scholarly journals Traditional serrated adenoma has two pathways of neoplastic progression that are distinct from the sessile serrated pathway of colorectal carcinogenesis

2014 ◽  
Vol 27 (10) ◽  
pp. 1375-1385 ◽  
Author(s):  
Jia-Huei Tsai ◽  
Jau-Yu Liau ◽  
Yu-Lin Lin ◽  
Liang-In Lin ◽  
Yi-Chen Cheng ◽  
...  
Keyword(s):  
Colorectal Carcinogenesis ◽  
Neoplastic Progression ◽  
Serrated Adenoma ◽  
Traditional Serrated Adenoma ◽  
Serrated Pathway

scholarly journals Traditional serrated adenoma has two distinct genetic pathways for molecular tumorigenesis with potential neoplastic progression

2020 ◽  
Vol 55 (9) ◽  
pp. 846-857
Author(s):  
Yoshihito Tanaka ◽  
Makoto Eizuka ◽  
Noriyuki Uesugi ◽  
Keisuke Kawasaki ◽  
Hiroo Yamano ◽  
...  
Keyword(s):  
Neoplastic Progression ◽  
Serrated Adenoma ◽  
Genetic Pathways ◽  
Traditional Serrated Adenoma

scholarly journals Pure somatic pathogenic variation profiles for patients with serrated polyposis syndrome

2021 ◽  
Author(s):  
Misaki Hidaka ◽  
Moriya Iwaizumi ◽  
Terumi Taniguchi ◽  
Satoshi Baba ◽  
Satoshi Osawa ◽  
...  
Keyword(s):  
Pathogenic Variant ◽  
Colorectal Carcinogenesis ◽  
Epigenetic Mechanism ◽  
Phenotypic Correlation ◽  
Genetic Profile ◽  
Tubular Adenoma ◽  
Serrated Adenoma ◽  
Serrated Pathway ◽  
Serrated Lesions ◽  
Genetic Profiles

Abstract Background The serrated pathway is a distinct genetic/epigenetic mechanism of the adenoma-carcinoma sequence in colorectal carcinogenesis. Although many groups have reported the genetic-phenotypic correlation of serrated lesions (SLs), previous studies regarding the serrated pathway were conducted on patients with SLs that have heterogeneous germline genetic backgrounds. We aimed to compare pure somatic genetic profiles among SLs within identical patients with SPS as a homogenous germline background. Methods We analysed SLs from one patient with SPS (Case #1) and compared DNA variant profiles using targeted DNA multigene panels via NGS among the patient’s hyperplastic polyp (HP), three sessile serrated lesions (SSLs), and one traditional serrated adenoma (TSA), in addition to leucocytes as a germline variant, and separately analysed three SSLs and one tubular adenoma (TA) within another patient with SPS (Case #2). Results In two patients, no germline pathogenic variant was observed, and a known pathogenic variant of BRAF (c.1799T > A, p.Val600Glu) was observed in one TSA and one SSL in Case #1, while three SSLs exhibited the BRAF variant in Case #2. Further, the genetic profile of TA is consistent with the adenoma-carcinoma sequence pathway profile and distinct from that of the other SLs within the same patient with SPS. Conclusions These findings of pure somatic genetic variant profiles among SLs with identical germline genetic background support the previous results analysed among SLs with heterogeneous germline genetic backgrounds.

scholarly journals Serrated Polyps and Their Alternative Pathway to the Colorectal Cancer: A Systematic Review

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Łukasz Szylberg ◽  
Marlena Janiczek ◽  
Aneta Popiel ◽  
Andrzej Marszałek
Keyword(s):  
Colorectal Cancer ◽  
Alternative Pathway ◽  
Meta Analysis ◽  
Complete Removal ◽  
Colorectal Carcinogenesis ◽  
Rapid Progression ◽  
Serrated Adenoma ◽  
Serrated Polyps ◽  
Serrated Pathway ◽  
Long Time

Colorectal cancer (CRC) is the third most frequently diagnosed cancer in the world. For a long time, only one pathway of colorectal carcinogenesis was known. In recent years, a new “alternative” pathway through serrated adenoma was described. Recent meta-analysis estimated these cancers as about 10% to 30% of all CRCs. Serrated polyps are the second most popular groups of polyps (after conventional adenomas) found during colonoscopy. Serrated polyps of the colon are clinically and molecularly diverse changes that have common feature as crypt luminal morphology characterized by glandular serration. Evidence suggests that subtypes of serrated polyps, particularly TSA and SSA/P, can lead to adenocarcinoma through the serrated pathway. Moreover, the data indicate that the SSA/P are the precursors of colorectal carcinoma by MSI and may be subject to rapid progression to malignancy. An important step to reduce the incidence of CRC initiated by the serrated pathway is to improve the detection of serrated polyps and to ensure their complete removal during endoscopy. Understanding of the so-called serrated carcinogenesis pathway is an important step forward in expanding possibilities in the prevention of CRC.

RNF43 Is an Early and Specific Mutated Gene in the Serrated Pathway, With Increased Frequency in Traditional Serrated Adenoma and Its Associated Malignancy

2016 ◽  
Vol 40 (10) ◽  
pp. 1352-1359 ◽  
Author(s):  
Jia-Huei Tsai ◽  
Jau-Yu Liau ◽  
Chang-Tsu Yuan ◽  
Yu-Lin Lin ◽  
Li-Hui Tseng ◽  
...  
Keyword(s):  
Serrated Adenoma ◽  
Traditional Serrated Adenoma ◽  
Serrated Pathway ◽  
Associated Malignancy

TRADITIONAL SERRATED ADENOMA – SIGNS OF SERRATED AND NONSERRATED TYPES OF COLON POLYPS

2019 ◽  
Author(s):  
N Ageykina ◽  
N Oleynikova ◽  
P Malkov ◽  
E Fedorov ◽  
N Danilova ◽  
...  
Keyword(s):  
Colon Polyps ◽  
Serrated Adenoma ◽  
Traditional Serrated Adenoma

Colchicine Effect in a Colonic Hyperplastic Polyp

2002 ◽  
Vol 126 (5) ◽  
pp. 615-617
Author(s):  
Michael Torbenson ◽  
Elizabeth A. Montgomery ◽  
Christine Iacobuzio-Donahue ◽  
John H. Yardley ◽  
Tsung-Teh Wu ◽  
...  
Keyword(s):  
Primary Biliary Cirrhosis ◽  
Hyperplastic Polyp ◽  
Surface Epithelium ◽  
Biliary Cirrhosis ◽  
Neoplastic Progression ◽  
Serrated Adenoma ◽  
Management Implications ◽  
Nuclear Polarity

Abstract Colchicine effect has been described recently in gastrointestinal biopsies, where it can result in accumulation of metaphase mitoses and epithelial disorganization. We describe the case of a colonic hyperplastic polyp with colchicine effect from a 52-year-old woman who was receiving colchicine for primary biliary cirrhosis. Biopsy of the polyp revealed prominent metaphase mitoses and focal loss of nuclear polarity in the surface epithelium, features that mimicked a serrated adenoma. Distinguishing between hyperplastic polyp and serrated adenoma is important because of the different management implications and the increased potential for neoplastic progression in the latter.

Su1940 Do Traditional Serrated Adenoma Coexist With Other Polyp Types?

2015 ◽  
Vol 148 (4) ◽  
pp. S-556
Author(s):  
Sara Hafezi-Bakhtiari ◽  
Stefano Serra ◽  
Richard Colling ◽  
Lai Mun Wang ◽  
Runjan Chetty
Keyword(s):  
Serrated Adenoma ◽  
Traditional Serrated Adenoma

Traditional serrated adenoma withBRAFmutation is associated with synchronous/metachronousBRAF-mutated serrated lesions

2015 ◽  
Vol 68 (6) ◽  
pp. 810-818 ◽  
Author(s):  
Jia-Huei Tsai ◽  
Chien-Hsuan Cheng ◽  
Chien-Chuan Chen ◽  
Yu-Lin Lin ◽  
Liang-In Lin ◽  
...  
Keyword(s):  
Serrated Adenoma ◽  
Traditional Serrated Adenoma ◽  
Serrated Lesions

Die Pathogenese des kolorektalen Karzinoms

Praxis ◽  
2002 ◽  
Vol 91 (39) ◽  
pp. 1589-1593
Author(s):  
Reinacher-Schick ◽  
Schmiegel
Keyword(s):  
Familiäre Adenomatöse Polyposis ◽  
Serrated Adenoma ◽  
Serrated Pathway ◽  
Genetische Instabilität

Die Identifizierung der Adenom-Karzinom-Sequenz mit ihren korrespondierenden molekulargenetischen Veränderungen hat entscheidend zum Verständnis der Pathogenese des kolorektalen Karzinoms (KRK) beigetragen. Aufgrund des häufigen biallelischen Verlustes, bzw. der Inaktivierung bestimmter Tumorsuppressorgene (APC, p53 u.a.) wird dieser Karzinogeneseweg üblicherweise «suppressor pathway» genannt. Hierfür charakteristisch ist eine genetische Instabilität auf chromosomaler Ebene. Nicht alle genetischen Veränderungen, die in der Kolonkarzinogenese eine Rolle spielen, lassen sich jedoch in dieses lineare Tumorprogressionsmodell einordnen. So entwickelt sich ein Teil der hereditären und sporadischen KRK auf dem Boden einer genetischen Instabilität auf DNA-Ebene (nachgewiesen als sog. Mikrosatelliteninstabilität, MSI). Dieser Weg der Kolonkarzinogenese wird auch «mutator pathway» genannt. Während sich die Familiäre Adenomatöse Polyposis (FAP) dem «suppressor pathway» zuordnen lässt, folgen die hereditären nicht-polypösen kolorektalen Karzinome (HNPCC) typischerweise dem «mutator pathway». Obwohl sich wahrscheinlich die meisten MSI-Karzinome ebenfalls aus kolorektalen Adenomen entwickeln, gibt es erste Hinweise, dass ein Teil der MSI-Tumoren möglicherweise aus bestimmten hyperplastischen Polypen über sog. «serrated adenoma» entsteht (sog. «serrated pathway»). In dieser Übersicht sollen die unterschiedlichen Wege der Kolonkarzinomentstehung dargestellt werden. Neben den molekularen Veränderungen sollen die morphologischen und klinischen Korrelate, die diese Karzinogenesewege kennzeichnen, aufgezeigt werden. Abschliessend werden praxisrelevante Aspekte des Themas diskutiert.

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