β-catenin helices in the cytoplasm of sessile serrated adenoma/polyps and conventional colorectal adenomas.

Initiation and progression in conventional adenomas is triggered by deregulation of WNT/β-catenin signaling. In the absence of WNT signal (off-state), β-catenin prevents phosphorylation of GSK3β, leading to aberrant nuclear accumulation in human tumors. It has been postulated that mutations in the β-catenin gene are always associated with a morphologically-neoplastic course. While investigating the nuclear expression of β-catenin in 170 colorectal biopsies, we observed a non-previously reported phenomenon, namely the presence of β-catenin cytoplasmic helices in 29% (n=7) of 24 sessile serrated adenoma/polyps (SSA/P), in 24% (n=13) of 54 adenomas, in 8% (n=3) of 38 specimens with IBD, but in none (0/54) with normal mucosa. The earliest β-catenin helices were found at the bottom of SSA/P glands (the domain of stem cells in the colorectal mucosa). It is submitted that β-catenin helices might highlight a non-previously described cytoplasmic phenomenon evolving during the serrated-carcinoma pathway in SSA/P, and during the adenoma-carcinoma pathway in conventional adenomas.