下咽鳞状细胞癌中HPV感染、p16表达及其与患者预后的关系

目的探讨下咽鳞状细胞癌中HPV感染、p16表达及其与患者预后的关系。方法收集46例下咽鳞状细胞癌手术标本,应用免疫组化SP法检测p16的表达;采用PCR-DNA反向点杂交技术检测HPV感染情况,收集临床病理资料并进行随访。结果下咽鳞状细胞癌组织中HPV感染率为26.1%(12/46),HPV感染与患者年龄、性别、发病部位、分化程度、TNM分期无关(P0.05)。下咽鳞状细胞癌患者p16蛋白阳性率为39.1%(18/46),p16蛋白阳性率与患者年龄、性别、发病部位、分化程度、TNM分期无关(P0.05)。HPV感染与p16蛋白表达呈正相关(r=0.437,P=0.002)。Kaplan-Meier生存分析显示:HPV阳性者比HPV阴性者中位生存期高(P=0.001);HPV阳性者中位无进展生存期亦高于HPV阴性者(P=0.002)。p16蛋白阳性者比p16阴性者中位生存期高(P=0.001);p16蛋白阳性者中位无进展生存期亦高于p16阴性者(P=0.003)。多因素Cox回归模型分析显示:临床分期、HPV感染及p16表达,是影响患者预后的独立因素(RR值分别为1.969、4.324、0.294,P值分别为0.018、0.015、0.013)。结论下咽鳞状细胞癌中HPV感染与p16蛋白表达相关,临床分期早、HPV感染及p16阳性的患者预后较好。     

乳腺浸润性导管癌中HPV18、HPV16感染的研究

目的 :了解乳腺浸润性导管癌中HPV18、HPV16的感染情况 ,分析其是否是乳腺癌发生的危险因素及与临床病理的相关性。方法 :根据HPV16、HPV18的DNA序列 ,合成相应特异的寡核苷酸片段 ,用加尾标记法制备地高辛标记探针 ,用原位杂交法检测 5 1例乳腺浸润性导管癌、10例相应正常乳腺上皮及 15例良性乳腺病变中HPV18、HPV16的感染 ,并分析其与患者发病年龄、肿块大小及淋巴结转移的相关性。结果 :浸润性导管癌中HPV18或 16的总阳性率达 70 6 % ,其中HPV18与HPV16的阳性率分别为 5 8 8%、4 5 1% ,均明显高于正常乳腺上皮的感染率 (30 0 %、10 0 % ;P <0 0 5 ) ;乳腺良性病变的HPV18、16阳性率分别是 6 0 0 %、6 0 % ,其中HPV18的阳性率亦显著高于正常乳腺上皮 (P <0 0 5 )。结论 :(1)HPV16和18可能是乳腺浸润性导管癌发生的致病因子 ,HPV18尚可能与乳腺良性病变的发生有关。 (2 )HPV的感染与患者年龄、肿块大小及淋巴结转移无相关性。     

新疆地区贲门腺癌HPV、HP感染和p53异常改变的病理生物学意义

目的了解人乳头瘤病毒（HPV）、幽门螺杆菌（HP）感染及p53突变在新疆不同民族贲门癌发生、发展中的作用。方法应用PCR技术对90例贲门腺癌（包括哈族29例,维族30例,汉族31例;癌组织高、中、低不同分化程度分别有17、55、18例）及21例切缘正常组织进行HPV16／18和HP的检测,并用免疫组化LSAB法检测以上病例的p53异常表达;同时应用上述不同方法分别检测20例胃窦部腺癌HPV16／18、HP感染和p53的表达。结果HPV16／18和HP感染及t）53在新疆贲门腺癌患者中的阳性检出率分别为34．4％（31／90）,14．4％（13／90）和73．33％（66／90）,在切缘正常组织中的检出率分别为0、0、4．76％（1／21）;它们的阳性检出率在癌和非癌组织间差异均存在显著性（P〈0．05）;哈、维、汉各民族之间HPV16／18、HP及p53的阳性率的差异均无统计学意义（P〉0．05）;HPV16／18和HP感染阳性率与贲门腺癌病理分级及淋巴结转移无明显相关（P〉0．05）;p53的阳性表达与组织分级无关（P〉0．05）,而与淋巴结转移相关（P〈0．05）;贲门腺癌患者中p53与HPV16／18和HP的感染之间未发现相关关系（P〉0．05）。胃窦部腺癌患者中HPV16／18及HP阳性检出率分别为10％（2／20）、55％（11／20）与其在贲门腺癌的阳性检出率差异有显著性（P〈0．05）,胃窦部腺癌组织中p53的阳性检出率为80％（16／20）,与其在贲门腺癌的阳性检出率差异无显著性（P〉0．05）。结论（1）HPV16／18感染和p53的异常表达在贲门癌变过程中可能具有重要的作用,而HP感染与贲门癌的发生关系不大;胃窦部HPV16／18感染率较低,而HP感染检出率较高;（2）贲门癌组织中HPV16／18、HP感染和p53的异常表达与肿瘤病理分级和民族之间均无明显相关;p53的阳性表达与淋巴结转移相关;（3）p53的异常表达与HPV16／18或HP感染在胃贲门、幽门区腺癌的发生可能均有重要作用。     

宫颈鳞状细胞癌HPV16/18、p53、p21表达及意义

目的　探讨人乳头状瘤病毒 (HPV) 16型、18型及 p5 3、p2 1基因蛋白的表达情况以及与宫颈癌的关系。 方法　应用免疫组化二步法检测 5 0例宫颈鳞癌、4 0例正常宫颈黏膜中HPV16、HPV18、p5 3、p2 1的表达。肿瘤组分 <6 0岁和≥ 6 0岁 2个年龄组 ,观察HPV感染情况。结果　宫颈鳞癌中HPV16、HPV18、p5 3、p2 1表达分别为 4 8%、2 0 %、5 4 %和 5 0 % ,而正常宫颈黏膜中的表达分别为 10 %、0、0、10 % ,两者经统计学比较差异有显著性 (P <0 0 1) ;<6 0岁组和≥ 6 0岁组HPV16阳性率分别为 84 2 %和 2 5 8% ,年青组明显高于年老组 ,经统计学比较差异有显著性 (P <0 0 1)。结论　 (1)宫颈鳞癌的发生与HPV16、HPV18感染有密切关系 ,提示检测宫颈HPV16、HPV18感染情况对于宫颈鳞癌的随访和早期诊断有着重要的参考价值。 (2 )提示宫颈黏膜在HPV感染后 ,可能在p5 3、p2 1多种癌基因的共同作用导致宫颈鳞癌的发生发展。     

食管鳞状细胞癌癌变过程中HPV16/18 E6蛋白与PIK3CA、PIK3CB突变的相关性及其临床意义

目的 探讨HPV感染与PIK3CA、PIK3CB突变在食管鳞状细胞癌(esophageal squamous cell carcinoma, ESCC)癌变过程中的表达差异及其临床意义。方法 采用免疫组化EnVision法检测32例食管正常黏膜、35例食管低级别异型增生(low-grade intraepithelial neoplasia, LGIN)、34例食管高级别异型增生(high-grade intraepithelial neoplasia, HGIN)及137例ESCC中HPV16/18 E6蛋白、p53、PIK3CA、PIK3CB的表达，并分析蛋白表达之间的相关性及与临床病理特征的关系。结果 HPV16/18 E6蛋白在食管正常黏膜组、LGIN组、HGIN组、ESCC组的阳性率分别为0、8.6%、26.5%、29.9%,HPV16/18 E6蛋白在ESCC和HGIN中的表达高于食管正常黏膜和LGIN(P<0.05);p53蛋白在食管正常黏膜组、LGIN组、HGIN组、ESCC组的阳性率分别为9.4%、28.6%、50.0%、68.6%,p53在HGIN中的表达高于...     

HPV感染和p53异常表达与宫颈鳞癌的关系

目的研究宫颈鳞癌与p53蛋白表达和HPV感染的关系,探讨宫颈鳞癌的形成机制。方法采用RT-PCR法分别检测p53基因在39例宫颈鳞癌组织和39例正常宫颈黏膜组织中的表达情况以及PCR方法检测HPV在这些组织中的感染情况。结果 HPV在宫颈鳞癌组中阳性率为48.72%(19/39),正常组织中为14.81%(4/27),p53基因表达在宫颈鳞癌组中阳性率为53.85%(21/39),正常组织中为18.52%(5/27),宫颈癌组的HPV感染和p53表达均高于正常组(P0.05)。结论 HPV感染与p53基因的异常表达与宫颈鳞癌发生密切相关,联合检测能提高准确性。     

p16蛋白与HPV mRNA检测在口咽部鳞状细胞癌诊断中的意义

目的 探讨p16蛋白与HPV mRNA检测在口咽部鳞状细胞癌(oropharyngeal squamous cell carcinoma, OPSCC)诊断中的意义。方法 收集2019年11月～2021年10月首都医科大学附属北京同仁医院诊治的105例OPSCC,采用免疫组化EnVision两步法检测p16、Ki-67、p53蛋白表达，并检测其中61例HPV16/18 mRNA的表达，分析其与临床病理特征的关系。结果 105例OPSCC中p16蛋白阳性58例(55.24%),阴性47例(44.76%);p16蛋白阳性患者比阴性患者的吸烟、饮酒史比例低(26/58 vs 37/47,16/58 vs 31/47),以扁桃体为常见发病部位(51/58 vs 18/47),易出现淋巴结转移(43/58 vs 23/47),Ki-67增殖指数较高(73.10%vs 47.45%),p53多为野生型(57/58 vs 16/47),形态学特征以非角化型鳞状细胞癌为主(29/58 vs 15/47),差异均有统计学意义(P<0.05)。61例HPV mRNA检测结果与p16蛋白表达完全一致(...     

外阴上皮内瘤变与人乳头状瘤病毒感染的相关性

目的 探讨人乳头状瘤病毒(HPV)在外阴上皮内瘤变(VIN)中的感染情况及与p53、Ki-67蛋白表达的关系.方法 用原位杂交法(ISH)检测HPV6/11、16/18、31/33型在55例VIN及10例外阴正常皮肤组织中的表达.同时用免疫组化SP法检测p53、Ki-67蛋白的表达.结果 HPVl6/18、31/33、6/11在VINⅢ中的阳性表达率分别为60%(6/10)、20%(2/10)和0%(0/10);在VIN Ⅱ中为53.57%(15/28)、39.28%(11/28)和10.71%(3/28);在VIN Ⅰ中为17.65%(3/17)、5.88%(1/17)和29.41%(5/17);正常对照组没有表达.p53、Ki-67蛋白在VINHI中的阳性表达率分别为70%(7/10)和90%(9/10);在VINⅡ中为78.57%(22/28)和78.57%(22/28);在VIN Ⅰ中为64.71%(11/17)和35.29%(6/17);在正常对照组没有表达.经统计学分析,VINⅢ、Ⅱ组中的HPVl6/18感染与正常组差异有显著性(P＜0.05);VINⅡ组的HPV31/33感染与正常组差异有显著性(P＜0.05);VINⅢ、Ⅱ组p53、Ki-67及VIN Ⅰ组p53阳性表达率与正常组差异有显著性(P＜0.05);VIN Ⅰ组Ki-67阳性表达率与VINⅡ组相比差异有显著性(P＜0.05).结论 VIN的发生与HPV感染有关,尤其与HPVl6/18、31/33型感染密切相关.VIN与外阴癌感染的HPV型别相同.在VIN的发生发展中,HPV感染以及p53突变可能起重要的作用.     

子宫颈腺癌中HPV16/18感染对p16Ink4a、Rb蛋白表达的影响

目的研究16、18型人乳头瘤病毒(HPV16/18)DNA与细胞周期相关蛋白p16Ink4a、Rb在子宫颈腺癌中的表达情况及HPV16/18感染对p16Ink4a、Rb蛋白表达的影响。方法采用组织微阵列技术结合原位杂交和免疫组化EliVision二步法标记检测HPV16/18DNA和p16Ink4a、Rb蛋白在86例子宫颈腺癌、15例子宫颈腺上皮异型增生及24例慢性子宫颈炎组织中的表达。结果子宫颈腺癌组和子宫颈腺上皮异型增生组HPV16/18DNA阳性表达率分别为65·1%和46·7%,均明显高于慢性子宫颈炎组8·3%(P<0·01);p16Ink4a蛋白在子宫颈腺癌组的阳性表达率为74·4%,显著高于慢性子宫颈炎组33·4%(P<0·01)。Rb蛋白在子宫颈腺癌组的阳性表达率为33·7%,低于慢性子宫颈炎组45·8%,但差异无显著性(P>0·05)。HPV16/18感染与子宫颈腺癌的病理分级和组织学类型无关,但与p16Ink4a蛋白表达呈正相关(P<0·05)。p16Ink4a与Rb蛋白表达与子宫颈腺癌的病理分级有关,G2、G3组p16Ink4a阳性表达率明显高于G1组(P<0·05),G3组Rb阳性表达率明显低于G1组(P<0·05)。p16Ink4a表达与子宫颈腺癌组织学类型有明显相关性,子宫内膜样腺癌p16Ink4a阳性表达率明显高于透明细胞腺癌(P<0·05)。结论子宫颈腺癌的发生与HPV16/18感染有关,HPV16/18感染可能影响p16Ink4a、Rb蛋白表达,使子宫颈腺上皮发生癌变并促进恶性发展。     

子宫颈病变中p16~(INK4A)蛋白表达及其与HPV16/18感染的关系

目的 探讨p16INK4A 蛋白在子宫颈鳞癌(SCC)和子宫颈上皮内肿瘤(CIN)中的表达及其与HPV16/18感染的关系.方法 用原位杂交法检测HPV16/18在25例子宫颈癌、45例CIN及10例慢性子宫颈炎中的表达,同时用免疫组化EliVision法检测p16INK4A 蛋白的表达.结果 (1)与慢性子宫颈炎相比,CIN Ⅱ级、CIN Ⅲ级、浸润癌HPV16/18杂交信号阳性率显著增高(P<0.01);(2)子宫颈鳞癌组织、CIN Ⅰ级、CIN Ⅱ级、Ⅲ级及慢性子官颈炎标本中p16INK4A 蛋白阳性率分别为100.0%、20.0%、46.7%、100.0%和10.0%;(3)在子宫颈鳞癌及CIN HPV16/18感染的标本中p16INK4A 蛋白表达均是阳性.结论 子宫颈鳞癌的形成与HPV感染、p16INK4A 蛋白过表达是呈正相关关系,p16INK4A蛋白可能作为子宫颈鳞癌及CIN的标志物,对子宫颈癌筛查和预防有重要意义.     

人乳头瘤病毒与P 53协同致膀胱移行细胞癌关系的研究

目的 研究人类乳头瘤病毒（ＨＰＶ）６、１１、１６和１８型及Ｐ５３与膀胱移行细胞癌的关系。方法 采用聚合酶链反应（ＰＣＲ）方法检测了７５例膀胱移行细胞癌组织中ＨＰＶ的感染,免疫组化ＳＰ法检测Ｐ５３蛋白表达情况。结果 膀胱移行细胞癌组织中ＨＰＶ６、１１、１６和１８的阳性率分别为６．７％（５／７５）,５．３％（４／７５）,３３．３％（２５／７５）和６．７％（５／７５）。低危型ＨＰＶ（６或１１）阳性率为９．３％（７／７５）,高危型ＨＰＶ（１６或１８）阳性率为３４．７％（２６／７５）。同一膀胱癌组织中两种以上（包括两种）ＨＰＶ亚型感染８例,占１０．６％。ＨＰＶ６、１６和１８型之间感染阳性率在肿瘤有无转移组中差异显著（Ｐ〈０．０５）,ＨＰＶ１６、１８的阳性率在肿瘤病理分级中差异有极显著性（Ｐ〈０．０１）。ＨＰＶ ＤＮＡ型别     

Detection and localization of human papillomavirus in penile condylomas and squamous cell carcinomas using in situ hybridization with biotinylated DNA viral probes

Human papillomavirus (HPV) has been previously demonstrated in male genital neoplasms using Southern blot hybridization (SBH) and in situ hybridization with radiolabeled probes (ISH-R). In this study we used in situ hybridization with biotinylated DNA viral probes (ISH-B), a technique that can be applied to routinely collected and processed tissue. Thirty cases of exophytic penile condyloma acuminatum and nine cases of invasive squamous cell carcinoma of the penis were examined for the presence of HPV using ISH-B for HPV types 6, 11, 16, 18, 31, and 33. HPV DNA was found in 25 of 30 (83%) penile condylomas; HPV type 6 in 13 (43%); and HPV type 11 in 12 (40%). Slight cross-reactivity between HPV types 6 and 11 was noted. None of the condyloma cases was positive for HPV types 16, 18, 31, or 33. One of the nine patients with squamous cell carcinoma of the penis was positive for HPV 16. In situ hybridization with biotinylated DNA viral probes is a highly sensitive method for detecting and localizing HPV in penile condylomas. This method, however, may not be as sensitive as SBH for detecting HPV in invasive penile squamous cell carcinomas.     

p53蛋白在宫颈鳞状上皮内病变与宫颈癌中的过度表达及其与H…

目的 探讨宫颈鳞状上皮内病变（ＳＩＬ）和宫颈癌中抑癌基因ｐ５３基因表达水平以及与ＨＰＶ的关系。方法 用免疫组化和ＰＣＲ－ＲＦＬＰ方法，对２６８例宫颈石蜡包埋组织（２９例慢性宫颈炎、６８例ＳＩＬ、１７１例宫颈癌）进行了ｐ５３蛋白水平及多型ＨＰＶ检测。结果 宫颈癌ｐ５３蛋白的过度表达率及强阳性过度表达率高于ＬＳＩＬ，ＨＰＶ１８阳性的ＳＩＬ及宫颈癌ｐ５３蛋白的过度表达率高于ＨＰＶ１６阳性和ＨＰＶ阴性者。     

Relation between retinoblastoma and p53 proteins in human papilloma viruses 16/18 positive and negative cancers of the uterine cervix.

AIM: To ascertain the extent of retinoblastoma protein (pRB) expression in comparison to p53 protein and human papilloma viruses (HPV) 16/18 status in cervical carcinomas. METHODS: Fifty cases of invasive cervical carcinoma were HPV typed for genotypes 16 and 18 using consensus primers by polymerase chain reaction (PCR). Immunohistochemistry for pRB and p53 was done on formalin fixed tissue using microwave antigen retrieval and commercially available antibodies. RESULTS: Forty five cases were squamous carcinomas, three were adenocarcinomas, and two were adenosquamous carcinomas. Thirty one cases were HPV 16 positive and one was HPV 18. Sixteen cases showed +4 pRB expression and a further 11 were +3 positive. Seven cases were negative. Only five cases (10%) showed +4 p53 immunostaining, while seven were negative and 15 were +1. Of the 16 pRB +4 positive cases, one was negative for p53 and a further seven were +1 positive. This inverse pattern of staining between pRB and p53 had a p value of < 0.001. No correlation was observed between HPV 16/18 status and p53 and/or pRB staining. CONCLUSIONS: pRB is expressed in the majority of cases of cervical cancer (86%), with more than 75% (+4) of the tumour cell population being positive in 16 cases (32%). There appears to be a general inverse pattern of staining between pRB (high) and p53 (low) in cervical cancer. The expression of both pRB and p53 proteins is independent of the HPV 16/18 status of the tumour.     

Detection of human papilloma virus and p16 expression in high-grade adenoid cystic carcinoma of the head and neck

Squamous cell carcinoma of the head and neck, particularly basaloid squamous cell carcinoma, may be difficult to distinguish from high-grade adenoid cystic carcinoma. Evidence of human papilloma virus (HPV) infection, particularly HPV 16, is frequently found in non-keratinizing oropharyngeal squamous cell carcinoma. Immunoreactivity for p16, a surrogate marker for HPV infection, often parallels the HPV infection status in oropharyngeal squamous cell carcinoma. However, the incidence and correlation between p16 expression and HPV infection in high-grade adenoid cystic carcinoma is unknown. Sixteen cases of high-grade adenoid cystic carcinoma, three cases of dedifferentiated adenoid cystic carcinoma and eight cases of low-/intermediate-grade adenoid cystic carcinoma were identified for inclusion in the study. All cases were tested by immunohistochemistry for p16 expression and in situ hybridization for high- and low-risk HPV. Eight cases (100%) of low-to-intermediate-grade adenoid cystic carcinoma were focally positive for p16, all of which were negative for HPV. In all, 14 of 16 cases (88%) of high-grade adenoid cystic carcinoma and three cases (100%) of dedifferentiated adenoid cystic carcinoma were positive for p16; strong and diffuse staining was noted in three cases (3 of 19, 16%). Two cases (11%) of high-grade adenoid cystic carcinoma, which were also diffusely positive for p16, showed the presence of high-risk HPV. These findings suggest that the presence of HPV infection in high-grade adenoid cystic carcinoma is infrequent, even in the presence of p16 immunostaining. Nevertheless, HPV positivity should not be used to exclude the possibility of high-grade adenoid cystic carcinoma when the differential diagnosis includes squamous cell carcinoma. Moreover, although p16 overexpression is often used as a surrogate marker for HPV in squamous cell carcinoma, it cannot be used in this manner in high-grade adenoid cystic carcinoma.     

子宫颈癌及癌前病变HPV16、Ki-67的表达及其相关性

目的对子宫颈癌及癌前病变中HPV感染和增殖细胞核抗原Ki-67表达情况进行研究。方法对45例子宫颈浸润性鳞状细胞癌、5例子宫颈腺癌、35例子宫颈上皮内瘤变（CIN）和5例正常宫颈组织采用免疫组化EnVision法进行HPV16和Ki-67表达的检测。结果HPV16阳性率为78．9％（71／90）,其中HPV16阳性率在子宫颈癌组织中为76．0％（38／50）,在CIN病变中为94．3％（33／35）,在正常子宫颈黏膜上皮组织中为阴性（0／5）。Ki-67阳性细胞在正常子宫颈、CIN和子宫颈癌组织中表达逐级增加,显示Ki-67表达程度与组织学类型有关。HPV和Ki-67在CIN和癌组织中的表达呈显著相关（P〈0．005）。结论瑞安地区子宫颈癌及癌前病变组织中存在HPV感染,HPV感染可能在子宫颈癌的发生、发展中起着重要作用。联合应用Ki-67与HPV可作为筛选子宫颈癌高危个体有价值的生物学标记。     

喉癌发生中人乳头瘤病毒感染与Langerhans细胞、p53表达的关系

目的：探讨喉癌的发生机理。方法：应用免疫组化ＬＳＡＢ法对３０例喉鳞状细胞癌人乳头瘤病毒（ＨＰＶ）感染、Ｌａｎｇｅｒｈａｎｓ细胞（ＬＣ）及ｐ５３蛋白表达进行了研究。结果：２６．７％的病例可以检测到ＨＰＶ抗原成分。ＨＰＶ感染的癌旁粘膜内ＬＣ数量明显少于无感染者，且形态也发生改变。ｐ５３蛋白表达阳性率在ＨＰＶ感染组（３７．５％）明显低于ＨＰＶ检测阴性组（８３．３３％）。结论：提示ＨＰＶ、ＬＣ、ｐ５３在喉癌发生发展过程中起一定作用，且相互影响，ＨＰＶ感染引起ＬＣ数量减少，局部免疫功能降低，ＨＰＶ感染还可能通过表达的肿瘤蛋白或其他机制使抑癌基因ｐ５３失活，进而导致肿瘤的发生。     

Proliferating cell nuclear antigen but not p53 or human papillomavirus DNA correlates with advanced clinical stage in renal cell carcinoma

In this study we investigated 56 renal cell carcinomas immunohistochemically for the expression of proliferating cell nuclear antigen (PCNA) and tumour suppressor protein p53 . We also analyzed for the presence of human papilloma virus (HPV) DNA subtypes 6, 11, 16, 18, 31 and 33 by in situ hybridization. In carcinomas which showed more than 10% of PCNA positive nuclei there were significantly more cases with invasion ( P = 0.032) or metastatic disease ( P = 0.047). Nine out of 22 grade III-IV tumours (40.9%) but only six out of 30 grade I-II tumours (20%) showed more than 10% of PCNA positive cells ( P = 0.097). Patients with 10% or more PCNA positive cells in kidney tumours had more advanced disease at the time of diagnosis than those showing less PCNA positive cells ( P = 0.05).
Six p53 positive cases were found among 56 tumours (11%), but only one case had more than 10% positive cell nuclei. The presence of HPV DNA was found in 29 out of 56 cases (52%). Multiple subtypes were found in 19 cases (34%). The most commonly occurring subtypes were 18 and 33. There was no association between PCNA, p53 and the presence of HPV DNA subtypes. Because of the association of PCNA with invasion and metastatic disease, it would be worth while to study PCNA further as a possible marker for aggressiveness of renal carcinomas. Both this study and those concentrated on mutational analysis suggest that p53 is generally not important for the development of renal cell carcinoma. On the other hand, the presence of HPV DNA in these tumours implicates HPV viral infection in the aetiology of renal cancer.     

Human papillomavirus infection and anal carcinoma. Retrospective analysis by in situ hybridization and the polymerase chain reaction.

To examine the association of human papillomavirus (HPV) infection with anal squamous cell carcinoma, the authors applied the highly sensitive polymerase chain reaction (PCR) and in situ hybridization (ISH) techniques to detect HPV DNA in formalin-fixed, paraffin-embedded tissues from 18 patients. The presence of HPV types 16/18 in 3 (16.7%) of 18 patients with anal carcinoma was found, using a colorimetric ISH technique for HPV types 6, 11, 16, 18, 31, 35, and 51. Results from one of these three patients were also positive for HPV 31, 35, 51 by ISH techniques. When the same series was analyzed using the PCR and consensus primers to the L1 open reading frame of the HPV genomes, the frequency of positive patients rose to 14 (77.8%) of 18. PCR analysis of the 14 lesions containing HPV DNA, using type-specific primers and probes for HPV 6, 11, 16, 18, and 33, showed that 1 contained HPV 6, 1 contained HPV 11, 4 contained HPV 16, 1 contained HPV 18, 1 contained HPV 33, 5 contained HPV of unclassified type(s), and 1 contained a mixture of three HPV types. There was concordance between typing of cases that were positive by ISH and PCR methods. These data agree with the concept that HPV, in particular type 16, is implicated in the pathogenesis of anal cancer.