OBJECTIVES: To investigate the clinicopathologic and endoscopic features of precursor lesions associated with traditional serrated adenomas (TSAs). METHODS: Mutation studies for BRAF, KRAS, PIK3CA, and EGFR and immunohistochemical staining for Ki-67 were performed on 107 TSAs from 104 patients. RESULTS: Nondysplastic hyperplastic polyp (HP) or sessile serrated adenoma/polyp (SSA/P) precursor lesions were found in 56 (52.3%) TSAs, among which 32 (57.1%) cases showed a flat-elevated lesion with a type II pit pattern during endoscopy. TSAs with an SSA/P precursor lesion were usually found in the proximal colon, while TSAs with an HP or with no precursor lesion were mainly located in the distal colon and rectum (P < .001). TSAs with a precursor lesion showed a lower frequency of conventional epithelial dysplasia and KRAS mutation as well as a higher frequency of BRAF mutation compared with those with no precursor lesion (P = .002, P < .001, and P < .001, respectively). CONCLUSIONS: A significant proportion of HP or SSA/P precursor lesions accompanied by TSAs can be detected by endoscopy based on both their flat-elevated growth and type II pit patterns. The heterogeneity of TSAs in terms of clinicopathologic and molecular features correlated with the status or type of precursor lesions.
OBJECTIVES: To investigate the clinicopathologic and endoscopic features of precursor lesions associated with traditional serrated adenomas (TSAs). METHODS: Mutation studies for BRAF, KRAS, PIK3CA, and EGFR and immunohistochemical staining for Ki-67 were performed on 107 TSAs from 104 patients. RESULTS:Nondysplastic hyperplastic polyp (HP) or sessile serrated adenoma/polyp (SSA/P) precursor lesions were found in 56 (52.3%) TSAs, among which 32 (57.1%) cases showed a flat-elevated lesion with a type II pit pattern during endoscopy. TSAs with an SSA/P precursor lesion were usually found in the proximal colon, while TSAs with an HP or with no precursor lesion were mainly located in the distal colon and rectum (P < .001). TSAs with a precursor lesion showed a lower frequency of conventional epithelial dysplasia and KRAS mutation as well as a higher frequency of BRAF mutation compared with those with no precursor lesion (P = .002, P < .001, and P < .001, respectively). CONCLUSIONS: A significant proportion of HP or SSA/P precursor lesions accompanied by TSAs can be detected by endoscopy based on both their flat-elevated growth and type II pit patterns. The heterogeneity of TSAs in terms of clinicopathologic and molecular features correlated with the status or type of precursor lesions.
Authors: Mark L Bettington; Neal I Walker; Christophe Rosty; Ian S Brown; Andrew D Clouston; Diane M McKeone; Sally-Ann Pearson; Kerenaftali Klein; Barbara A Leggett; Vicki L J Whitehall Journal: Mod Pathol Date: 2014-09-12 Impact factor: 7.842
Authors: José García-Solano; María Eulalia García-Solano; Daniel Torres-Moreno; Pablo Carbonell; Javier Trujillo-Santos; Miguel Pérez-Guillermo; Pablo Conesa-Zamora Journal: Cell Oncol (Dordr) Date: 2016-02-01 Impact factor: 6.730
Authors: Tilman T Rau; Raja Atreya; Daniela Aust; Gustavo Baretton; Matthias Eck; Katharina Erlenbach-Wünsch; Arndt Hartmann; Alessandro Lugli; Robert Stöhr; Michael Vieth; Anna M Wirsing; Inti Zlobec; Tiemo Katzenberger Journal: J Pathol Clin Res Date: 2016-02-25
Authors: Jon A Lorentzen; Krzysztof Grzyb; Paula M De Angelis; Geir Hoff; Tor J Eide; Per Arne Andresen Journal: Clin Med Insights Pathol Date: 2016-09-07