Serrated polyps of the colon and rectum (hyperplastic polyps, sessile serrated adenomas, traditional serrated adenomas, and mixed polyps)—proposal for diagnostic criteria

2010 ◽  
Vol 457 (3) ◽  
pp. 291-297 ◽  
Author(s):  
Daniela E. Aust ◽  
◽  
Gustavo B. Baretton
2009 ◽  
Vol 55 (2) ◽  
pp. 206-213 ◽  
Author(s):  
Dominique Sandmeier ◽  
Jean Benhattar ◽  
Patricia Martin ◽  
Hanifa Bouzourene

2015 ◽  
Vol 139 (6) ◽  
pp. 730-741 ◽  
Author(s):  
Hui-Min Yang ◽  
James M. Mitchell ◽  
Jorge L. Sepulveda ◽  
Antonia R. Sepulveda

Context Colorectal cancer is a heterogeneous disease resulting from different molecular pathways of carcinogenesis. Recent data evaluating the histologic features and molecular basis of the serrated polyp–carcinoma pathway have significantly contributed to more comprehensive classifications of and treatment recommendations for these tumors. Objective To integrate the most recent molecular findings in the context of histologic classifications of serrated lesions and their implications in diagnostic pathology and colorectal cancer surveillance. Data Sources Published literature focused on serrated polyps and their association with colorectal cancer. Conclusions Three types of serrated polyps are currently recognized: hyperplastic polyps, sessile serrated adenomas/polyps, and traditional serrated adenomas. The BRAF V600E mutation is one of the most frequent molecular abnormalities identified in hyperplastic polyps and sessile serrated adenomas. In contrast, in traditional serrated adenomas, either BRAF V600E or KRAS mutations can be frequently identified. CpG methylation has emerged as a critical molecular mechanism in the sessile serrated pathway. CpG methylation of MLH1 often leads to reduced or lost expression in dysplastic foci and carcinomas arising in sessile serrated adenomas/polyps.


2007 ◽  
Vol 128 (5) ◽  
pp. 445-455 ◽  
Author(s):  
Akiyoshi Mochizuka ◽  
Takeshi Uehara ◽  
Takamichi Nakamura ◽  
Yukihiro Kobayashi ◽  
Hiroyoshi Ota

2017 ◽  
Vol 48 (4) ◽  
pp. 291-298 ◽  
Author(s):  
Bita Geramizadeh ◽  
Scott Robertson

Gut ◽  
2021 ◽  
pp. gutjnl-2021-324301
Author(s):  
Dan Li ◽  
Amanda R Doherty ◽  
Menaka Raju ◽  
Liyan Liu ◽  
Nan Ye Lei ◽  
...  

ObjectiveThe longitudinal risk of colorectal cancer (CRC) associated with subtypes of serrated polyps (SPs) remains incompletely understood.DesignThis community-based, case–control study included 317 178 Kaiser Permanente Northern California members who underwent their first colonoscopy during 2006–2016. Nested within this population, we identified 695 cases of CRC and 3475 CRC-free controls (matched 5:1 to cases for age, sex and year of colonoscopy). Two expert pathologists reviewed the tissue slides of all SPs identified on the first colonoscopy and reclassified them to sessile serrated lesions (SSLs), hyperplastic polyps (HPs) and traditional serrated adenomas. SPs with borderline characteristics of SSLs but insufficient to make a definitive diagnosis were categorised as unspecified SPs. The association with development of CRC was assessed using multivariable logistic regression.ResultsCompared with individuals with no polyp, the adjusted ORs (aORs) for SSL alone or with synchronous adenoma were 2.9 (95% CI: 1.8 to 4.8) and 4.4 (95% CI: 2.7 to 7.2), respectively. The aORs for SSL with dysplasia, large proximal SSL,and small proximal SSL were 10.3 (95% CI: 2.1 to 50.3), 12.8 (95% CI: 3.5 to 46.9) and 1.9 (95% CI: 0.8 to 4.7), respectively. Proximal unspecified SP also conferred an increased risk (aOR: 5.8, 95% CI: 2.2 to 15.2). Women with SSL were associated with higher risk (aOR: 4.4; 95% CI: 2.3 to 8.2) than men (aOR: 1.7; 95% CI: 0.8 to 3.8).ConclusionIncreased risk of CRC was observed in individuals with SSLs, particularly large proximal ones or with dysplasia, supporting close endoscopic surveillance. Proximal unspecified SPs were also associated with increased risk of CRC and should be managed as SSLs.


2004 ◽  
Vol 99 (11) ◽  
pp. 2242-2255 ◽  
Author(s):  
Christopher S. Huang ◽  
Michael J. O'Brien ◽  
Shi Yang ◽  
Francis A. Farraye

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