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目的:探讨人类乳头状瘤病毒(Human Papillomavirus,HPV)感染和抑癌基因P16的失活与喉癌(Laryneal carcinoma,LC)和喉乳头状瘤(Laryngeal papilloma,LP)发生的相关性,以进一步阐明LC和LP的病因和发病机理。方法:收集LP 46例[其中成人型喉乳头状瘤(ALP)21例,青少年型喉乳头状瘤(JLP)25例]、LC 26例、癌旁正常组织6例、声带小结15例,用标记的HPV_(1,6,8,11,13,16,18,30,31,32,33,45,51)通用引物直接法原位PCR方法和免疫组化(SP法)方法分别检测HPV-DNA和P16蛋白。结果:1、HPV阳性率JLP组(84%,21/25)显著高于ALP组(38.1%,8/21)、LC组(19.2%,5/26)、声带小结组(0%,0/15)和癌旁组织组(0%,0/6)(卡方检验,P<0.05);而ALP组、LC组、声带小结组和癌旁组织组之间HPV阳性率无显著差别(卡方检验或Fisher’s精确概率法,P>0.05)。2、P16蛋白的阳性率ALP组(57.1%,12/21)和LC组(38.5%,10/26)均显著低于JLP组(88%,22/25)、癌旁组织组(100%,6/6)和声带小结组(93.3%,14/15)(卡方检验,P<0.05);ALP组和LC组之间及JLP组和声带小结组之间P16蛋白阳性率无显著差别(卡方检验,P>0.05)。3、LP中P16蛋白的阳性率在HPV阳性和阴性组中有显著差别(x~2检验,P<0.05);喉癌中P16蛋白的阳性率在HPV阳性组和阴性组中无显著差别(Fisher’s精确概率法,P>0.05)。结论:青少年型喉乳头状瘤的发生与HPV感染密切相关而与抑癌基因P16的失活无明显相关。成人型喉乳头状瘤和喉癌的发和与HPV感染可能无明显关系,而与抑癌基因P16的失活密切相关。HPV感染和P16基因失活在致瘤过程中无明显协同作用。
Objective: To investigate the relationship between human papillomavirus (HPV) infection and inactivation of tumor suppressor gene P16 and the development of Laryngeal carcinoma (LC) and Laryngeal papilloma (LP) Elucidate the etiology and pathogenesis of LC and LP. Methods: Forty-six patients with LP, including 21 cases of adult laryngeal papilloma (ALP) and 25 cases of juvenile laryngeal papilloma (JLP), were enrolled in this study. LC (26 cases), paracancer normal tissue (6 cases) and vocal nodules Labeled HPV_ (1,6,8,11,13,16,18,30,31,32,33,45,51) universal primer direct in situ PCR method and immunohistochemistry (SP method) were detected HPV -DNA and P16 protein. The positive rates of HPV in JLP group (84%, 21/25) were significantly higher than those in ALP group (38.1%, 8/21), LC group (19.2%, 5/26), vocal nodules group (0%, 0 / 15) and paracancerous tissues (0%, 0/6) (chi square test, P <0.05). There was no significant difference in HPV positive rates between ALP, LC, Chi-square test or Fisher’s exact test, P> 0.05). The positive rate of P16 protein in ALP group (57.1%, 12/21) and LC group (38.5%, 10/26) were significantly lower than those in JLP group (88%, 22/25) , 6/6) and vocal nodules (93.3%, 14/15) (chi square test, P <0.05). There was no significant difference in the positive rates of P16 between ALP and LC groups and between JLP and vocal nodules (Chi-square test, P> 0.05). The positive rate of P16 protein in LP was significantly different between HPV positive and negative groups (P <0.05). The positive rate of P16 protein in laryngeal carcinoma was not significantly different between HPV positive group and negative group Fisher’s exact test, P> 0.05). Conclusion: The incidence of juvenile laryngeal papilloma is closely related to HPV infection but not to the inactivation of tumor suppressor gene P16. The development of human laryngeal papilloma and laryngeal carcinoma may not have a significant relationship with HPV infection, but is closely related to the inactivation of tumor suppressor gene P16. HPV infection and P16 gene inactivation in the process of tumor no significant synergy.