Abstract 5176: Expression of the atypical protein kinase C combined with expression of other factors is important for determination of structures in lateral spreading type tumors of the colon or the rectum
Authors: Ichikawa Yasushi , Ishikawa Takashi , Shimizu Daisuke , Goto Ayumu , Suwa Hirokazu , Yamagishi Shigeru , Osada Shunichi , Ota Mitsuyoshi , Fujii Shoichi , Kawamata Mayumi , Akimoto Kazunori , Nagashima Yoji , Takahashi Hirokazu , Nakajima Atsushi , Endo Itaru , Ohno Shigeo 
Published: February 2011

Background: LSTs grow superficially along the colonic wall but are short in height despite diameters larger than 10 mm. In our investigation, LSTs maintain cell polarity in spite of neoplasms comparing with polypoid-type tumor. In the present study, we examined the microscopic morphologies and functional characteristics of LSTs using immunohistochemical studies. Material and Methods: 30 LSTs and 20 polypoid-type colorectal tumors resected endoscopically or surgically in the department of Gastroenterological Surgery of Yokohama City University Hospital from 1998 to 2007, were examined. Localization of beta-catenin or E-cadherin, conservation of basement membrane and aPKCl/i were investigated by immunohistochemistry.

Results: The expression of beta-catenin was of the preserved type in 7 (87.5%) of the LST adenomas, 11 (100%) of the polypoid-type adenomas and 7 (77.8%) of the LST intramucosal cancers. The expression of beta-catenin was of the nucleic type in 5 (55.6%) and the preserved type in only 2 (22.2%) of the polypoid-type cancers in adenoma. The expression of E-cadherin was also of the cytoplasmic or preserved type in all cases of the LST adenomas and polypoid-type adenomas and 8 (88.9%) of the LST intramucosal cancers. The expression of E-cadherin was of the lost type in none (0%) of the LST adenomas and polypoid-type adenomas while it was of the lost type in 5 (55.6%) of the polypoid-type cancers in adenoma. The expression of type IV collagen was of the continuous type in 8 (100%) of the LST adenomas and 6 (66.7%) of the LST intramucosal cancers. The expression of type IV collagen was discontinuous in 8 (72.7%) of [the] polypoid-type adenomas and lost in 7 (77.8%) of the polypoid-type cancers in adenoma. The expression of type IV collagen was of the lost type in all cases of LST invasive cancers with adenoma.

Conclusion: In aPKC lambda/iota e xpression, &gt;90% of adenoma was 1+ or 2+. 87% of LST adenomas were 1+ and 45% of polypoid-type adenomas were 2+. About 70% of cancer in polypoid-type adenoma and invasive cancer of LSTs were 3+. On the other hands, about 60% of LST intramucosal cancers were 1+. LST adenomas or LST cancer in situ showed weaker expression of aPKC than polypoid-type adenomas or cancers.

In the site of strong expression of aPKCl ambda/iotab eta-catenin was expressed in nucleus and in the site of weak expression of aPKC lambda/iota, beta-catenin was expressed in cytoplasm and cell membrane

Conclusions: In the present study, we showed that in LSTs, not only adenomatous lesions, but also intramucosal cancerous lesions, maintained the characteristics of normal epithelial cells in the expression of beta-catenin, E-cadherin and Type IV collagen. They also showed weak expression of aPKC lambda/iota. (Supported by the grants of Japanese Ministry of Education, Culture, Sports and Science)

Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend.

Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5176.