| Objective:To investigate the distribution of Human Papillomavirus genotyping in paraffin-embedded tissues in cervical cancer leision patients, and to compare the consistency between cervical cancer leision and cancer adjacent squamous intraepithelial lesion, we try to discuss the mechanism of different HPV genotyping in squamous intraepithelial lesion progressing to cervical cancer.Methods:We selected 104 cervical cancer patients'tissue from Loop electrical excison procedure (LEEP), hysterectomy and colposcopy biopsy, made paraffin sections by"Sandwich"Method, and then separated cervical cancer lesion by microdissection. When different degrees of SIL and cervical cancer lesion coexistent with the same paraffin block, we separated different lesion and detected the genotype in these samples by HPV gene chips.Results:1 There are HPV 92 positive cases in 104 cervical cancer cases, the positive rates is 88.46%. There are 10 genotypes in those cases, they are HPV-16, HPV-18, HPV-31, HPV-33, HPV-35, HPV-45, HPV-58, HPV-59, HPV-66 and HPV-73. All the genotypes we detect are high-risk types and HPV-16 (73 cases ,70.19% in all the positive cases)is the most prevalent type, following are HPV-18( 7 cases, 6.73%),HPV-33( 4 cases, 3.85%)and HPV-73(2 cases, 1.92%). There are 101 single HPV infection cases, only 1 double HPV infection case (HPV-16/33).The lowest age and highest age were 25 years old and 66 years old respectively, average age was 34 years old. HPV16 was the predominant type in all the age groups. We can detect 7 different genotypes in 25~39 age group, and that is more than other age groups.2 We found 53 cases that there are different degrees of SIL and cervical cancer lesion coexistent with the same paraffin blocks , in these cases:2.1 There are 24 adjacent cervical cancer lesions and HSIL cases in the same block, 20 cases can detect the same genotype(HPV-16 17 cases, HPV-18, -58 and -33 1 case, respectively), 1 HSIL sample can't detect HPV DNA, its cervical cancer lesion is HPV-16; 3 cases can't detect HPV DNA in both cervical cancer lesions and HSIL.2.2 There are 32 adjacent cervical cancer lesions and LSIL cases in the same block, 9 cases can detect the same genotype (HPV-16 8 cases, HPV-73 1 case);1 case can detect HPV-33 in cervical cancer lesion, but can detect HPV-16/-33 in its adjacent LSIL. 16 LSIL sample can't detect HPV DNA, their cervical cancer lesion are HPV-16 12 cases, HPV-31, -33, -66, -16/-33 1 case respectively); 6 cases can't detect HPV DNA in both cervical cancer lesions and LSIL.In different degree of SIL that coexistent with cervical cancer lesion, we found that there were 20 cases in HSIL(83.33%,20/24), 10 cases in LSIL(31.25%,10/32), there is significant different between the positive rates of HSIL and LSIL (χ2=14.957,p<0.05). We can detect the same HPV genotype in 20 cases (83.33%,20/24) cervical cancer lesions and their adjacent HSIL, the highest infection frequency of HPV genotype is HPV-16 (17 cases, 85.00%), and other genotypes are HPV-18, -33, -58( 1 case respectively, 15%); we detect the same HPV genotype in 9 cases (28.13%,9/32) cervical cancer lesions and their adjacent LSIL, the highest infection frequency of HPV genotype is HPV-16(17 cases, 85.00%), too, and the other genotype is HPV-73. There are no significant differents in HPV genotype distribution between HSIL and LSIL, when they coexistent with the same cervical cancer patients.Conclusion:1 HPV infection is the main pathogenic factor of cervical cancer, HPV-16 and HPV-18 are the main pathogenic genotype;2 Single HPV infection can't increase the risk in cervical cancer tumorigenesis than multiple HPV infection. 3 When there are different degrees of SIL and cervical cancer lesion coexistent with the same cervical cancer patients, the rate of detecting same HPV genotype in cancer and adjacent HSIL is higher than that of LSIL.4 There are no significant differents in HPV genotype distribution between HSIL and LSIL, when they coexistent with the same cervical cancer patients.
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