The Study Of Endoscopy And Molecular-mechanisms About The Relationship Of Laterally Spreading Tumor, Colorectal Adenoma And Carcinoma

Colorectal tumorigenesis is a mulpathway procedure refer to moleculargenetics and histomorphology. Treatment and diagnosis to the precancerosis ofcolorectal carcinoma timly can lower the morbidity and mortality. With thedevelopment of endoscopy, including indigo carmine and magnifyingendoscopy et al, early-stage colorectal carcinoma,laterally spreading tumor(LST) and little lesion can be diagnosed and treated. The samples can bestudied in histology and molecular biology. This article studied therelationship of LST, colorectal adenoma and carcinoma1. Study of endoscopyRecently,the application of indigo carmine and magnifying endoscopymake the observing of Laterally spreading tumor(LST), ECC, small polypouslesion or other small mucosal lesion more detailful, but now, indigo carmineand magnifying endoscopy are on the primary stage, the studies about this arevery few.This article studied the pit patterns of 78 polypous lesions of colorectumand 10 invasive carcinoma .Pit patterns of Ⅰand Ⅱwere hyperplastic polypusor inflammatory polypus and were 65.4%(17/26).39 pit patterns of ⅢL and Ⅳwere adenomatous polypus, among them ,14 were caralicular adenoma, 17were canalicular villous adenoma, 8 were villous adenoma and 8 were mixedpit pattern including 5 ⅢL + Ⅳand 3 Ⅱ+ Ⅳ.In the tumorous lesions, the pitpatterns of caralicular adenoma and canalicular villous were ⅢL mainly, butvillous adenoma were almost Ⅳ, All the invasive carcinoma have thedestructions of pit pattern even ⅤN type. The relationship between the type ofpit pattern and pathology type reflected the significance of pit pattern .Observing the pit pattern with magnifying endoscopy is simple andpractical ,it is important development of endoscopy, with it, the pathology typeand infiltration depth can be indentified more or less,and the doctor canselect the project with endoscopy or operation according to it . 29 LST were diagnosed by indigo carmine and magnifying endoscopy, 12homogenous type,15 nodular-mixed type,1 flat elevate type and 1 pseudodepressed type in them. Ⅳwas the main pit pattern(69%),3 were intramucosalcarcinoma,about 10.3% of LST. Among them, the lesions in hepatic flexue andascending colon were11, 18 were in rectum, the biggest leison was 45mm×55mm and the smallest lesion was 11mm×12mm. Ⅳwas the main pit patternand 65.5%(19/27), ⅢL was 7. Among these 7, 5 were canalicular villousadenoma.15 were villous adenoma among Ⅳpit pattern,2 were mixed type,one of them was ⅢL + Ⅳ,the pathology type was villous adenoma, anotherwas Ⅳ+ⅤA and was intramucosal carcinoma. LST is different to usual adenoma and have intimate relationship withcolorectal carcinoma according to the big study , the rate of companied withcolorectal carcinoma was 8.4~52.5% and there was study indicted LST coulddeveloped invasive carcinoma in 3 years. The feature and the tumorigenesis ofLST was focus and main aspect . The reports about LST in our country were very few .According to ourexperience,in the process of endoscopy ,it is necessary to make indigo carmineto the lesions of congestion ,rough. LST including granular type and nongranular type, it have 4 subtypeincluding homogenous type, nodular-mixed type, flat elevate type and pseudodepressed type according to our study. The pit patterns of LST are ⅢL and Ⅳmainly, ⅤA is the sign of canceration.Endoscopy is the suitable treatment about LST, EMR and EPMR are themain way. 2. Study of MolecularMechanism We study the expression and mutation of P53, Bcl-2, APC,Caspase 9,andSurvivin in the LST, colorectal adenoma and carcinoma to interpret themolecular mechanism of colorectal carninoma. ①We studied the mutation of P53 exon 5,6,7,8 with PCR-SSCP. Themutation rate of LST group was 18.2% and was similar to adenoma (20.0%).Carcinoma group was 33.3%and was higher than other groups significantly. Atthe same time, the expression of P53 was detected by immunohistochemicaltechnique (S-P). The result was that expression was negative in normal group,positive cell were weaker in adenoma group and the positive cell is stronger incarcinoma group. There were significant differences in LST, colorectaladenoma and carcinoma group. ②We detected the expression of bcl-2 with immunohistochemicaltechnique. The results were that bcl-2 was positive in basilar part, but wasnegative on surface epithelium in normal mucosa .The expression of bcl-2 incarcinoma was significantly lower than adenoma and LST groups (p<0.05). ③We investigated the mutation cluster region (MCR) of APC geneincluding 10 normal colorectal mucosa,10 LST, 18 colorectal adenoma and 20colorectal carcinoma .The results were that the mutation rates were 25%,30%and 27.8%.There were no significant difference .At the same time ,we detectedthe expression of APC gene protein production. APC protein was significantlylower than LST, colorectal adenoma and carcinoma groups .That means theinactivation of APC gene is the early molecule event in tumorigenesis . ④We detected the expression of Caspase 9 by immunohistochemicaltechnique .The results were that the expression was significantly lower in LST,colorectal adenoma and carcinoma groups than normal mucosa. That meansthe suppression of Caspase 9 suppress the apoptosis pathway and make thetumor grew.