41例胃癌标本HPV16,18感染状况研究

目的：对本地区胃癌病人中人乳头瘤病毒（ＨＰＶ）的感染状况做一调查研究。方法：采用ＰＣＲ技术对４１例新鲜胃癌组织中ＨＰＶ１６和１８型病毒的感染进行检测。结果：４１例新鲜胃癌组织中ＨＰＶ１６型阳性率为４．８８％（２／４１）；ＨＰＶ１８型阳性率为９．７６％（４／４１）；两型合计阳性率为１４．６４％。结果：本地的ＨＰＶ１６和１８型病毒的感染率与文献报道的比较居中等水平，没有两型病毒双重感染的结果与文献报道     

人乳头瘤病毒16、18型在乳腺癌组织中的表达

目的：探讨人乳头瘤病毒（ＨＰＶ）１６、１８型感染与人乳腺癌病因学的关系。方法：采用免疫组化法（ＳＰ）检测ＨＰＶ１６、１８Ｅ６蛋白在１０例正常乳腺组织,４５例乳腺癌组织中的表达并对癌组中１３例ＨＰＶ１６、１８Ｅ６蛋白阳性材料进行ＨＰＶ１６、１８ＤＮＡ原位杂交检测。结果：癌组中ＨＰＶ１６、１８Ｅ６阳性率为５３．３％（２４／４５）,而正常乳腺组织中均为阴性表达。ＨＰＶ１６、１８ＤＮＡ阳性率为３８．５％（     

应用聚合酶链反应和核酸杂交技术研究人乳头瘤病毒与膀胱癌的相关性

目的研究人乳头瘤病毒（ＨＰＶ）与膀胱癌的关系。方法应用聚合酶链反应与核酸分子杂交方法，检测４８例膀胱癌组织中ＨＰＶ·ＤＮＡ。结果膀胱癌中ＨＰＶ１６感染率为５６．２％（２７／４８），ＨＰＶ１８感染率为８．４％（４／４８）。分化差者ＨＰＶ１６ＤＮＡ阳性率为７４％，显著高于分化好者（２７．３％Ｐ＜０．０５）。浸润性者（Ｔ２～Ｔ４）ＨＰＶ１６阳性率为７２％，明显高于浅表性者（２５％，Ｐ＜０．０５）。结论ＨＰＶ１６感染可能是膀胱癌发生、发展的重要因素。     

HPV16,HPV18感染及p53,p21基因突变与胃癌预后研究

目的：了解胃癌组织中ＨＰＶ１６、ＨＰＶ１７８的感染及Ｐ５３、Ｐ２１基因突变是否存在协同致癌作用及其与胃癌患者的预后的关系。方法：采用聚合酶链（ＰＣＲ）技术,检测６４例胃癌组织标本中人乳头瘤病毒１６、１８型感染,并采用免疫组化Ｓ－Ｐ法对胃癌Ｐ５３、Ｐ２１基因突变进行检测。结果：ＨＰＶ１６阳性率为４３．７５％,ＨＰＶ１８阴性;Ｐ５３基因突变率为４６．８７％;Ｐ２１阳性表达为５３．１２％。三项同时发生率     

人膀胱移行细胞癌内的16／18型人乳头状瘤病毒感染

目的 探讨人膀胱移行细胞癌与高危型人乳头瘤病毒感染的关系。方法 采用聚合酶链式反应（ＰＣＲ法）检测１１２例膀胱移行细胞组织（包括７５例石蜡包埋组织和３７例手术切除组织）和７例正常膀胱粘膜组织的ＨＰＶ－１６／１８感染率及ＨＰＶ－１６／１８感染与膀胱移行细胞癌病理分极及临床分期的关系。同时检测了２４例膀胱癌病人尿液沉淀中ＨＰＶ阳性率。结果 膀胱移行细胞癌的ＨＰＶ－１６／１８的总感染率为６２．５０％（７     

人乳头瘤病毒DNA6／11,16,18在成人喉乳头状瘤中的表达探讨

为探讨乳头瘤病毒在成人喉乳头状瘤的表达变化，采用原位杂交技术，用荧光素标记的人乳头瘤病毒（ＨＰＶ）６／１１，１６，１８型探针，对３６例尔马林固定，石蜡包埋的喉乳头瘤组织进行了ＨＰＶ６／１１，１６和１８型检测，结果：３６例喉乳头状瘤中２１例ＨＰＶ６Ｂ／１１阳性，３例ＨＰＶ１６阳性，ＨＰＶ１８无一例阳性，且阳性细胞主要分布于乳头浅层。结果提示喉乳头状瘤的发生与ＨＰＶ６／１１和１６型有关，乳头浅层可能是     

人乳头状瘤病毒18型DNA在乳腺癌组织中的表达

目的：探讨人乳头状瘤病毒（ＨＰＶ）１８型感染与人乳腺癌病因学之间的关系。方法：采用生物素标记的分子原位杂效技术检测柳州地区女性乳腺癌、导管内乳头状瘤和正常乳腺组织中ＨＰＶ １８ ＤＮＡ。结果：乳腺癌、导管内乳头状瘤和正常乳腺组织中ＨＰＶ １８ ＤＮＡ的阳性率分别为４８．０％、３０．０％和１６．７％。多种组织学类型的乳腺癌组织中有ＨＰＶ １８ ＤＮＡ的存在且以整合型感染为主。癌组中淋巴结转移组ＨＰＶ     

人咽喉部肿瘤组织HPV免疫组化及DNA斑点杂交的检测

用免疫组化及ＤＮＡ斑点杂交技术检测人咽喉部乳头状瘤及鳞状细胞癌组织中ＨＰＶ壳蛋白抗原及ＨＰＶ６、１１、１６、１８型ＤＮＡ《结果显示，５例正常粘膜、１５例声带息肉ＨＰＶ抗原及ＤＮＡ检测均阴性。１１例乳状状瘤ＨＰＶ怕与ＨＰＶＤＮＡ阳性率均为４５．５％。２２例鳞状细胞癌ＨＰＶ抗原阳性率为２２．７％，ＨＰＶＤＮＡ阳性率为２７．３％，乳头瘤ＨＰＶ检出率与组织学的检查的结果相符。结果提示咽喉部乳头瘤及鳞状细胞     

应用 PCR 方法检测大肠癌组织中的 HPV DNA

本文采用聚合酶链式反应（ＰＣＲ）的方法，对２０例大肠癌患者的手术切除标本进行了人体乳头瘤病毒（ＨＰＶ）ＤＮＡ的检测。结果发现４例（２０％）ＨＰＶ１６型扩增阳性，其中１例显示ＨＰＶ１６．１８型双重阳性。初步表明大肠癌组织中存在ＨＰＶ的感染。     

人乳头瘤病毒感染和p53基因突变与宫颈癌的关系

目的：探讨人乳头瘤病毒１６和１８型及抑癌基因ｐ５３突变对宫颈的致癌作用以及ＨＰＶ感染与ｐ５３基因突变的相关性。方法：采用聚合酶链反应技术和限制性睛段多态性分析技术对３４例原发性宫颈癌组织及３０例正常宫颈组织ＨＰＶ１６，１８型ＤＮＡ及抑癌基因ｐ５３的基因突变进行了检测。     

Role of human papillomavirus in the development of urothelial carcinoma

It has been estimated that almost 10% of the worldwide cancer burden is linked to human papillomavirus (HPV) infection. Although the association between HPV and bladder carcinoma has been extensively investigated, data on the role of HPV in bladder carcinogenesis are controversial. The aim of the study was to assess the possible role of human papillomavirus in the development of urothelial bladder carcinomas. Formalin-fixed and paraffin-embedded archival tissue samples were used for DNA extraction. Seventy urothelial bladder carcinoma tissues were screened by nested-polymerase chain reaction (PCR) for HPV DNA with a control group of total 18 cervical tissues with invasive cervical carcinoma and cervical intraepithelial neoplasia III (CIN III). In the study group, we did not find HPV DNA positivity in any of the urothelial carcinomas. In the control group, 15 out of 18 (83.3%) samples were positive for the HPV DNA. These results indicated that there was no association between HPV infection and urothelial carcinomas.     

Low incidence of human papillomavirus type 16 DNA in bladder tumor detected by the polymerase chain reaction.

Human papillomavirus (HPV) detection was done using the polymerase chain reaction technique on tumor tissue from 44 patients with transitional cell carcinoma of the urinary bladder. Only one of the 44 was associated with HPV infection. The HPV-positive patient was not known to have immunodeficiency or genital warts, and the tumor was not morphologically different from the other tumors. Control experiments excluded the possibility that this finding was caused by contamination of the sample. This study confirms that HPV infection is a rare condition in bladder carcinoma.     

High frequency of human papillomavirus infection in carcinoma of the urinary bladder.

BACKGROUND AND METHODS. The prevalence of type 6, 11, 16, 18, and 33 human papillomavirus (HPV) was investigated with the polymerase chain reaction (PCR) on formalin-fixed, paraffin wax-embedded material, including 48 neoplastic and 21 normal urinary bladder specimens. The PCR-amplified DNA were analyzed by gel electrophoresis and dot blot and Southern blot hybridization. Some tissues were tested further by nonisotopic in situ hybridization. RESULTS. HPV DNA was detected in 39 (81%) of 48 carcinomas and 7 (33%) of 21 normal urinary bladder specimens. The presence of high-risk HPV (types 16, 18, and 33) was increased significantly in carcinoma cases (62%) as compared with normal specimens (14%) (P less than 0.01). Similarly, multiple HPV infections were significantly higher in carcinoma (60%) than in the normal tissues (5%) (P less than 0.01). The overall and high-risk HPV infections in both neoplastic and normal specimens were distributed almost equally in male and female patients. There was no significant correlation between positive results for HPV and histologic grades of the carcinoma. CONCLUSIONS. These results demonstrate that the urinary bladder in both sexes is another site where infection with the common genital tract HPV may carry a risk of malignant transformation.     

Etiologic role of human papillomavirus infection in bladder carcinoma

BACKGROUND:

The authors elucidated an etiologic role of human papillomavirus (HPV) infection in carcinoma of the bladder.

METHODS:

One hundred seventeen of 224 patients with bladder carcinoma who were treated between 1997 and 2009 were enrolled in this study. The presence of HPV DNA was tested on frozen carcinoma tissues that were obtained by transurethral resection using a polymerases chain reaction‐based method. Localization of HPV was observed on archival tissue specimens by in situ hybridization (ISH) for high‐risk HPV DNA. Cyclin‐dependent kinase (CDK) inhibitor 2A (inhibits CDK4) (p16‐INK4a) and minichromosome maintenance protein‐7 (mcm‐7)—surrogate markers for high‐risk HPV‐E7 oncoprotein—and HPV‐L1 (capsid) protein expression were evaluated by immunohistochemistry.

RESULTS:

HPV types 16, 18, 31, 33, 52, and 58, and an unknown HPV type were detected in 18 of 117 samples (15%) from patients with bladder carcinoma. HPV16 was identified in 6 samples, HPV18 was identified in 4 samples, and HPV33 was identified in 3 samples. All were single HPV type infections. HPV was detected in 38% (12 of 28) of histologic grade 1 bladder carcinomas, 8.5% (6 of 71) of grade 2 bladder carcinomas, and in 0% (0 of 18) of grade 3 bladder carcinomas. Multivariate analysis indicated that younger age (<60 years; odds ratio [OR], 10.9; 95% confidence interval [CI], 2.6‐45.3) and grade 1 tumors (OR, 4.5; 95% CI, 1.2‐17.0) were associated with HPV infection. ISH analysis indicated that high‐risk HPV DNA was localized in the nuclei of tumor cells of all HPV‐positive samples. p16‐INK4a and mcm‐7 were expressed in 94% and 89% of HPV‐positive carcinoma cells, respectively. HPV‐L1 protein expression, which suggested reproductive HPV infection, was not observed in any carcinoma.

CONCLUSIONS:

The current results indicated that high‐risk HPV is likely to be a causative agent of some low‐grade bladder carcinomas that develop in younger patients. Cancer 2011. © 2010 American Cancer Society.     

Association of human herpesvirus type 6 DNA with human bladder cancer

We examined the presence of human herpesvirus type 6 (HHV6) DNA in a series of 74 bladder carcinomas from a Mediterranean population to elucidate their possible role as cofactor in the development of bladder cancer with or without associated human papillomavirus (HPV) infection. HHV-6 type B DNA was present in 5 men (6.8%) out of the 74 tumors investigated; two of them had associated HPV-16 DNA in the same specimen. In one case that had associated urothelial carcinoma in situ, both HHV-6B and HPV-16 DNA were present. In conclusion, the low incidence of HHV-6B in bladder cancer and the ubiquitous nature of HHV-6 infection are more consistent with a bystander role rather than cofactor in the oncogenesis of bladder cancer.     

Presence and physical state of HPV DNA in prostate and urinary-tract tissues.

Neoplastic and non-neoplastic tissues from the urinary tract and the prostate were analyzed for the presence of human papillomavirus (HPV) DNA. The analysis was performed by PCR using primers specific for HPV 6/11 and 16. HPV DNA was present in bladder, ureter, kidney and prostate, with percentages ranging between 46% and 87%. Benign and oncogenic HPV types were detected with similar frequencies both in non-neoplastic and in neoplastic biopsies, and HPV 16 was not preferentially associated with malignant lesions. In all instances, small amounts of HPV DNA were present in the tissues, suggesting the absence of productive infection. Analysis of the physical state of HPV DNA performed by 2-dimensional gel electrophoresis and Southern blot hybridization revealed that HPV 16 DNA harbored in the urinary tract can be integrated also in non-neoplastic tissues. The results indicate that HPV 16 does not seem to be associated with urinary-tract and prostate oncogenesis, but that these tissues may represent an important reservoir for the transmission of HPV types normally infecting the genital tract.     

HPV16/18在膀胱癌中表达及其与bFGF、cyclinD1和cyclinE的相关关系

目的探讨人乳头瘤病毒(HPV)16/18与膀胱癌发病之间关系及其作用机制.方法应用免疫组化方法检测78例膀胱癌标本和11例正常膀胱组织中HPV16/18、碱性成纤维细胞生长因子(bFGF)、细胞周期蛋白(cyclin)D1和cyclinE的表达及相关关系.结果膀胱癌中HPV16/18阳性率为65.4%,显著高于正常的27.3%;而且与肿瘤病理分级、分期相关,但与肿瘤复发无相关.膀胱癌中HPV16/18与bFGF及cyclinD1表达之间有显著相关性,但与cyclinE表达之间无显著相关性.结论HPV16/18感染参与膀胱癌发病过程,而且通过多途径发挥作用.     

Human papilloma virus and p53 expression in bladder cancer in Egypt: Relationship to schistosomiasis and clinicopathologic factors

The aim of the current study was to compare the role of p53 and human papillomavirus (HPV) in schistosomiasis-related and schistosomiasis-unrelated carcinoma of the urinary bladder. To achieve this aim, we investigated 114 bladder carcinomas for p53 oncoprotein expression by immunohistochemistry and for human papillomavirus by in situ hybridization technique. The results revealed that 64 tumors (56.1%) were schistosomiasis-associated. Sixty seven (58.8%) were transitional cell carcinomas and 32 (28%) were squamous cell carcinomas. The remaining 15 tumors (13.2%) included adenocarcinomas and sarcomatoid carcinomas. In both schistosomiasis-associated and non-associated carcinomas, p53 oncoprotein expression was significantly higher in poorly differentiated tumors. However, it was significantly higher in locally more invasive tumors in the schistosomal carcinomas only. HPV types 16/18 could be detected in 1 of the 114 bladder carcinomas (0.95%), which was schistosomiasis-related squamous cell carcinoma in situ. These results suggest that p53 immunohistochemistry can be a prognostic factor in both schistosomal and nonschistosomal bladder cancer. More importantly, HPV does not seem to play a role in the pathogenesis of either type of bladder cancer in our country.(Pathology Oncology Research Vol 12, No 3, 173–178) An erratum to this article is available at .     

The Aetiological Role of Human Papillomavirus in Colorectal Carcinoma: An Iranian Population- Based Case Control Study

Background: Human papillomavirus (HPV) is one of the most common sexually transmitted infectionsworldwide and the association between HPV infection and genital cancers has been well established. This studyconcerned the possible role of HPV infection in colorectal carcinoma (CRC) in the Iranian population. Materialsand Methods: We examined 80 tissues obtained from patients with colorectal cancer consisting of 58 colon cancersamples and 22 rectal cancer samples and 80 tissues from patients with unremarkable pathologic changes asmatched controls by sex, study center and anatomical sites. HPV infection and genotypes were detected usingnested PCR and sequencing methods, respectively. Results: HPV DNA was detected in 5/80 (6.25%) cases including1 of 22 (4.54%) patients with rectum cancer and 4 of 58 (6.9%) patients with colon cancer and 1/80 (1.25%) ofcontrols. Furthermore, HPV-18 was detected as the most frequent type and we found no significant correlationbetween prevalence of HPV infection and anatomical sub- sites. Conclusions: Although a causal relation betweenhuman papillomavirus and colorectal cancer was not found through this study, analysis of medical recordspointed to a possible role for high- risk types of HPV in increasing the potential of aggressiveness in colorectalcancer. This study shows a particular frequency of HPV genotypes in patients with colorectal cancer in Iran.Since HPV vaccines are limited to a few types of virus, using cohort studies in different geographical zones toscreen for patterns of HPV infection in different organs might increase the efficacy and optimization of thecurrent vaccines.     

Prevalence and Distribution of High- and Low- Risk HPV Genotypes in Women Living in the Metropolitan Area of Naples: A Recent Update

Introduction: Human papillomavirus (HPV) can infect both male and female genitals, skin, and mucous membranes, causing benign or malignant lesions. HPV is a common sexually transmitted infection and it is the main cause of cervical cancer. The present retrospective study updated the previously published data on HPV genotypes distribution among women living in Naples. Materials and methods: In this study, 502 cervical scrape specimens were collected from women with abnormal cytological indication and analyzed for HPV DNA identification by Linear Array HPV genotyping test. Results: The HPV infection rate was 24.1%. HPV-16 (14.6%) was the most representative HR-HPV genotypes, followed by HPV-31 (13.8%), -18 (9.2%), and HPV-51 (8.5%). In addition, HPV-42 (16.4%) was the most prevalent genotype among LR-HPV  genotypes (low-risk human papillomavirus). It was also found that women at the age group of 23-29 years (42.5%) were at the highest risk of HPV infection. It was found that the HPV-16 frequency decreased, but HPV-31 and -18 frequency increased a little. The LR HPV-53 frequency decreased, leaving the first place for abundance to the LR HPV-42. HPV-6 frequency did not change. LR HPV -11 was no more present. Merging <23 and 23-29 age classes into one class followed the same result. Conclusion: HPV prevalence declined in comparison to the previous data. A frequency variation was recorded for several genotypes in this study.  Data can be useful to implement the preventative strategies and to promote HPV vaccination.