| ObjectiveHPV infection plays an important role in cervial carcinogenesis. however,HPV infection is not sufficient. The inactivation and deletion of TSG is considered the main reason of carcinogenesis. LOH is the middle step of loss of TSG. The abnormal of MI indicated the instability of Gene. To investigate the role of LOH, MI and infection of HPV in the development of cervical carcinoma, we studied the incidence of LOH , MI and infection of HPV using 6 polymorphic microsatellite markers. (D10S541, D10S583, D10S1687, D3S1234, D3S1300, D3S1481) and also to analyze the relationship among them and clinico-pathological characteristics in cervical carcinoma.Methods52 invasive cancers(12 I stage,21 II stage, 14 in stage,5 IV stage) were examined,there were 40 squamous cell carcinomas,9 ade-nocarcinomas,3 adenosquamous carcinomas out of 52 and 23 high dif-feretiated, 16 moderate differetiated and 13 poor differetiated among them. 43 CIN(15 CIN 1,12 CIN II ,6 CIN I ) and 12 normal cervical tissues were examined at the same time.DNA extraction was done by means of a DEXPAT kit. Primers forsix loci and HPV E6 were chosen from the Genome Data Base. The condition of reaction was according to the describing.The products of PCR electrophoresed in 8% polyacrylamide gels. The results were visualized by silver staining. Evaluation was performed by comparison with the intensity of the own blood. Tissues were scored as exhibiting LOH( + ) if there was an absence or 50% reduction in intensity and scored as MI( + ) if there was a moving and (or) increase and scored as HPV( + ) if there was PCR products of HPV.ResultsLOH occurred in 37 out of 52 invasive cancers (71.2% ) at least one of six loci and obviously higher than GIN (13. 0% ) and normal cervical tissues ( 0% ) ( P < 0. 01). The highest incidence was in D3S1234(51.9% ) ,LOH in 3p(51.0% ) was higher than that in lOq (28.1% ) ( P <0.05 ). LOH in stage 1 and IV was obviously higher than stage I and II ?As to the incidence of LOH, it is higher in squa-mous cell carcinoma at chromosome 3p,but higher in adenocarcinoma at chromosome lOq and there is no difference among high , moderate and poor differetiated(P >0. 05). The incidence of LOH in GIN ffi was 2 fold in GIN I at 3p and was obviously higher than normal tissues (P<0.05).The rate of infection of HPV was 88.5% in invasive cancer(46/ 52) and obviously higher than that in GIN ( 34.9% ) and normal cervical tissues(8.3% ). The incidence in GIN was higher than in normal tissues (P <0. 05). The incidence of LOH in 3 p is higher in HPV ( + ) thaninHPV( -).MI occured in 10 out of 52 invase cancers (19. 2% ) and therehavn't MI in normal and CIN. All of the MI( + ) are LOH( + ). There wereS HPV( +) and 5 HPV( -) in 10 MI ( +)(P>0.05).ConclusionWe tested LOH in 6 polymorphic microsatellite markers ( D10S541, D10S583, D10S1687, D3S1234, D3S1300, D3S1481) in cervical carcinoma, LOH occurred in 37 out of 52 invasive cancers (71.2% ) at least one of six loci. It indicated these loci might be the molecule symbol of cervical carcinoma.The highest incidence was in D3S1234 (51. 9% ) , LOH in 3p (51.0% ) was higher than that in 10q(28.1% ) ( P <0.05). It indicated that the high incidence of LOH was located in 3p,the putative suppressor genes are likely to be located on specific chromosome region 3p. FHTT gene might be relation with the development of cervical carcinoma.The incidence of LOH was gradually increaced from I to IV in in-vase carcinoma and indicated LOH in 3p was the main events and played an important role and was the symbol in the development of cervical carcinoma. LOH was not the first reason but was one of the importmant causes in the development of cervical carcinoma.As to the incidence of LOH,it is higher in squamous cell carcinoma at chromosome 3p,but higher in adenocarcinoma at chromosome 10q. This might be the different TSG plays role in diffrernt pathological tumors. There is no difference among high , moderate and poor differetiated carcinomas indicated LOH had no relation...
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