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Fig. 4 | Diagnostic Pathology

Fig. 4

From: Molecular characterization of sessile serrated adenoma/polyps with dysplasia/carcinoma based on immunohistochemistry, next-generation sequencing, and microsatellite instability testing: a case series study

Fig. 4

Schematic representation of differences in the molecular biological expressions and genetic alterations in the serrated neoplasia pathway. Sessile serrated adenoma/polyp (SSA/P) is an early precursor lesion in the serrated neoplasia pathway that progresses to cytological dysplasia and results in BRAF-mutated colorectal carcinomas that are commonly high levels of microsatellite instability (MSI-high) (diagram A) or microsatellite-stable (MSS) (diagram B). Both pathways are associated with a CpG island methylator phenotype and WNT/β-catenin signaling activation. a The upper arm, driven by BRAF mutation and MLH1 methylation, indicates progression to BRAF-mutated MSI-high carcinoma. FBXW7 mutations are potentially involved in progression of this pathway. b The lower arm, driven by BRAF mutation and methylation of unspecified tumor-suppressor genes, involves progression to BRAF-mutated MSS carcinoma. TP53 mutations are potentially involved in progression of this pathway

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