High BMI and high VFA can predict technical difficulties during laparoscopic gastric surgery and postoperative complications. Particularly, LADG should be performed cautiously to prevent surgical complications for male patients with high VFA. Predictive impact of VFA should be further determined in a larger set of patients.
Colorectal flat-type tumors include laterally spreading tumors (LSTs) and flat depressed-type tumors. The former of which shows a predominant lateral spreading growth rather than an invasive growth. The present study examined the morphological characteristics of LSTs, in comparison with polypoid- or flat depressed-type tumors, along with the expression of atypical protein kinase C (aPKC) λ/ι, a pivotal cell polarity regulator, and the hallmarks of cell polarity, as well as with type IV collagen, β-catenin and E-cadherin. In total, 37 flat-type (24 LSTs and 13 flat depressed-type tumors) and 20 polypoid-type colorectal tumors were examined. The LSTs were classified as 15 LST adenoma (LST-A) and nine LST cancer in adenoma (LST-CA). An immunohistochemical examination was performed on aPKC λ/ι, type IV collagen, β-catenin and E-cadherin. The LST-A and -CA showed a superficial replacing growth pattern, with expression of β-catenin and E-cadherin in the basolateral membrane and type IV collagen along the basement membrane. In addition, 86.6% of LST-A and 55.6% of LST-CA showed aPKC λ/ι expression of 1+ (weak to normal intensity staining in the cytoplasm compared with the normal epithelium). Furthermore, ~45% of the polypoid-type adenomas showed 2+ (moderate intensity staining in the cytoplasm and/or nucleus) and 66.7% of the polypoid-type cancer in adenoma were 3+ (strong intensity staining in the cytoplasm and nucleus). A statistically significant positive correlation was observed between the expression of aPKC λ/ι and β-catenin (r=0.842; P<0.001), or type IV collagen (r=0.823; P<0.001). The LSTs showed a unique growth pattern, different from the expanding growth pattern presented by a polypoid tumor and invasive cancer. The growth characteristics of LST appear to be caused by adequate coexpression of β-catenin, type IV collagen and aPKC λ/ι.
Aims: The clinical significance of measuring serum p53 antibodies in colorectal cancer patients was evaluated. Patients and Methods: Preoperative serum tumor markers including CEA, CA19-9 and p53 antibody were examined in 264 patients (stage I: 68, II: 73, III; 81) who were given diagnoses of colon and/or rectal cancer in Yokohama City University Hospital from 2007 to 2008. Correlativity of tumor markers to clinical findings was investigated. Results: In the overall patients, range, median and positive ratio of each tumor marker are shown in Table 1. Positive ratio of CEA and CA19-9 gradually increased according to clinical stage of the tumor, however, those of p53 showed almost the same concentration in any stage. Then, in stage I patients, positive ratio of p53 was higher than CEA and CA19-9 (p=0.0005). Thirty five cases (13.3%) of patients had synchronous or metachronous double or triple colorectal cancers. In that group, positive ratio of p53 was 48.3%, and median serum concentration of p53 was 0.915U/ml (0.15-295). Positive ratio and serum concentration of p53 of double or triple colorectal cancer patients were significantly higher than that of single cancer patients (p=0.0375). Conclusions: Serum concentration of p53 is sensitive, especially in early stage of colorectal cancer compared with other tumor markers. Colorectal cancer patients who showed high concentration of p53 have to be carefully checked for occult 2nd gastrointestinal tumor.1 nnCEA(ng/ml)CA19-9(ng/ml)p53 antibody(U/ml)Range (median)overall2640.3-3371(2.95)1-18927(12)0.15-443(0.53) Stage0180.3-5.7(1.45)1-44(9)0.15-2.36(0.28) StageI680.3-18.3(1.7)1-161(10)0.15-233(0.45) StageII730.5-148.1(3.9)1-1353(13)0.15-435.5(0.775) StageIII810.7-124.4(3.5)1-345(14)0.15-136.2(0.645) StageIV251.8-3371(23.9)1-18927(31)0.15-443(0.58) nCEA(%)CA19-9(%)p53 antibody(%)Positive ratiooverall26432.214.835.2 Stage0185.65.616.7 StageI687.45.929.4 StageII7337.012.341.1 StageIII8137.016.038.3 StaIV2588.048.036.0 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 830.
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, >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.
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