Sessile serrated adenoma/polyps(SSA/Ps) are early precursor lesions in the serrated neoplasia pathway, which results in colorectal carcinomas with BRAF mutations, methylation for DNA repair genes, a Cp G island methyl...Sessile serrated adenoma/polyps(SSA/Ps) are early precursor lesions in the serrated neoplasia pathway, which results in colorectal carcinomas with BRAF mutations, methylation for DNA repair genes, a Cp G island methylator phenotype, and high levels of microsatellite instability. Some of these lesions can rapidly become dysplastic or invasive carcinomas that exhibit high lymphatic invasion and lymph node metastasis potentials. Detecting serrated lesions, including SSA/Ps with and without dysplasia/carcinoma, is critical, but SSA/Ps can be difficult to detect, are inconsistently identified by endoscopists and pathologists, and are often incompletely resected. Therefore, SSA/Ps are considered to be major contributors to "interval cancers". If colonoscopists can identify the specific endoscopic characteristics of SSA/Ps, their detection and the effectiveness of colonoscopy may improve. Here, the endoscopic features of SSA/Ps with and without dysplasia/carcinoma, including the characteristics determined using magnifying endoscopy, are reviewed in the context of previous reports. Endoscopically, these subtle polyps are like hyperplastic polyps, because they are slightly elevated and pale. Unlike hyperplastic polyps, SSA/Ps are usually larger than 5 mm, frequently covered by a thin layer called the ‘‘mucus cap'', and are more commonly located in the proximal colon. Magnifying narrow-band imaging findings, which include dark spots inside the crypts and varicose microvascular vessels, in addition to the type II-open pit patterns detected using magnifying chromoendoscopy, effectively differentiate SSA/Ps from hyperplastic polyps. The lesions' endoscopic characteristics, which include their(semi)pedunculated morphologies, double elevations, central depressions, and reddishness, and the use of magnifying endoscopy, might help to detect dysplasia/carcinoma within SSA/Ps. Greater awareness may promote further research into improving the detection, identification, and complete resection rates of SSA/Ps with and without dysp展开更多
AIM: To validate the utility of Annexin A10 as a surrogate marker of the serrated neoplasia pathway in invasive colorectal cancers(CRCs).METHODS: A total of 1133 primary CRC patients who underwent surgical resection a...AIM: To validate the utility of Annexin A10 as a surrogate marker of the serrated neoplasia pathway in invasive colorectal cancers(CRCs).METHODS: A total of 1133 primary CRC patients who underwent surgical resection at Seoul National University Hospital between January 2004 and December 2007 were enrolled.Expression of Annexin A10 was evaluated by immunohistochemistry using tissue microarray and paired to our findings on clinicopathologic and molecular characteristics of each individual.Cp G island methylator phenotype was determined by Methy Light assay and microsatellite instability was determined by high performance liquid chromatography.KRAS and BRAF mutation status was evaluated by direct sequencing and allele-specific PCR.Univariate and stage-specific survival analyses were performed to reveal the prognostic value of Annexin A10 expression.RESULTS: Annexin A10 expression was observed in 66(5.8%) of the 1133 patients.Annexin A10 expression was more commonly found in females and was associated with proximal location,ulcerative gross type,advanced T category,N category and TNM stage.CRCs with Annexin A10 expression showed an absence of luminal necrosis,luminal serration and mucin production.CRCs with Annexin A10 expression were associated with Cp G island methylator phenotype,microsatellite instability and BRAF mutation.In survival analysis,Annexin A10 expression was associated with poor overall survival and progression-free survival,especially in stage Ⅳ CRCs.CONCLUSION: Annexin A10 expression is associated with poor clinical behavior and can be used a supportive surrogate marker of the serrated neoplasia pathway in invasive CRCs.展开更多
文摘Sessile serrated adenoma/polyps(SSA/Ps) are early precursor lesions in the serrated neoplasia pathway, which results in colorectal carcinomas with BRAF mutations, methylation for DNA repair genes, a Cp G island methylator phenotype, and high levels of microsatellite instability. Some of these lesions can rapidly become dysplastic or invasive carcinomas that exhibit high lymphatic invasion and lymph node metastasis potentials. Detecting serrated lesions, including SSA/Ps with and without dysplasia/carcinoma, is critical, but SSA/Ps can be difficult to detect, are inconsistently identified by endoscopists and pathologists, and are often incompletely resected. Therefore, SSA/Ps are considered to be major contributors to "interval cancers". If colonoscopists can identify the specific endoscopic characteristics of SSA/Ps, their detection and the effectiveness of colonoscopy may improve. Here, the endoscopic features of SSA/Ps with and without dysplasia/carcinoma, including the characteristics determined using magnifying endoscopy, are reviewed in the context of previous reports. Endoscopically, these subtle polyps are like hyperplastic polyps, because they are slightly elevated and pale. Unlike hyperplastic polyps, SSA/Ps are usually larger than 5 mm, frequently covered by a thin layer called the ‘‘mucus cap'', and are more commonly located in the proximal colon. Magnifying narrow-band imaging findings, which include dark spots inside the crypts and varicose microvascular vessels, in addition to the type II-open pit patterns detected using magnifying chromoendoscopy, effectively differentiate SSA/Ps from hyperplastic polyps. The lesions' endoscopic characteristics, which include their(semi)pedunculated morphologies, double elevations, central depressions, and reddishness, and the use of magnifying endoscopy, might help to detect dysplasia/carcinoma within SSA/Ps. Greater awareness may promote further research into improving the detection, identification, and complete resection rates of SSA/Ps with and without dysp
基金Supported by Grant from Basic Science Research Program through the National Research Foundation(NRF)funded by the Ministry of Education,No.2013R1A1A2059080a grant from the Korean Health Technology R&D Project,Ministry of Health&Welfare,No.HI13C1804+2 种基金Priority Research Centers Program through the NRF funded by the Ministry of Education,Science and Technology,No.2009-0093820the NRF grant funded by the Ministry of Science,ICT,and Future planning,No.2011-0030049a grant of the Korea Health Technology R&D Project,Ministry of Health&Welfare,Republic of Korea,No.HI14C1277."
文摘AIM: To validate the utility of Annexin A10 as a surrogate marker of the serrated neoplasia pathway in invasive colorectal cancers(CRCs).METHODS: A total of 1133 primary CRC patients who underwent surgical resection at Seoul National University Hospital between January 2004 and December 2007 were enrolled.Expression of Annexin A10 was evaluated by immunohistochemistry using tissue microarray and paired to our findings on clinicopathologic and molecular characteristics of each individual.Cp G island methylator phenotype was determined by Methy Light assay and microsatellite instability was determined by high performance liquid chromatography.KRAS and BRAF mutation status was evaluated by direct sequencing and allele-specific PCR.Univariate and stage-specific survival analyses were performed to reveal the prognostic value of Annexin A10 expression.RESULTS: Annexin A10 expression was observed in 66(5.8%) of the 1133 patients.Annexin A10 expression was more commonly found in females and was associated with proximal location,ulcerative gross type,advanced T category,N category and TNM stage.CRCs with Annexin A10 expression showed an absence of luminal necrosis,luminal serration and mucin production.CRCs with Annexin A10 expression were associated with Cp G island methylator phenotype,microsatellite instability and BRAF mutation.In survival analysis,Annexin A10 expression was associated with poor overall survival and progression-free survival,especially in stage Ⅳ CRCs.CONCLUSION: Annexin A10 expression is associated with poor clinical behavior and can be used a supportive surrogate marker of the serrated neoplasia pathway in invasive CRCs.
