic duodenal carcinomas, gains on chromosome 12 were not observed in duodenal carcinomas of patients with FAP. Identification of the genes in these regions of chromosome 12 could lead to a better understanding of the carcinogenesis pathways leading to sporadic and FAP-related duodenal carcinomas. Furthermore, hypermethylation seems to be a general feature of both FAP-related duodenal carcinomas as well as sporadic duodenal carcinomas with the exception of the PAX6 gene, which is methylated only in FAP-related carcinomas.

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Section: Discussioncontrasting

confidence: 55%

Chromosomal and methylation alterations in sporadic and familial adenomatous polyposis-related duodenal carcinomas

et al. 2007

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“…Our findings that p14 ARF expression was significantly low in mock-treated KRAS aMut colorectal cancer cells (HCT116, LoVo, LS174T, LS123, and SW620) in comparison with that in KRAS wild /p53 wild MRC5 and RKO cells (Fig. 2B and E) agree with the finding that ARF expression was frequently suppressed in many malignancies (28). Transduction of these KRAS aMut tumor cells by Ad-KRhdm2 led to increased p14 ARF , of which the fold increment was, however, much lower in comparison with that of Hdm2.…”

Section: Discussionsupporting

confidence: 90%

A Novel E1B-55kD-Deleted Oncolytic Adenovirus Carrying Mutant KRAS-Regulated hdm2 Transgene Exerts Specific Antitumor Efficacy on Colorectal Cancer Cells

Liu

et al. 2010

Molecular Cancer Therapeutics

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E1B-55kD-deleted adenoviruses have been used as conditionally replicative adenoviruses (CRAds) for therapeutic purposes in tumors with loss-of-function p53 mutation. To target cancer cells that harbor activating mutant KRAS (KRAS aMut ) but spare p53 wild normal cells, we constructed and examined by reporter assays a KRAS aMut but not p53-responsive promoter, the Δp53REP2 promoter. The Δp53REP2 promoter, derived from human double minute 2 (hdm2) P2 promoter with its p53 response elements being deleted, was used to regulate the expression of the hdm2 transgene in a novel E1B-55kD-deleted CRAd, the

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“…In the literature, aberrant p16 methylation was present in 18-61% of the lesions using the MSP method (Guan et al 1999;Liang et al 1999;Wiencke et al 1999;Esteller et al 2000;Burri et al 2001;Esteller et al 2001;Kanai et al 2001;Yi et al 2001;Hawkins et al 2002;Hibi et al 2002;Van Rijnsoever et al 2002;Maeda et al 2003;Norrie et al 2003;Schneider-Stock et al 2003;Van Rijnsoever et al 2003;Ward et al 2003;Kim et al 2005;SanzCasla et al 2005;Derks et al 2006;Iacopetta et al 2006;Ishiguro et al 2006;Lee et al 2006;Ogino et al 2006;Prall et al 2006;Goto et al 2009). Methylation frequencies examined by other methods were rather low ranging from 17 to 40% (Herman et al 1995;Ahuja et al 1997;Toyota et al 1999;Shannon and Iacopetta.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have shown that p16 methylation is a frequent phenomenon in older females (Hawkins et al 2002;Norrie et al 2003;Ward et al 2003;Ishiguro et al 2006) as well as with right-sided lesions (Hawkins et al 2002;Van Rijnsoever et al 2002;Norrie et al 2003;Ward et al 2003;Iacopetta et al 2006), circumscribed tumor margins (Norrie et al 2003), increased intratumoral/peritumoral lymphocytes (Hawkins et al 2002;Norrie et al 2003;Ward et al 2003;Iacopetta et al 2006), Crohn's type reactions (Norrie et al 2003), a mucinous phenotype (Hawkins et al 2002;Maeda et al 2003;Norrie et al 2003;Ward et al 2003;Iacopetta et al 2006), poor tumor diVerentiation (Shannon and Iacopetta 2001;Hawkins et al 2002;Van Rijnsoever et al 2002;Maeda et al 2003;Norrie et al 2003;Ward et al 2003;Lee et al 2006) and an advanced stage (Yi et al 2001;Maeda et al 2003;Ishiguro et al 2006;Goto et al 2009). This mirrors the clinicopathological features classically described with the CpG island methylator phenotype (CIMP), known to cause microsatellite instability through methylation of the hMLH1 promoter in colorectal cancers (Ahuja et al 1997;Toyota et al 1999;Hawkins et al 2002;Van Rijnsoever et al 2002Iacopetta et al 2006;…”

Section: Discussionmentioning

confidence: 99%

Aberrant p16INK4a methylation is a frequent event in colorectal cancers: prognostic value and relation to mRNA expression and immunoreactivity

Mitomi

Fukui

Tanaka

et al. 2009

J Cancer Res Clin Oncol

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Prognostic value of p16INK4a and p14ARF gene hypermethylation in human colon cancer

Cited by 56 publications

References 38 publications

Chromosomal and methylation alterations in sporadic and familial adenomatous polyposis-related duodenal carcinomas

Chromosomal and methylation alterations in sporadic and familial adenomatous polyposis-related duodenal carcinomas

A Novel E1B-55kD-Deleted Oncolytic Adenovirus Carrying Mutant KRAS-Regulated hdm2 Transgene Exerts Specific Antitumor Efficacy on Colorectal Cancer Cells

Aberrant p16INK4a methylation is a frequent event in colorectal cancers: prognostic value and relation to mRNA expression and immunoreactivity

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