PT - JOURNAL ARTICLE AU - CARLOS A. RUBIO AU - ANN KAUFELDT AU - RAFAT KOHA AU - MARIKO USHOIDA AU - JENNY LINDAHL AU - LORAND L. KIS TI - β-Catenin Helices in the Cytoplasm of Sessile Serrated Adenoma/Polyps and Conventional Colorectal Adenomas DP - 2015 Feb 01 TA - Anticancer Research PG - 929--934 VI - 35 IP - 2 4099 - http://ar.iiarjournals.org/content/35/2/929.short 4100 - http://ar.iiarjournals.org/content/35/2/929.full SO - Anticancer Res2015 Feb 01; 35 AB - 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.