Frequent Somatic Mutations ofhMSH3with Reference to Microsatellite Instability in Hereditary Nonpolyposis Colorectal Cancers

1997 ◽  
Vol 236 (2) ◽  
pp. 248-252 ◽  
Author(s):  
Yoshimitsu Akiyama ◽  
Naomi Tsubouchi ◽  
Yasuhito Yuasa
2011 ◽  
Vol 2011 ◽  
pp. 1-7
Author(s):  
D. Speake ◽  
J. O'Sullivan ◽  
D. G. Evans ◽  
F. Lalloo ◽  
J. Hill ◽  
...  

Aims. To compare methylation profiles, protein expression, and microsatellite instability (MSI) of sporadic, HNPCC, and familial hyperplastic polyps (HPs).Methods. Methylation-specific PCR (MSP) and pyrosequencing assessed p16, MGMT, hMLH-1, MINT 1, and MINT 31 methylation. IHC (Immunohistochemistry) assessed Ki67, CK20, hMLH-1, hMSH-2, and hMSH-6 protein expression. MSI analysis was performed on those polyps with adequate DNA remaining.Results. 124 HPs were identified 78 sporadic, 21 HNPCC, 25 familial, and the HNPCC group demonstrated no significant differences in overall methylation (P=.186Chi2). The familial group demonstrated significantly less over all methylation levels (P=.004Chi2).Conclusions. HPs that occur in HNPCC have no more worrying features at a molecular level than those patients with HPs in a sporadic setting.


1996 ◽  
Vol 87 (3) ◽  
pp. 279-287 ◽  
Author(s):  
Shi-Long Lu ◽  
Yoshimitsu Akiyama ◽  
Hiromi Nagasaki ◽  
Tadashi Nomizu ◽  
Eiichi Ikeda ◽  
...  

2001 ◽  
Vol 120 (5) ◽  
pp. A295-A295
Author(s):  
D CHANG ◽  
A GOEL ◽  
L RICCIARDIELLO ◽  
C ARNOLD ◽  
C BOLAND

2014 ◽  
Vol 146 (5) ◽  
pp. S-628
Author(s):  
Young Baek Kim ◽  
Sun-Young Lee ◽  
Jeong Hwan Kim ◽  
In Kyung Sung ◽  
Hyung Seok Park ◽  
...  

2011 ◽  
Vol 459 (1) ◽  
pp. 55-63 ◽  
Author(s):  
Jeong Mo Bae ◽  
Mi Jung Kim ◽  
Jung Ho Kim ◽  
Jae Moon Koh ◽  
Nam-Yun Cho ◽  
...  

2013 ◽  
Vol 145 (3) ◽  
pp. 540-543.e22 ◽  
Author(s):  
Alexandra E. Gylfe ◽  
Johanna Kondelin ◽  
Mikko Turunen ◽  
Heikki Ristolainen ◽  
Riku Katainen ◽  
...  

2016 ◽  
Vol 29 (04) ◽  
pp. 336-344 ◽  
Author(s):  
Jean Ashburn ◽  
Thomas Plesec ◽  
Matthew Kalady

AbstractColorectal serrated polyps are intermediate lesions in the serrated neoplastic pathway, which account for up to 30% of colorectal cancers. This pathway is biologically distinct from the adenoma-to-carcinoma sequence, with associated cancers exhibiting mutations in the BRAF oncogene, DNA promoter hypermethylation, and microsatellite instability. An evolving understanding of these unique lesions has led to the development of a more accurate classification, improved endoscopic identification, and tailored clinical management guidelines. This article reviews serrated polyps and serrated polyposis syndrome.


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