scholarly journals Diagnostic sensitivity for invasive cervical carcinoma of high risk HPV tests performed on SurePath™ liquid-based pap specimens

2013 ◽  
pp. 101 ◽  
Author(s):  
Keith Nance
2015 ◽  
Vol 123 (7) ◽  
pp. 421-427 ◽  
Author(s):  
Xiang Tao ◽  
Christopher C. Griffith ◽  
Xiangrong Zhou ◽  
Zhiheng Wang ◽  
Yabin Yan ◽  
...  

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 714
Author(s):  
Matthias Läsche ◽  
Horst Urban ◽  
Julia Gallwas ◽  
Carsten Gründker

Cervical cancer is responsible for around 5% of all human cancers worldwide. It develops almost exclusively from an unsolved, persistent infection of the squamocolumnar transformation zone between the endo- and ecto-cervix with various high-risk (HR) human papillomaviruses (HPVs). The decisive turning point on the way to persistent HPV infection and malignant transformation is an immune system weakened by pathobionts and oxidative stress and an injury to the cervical mucosa, often caused by sexual activities. Through these injury and healing processes, HPV viruses, hijacking activated keratinocytes, move into the basal layers of the cervical epithelium and then continue their development towards the distal prickle cell layer (Stratum spinosum). The microbial microenvironment of the cervical tissue determines the tissue homeostasis and the integrity of the protective mucous layer through the maintenance of a healthy immune and metabolic signalling. Pathological microorganisms and the resulting dysbiosis disturb this signalling. Thus, pathological inflammatory reactions occur, which manifest the HPV infection. About 90% of all women contract an HPV infection in the course of their lives. In about 10% of cases, the virus persists and cervical intra-epithelial neoplasia (CIN) develops. Approximately 1% of women with a high-risk HPV infection incur a cervical carcinoma after 10 to 20 years. In this non-systematic review article, we summarise how the sexually and microbial mediated pathogenesis of the cervix proceeds through aberrant immune and metabolism signalling via CIN to cervical carcinoma. We show how both the virus and the cancer benefit from the same changes in the immune and metabolic environment.


2012 ◽  
Vol 119 (3) ◽  
pp. 253-256 ◽  
Author(s):  
Krishnakumar Vinodhini ◽  
Santhanam Shanmughapriya ◽  
Sumathy Sanmugham ◽  
Ganesan Senthikumar ◽  
Bhudev C. Das ◽  
...  

2013 ◽  
Vol 2 (1) ◽  
pp. S33
Author(s):  
Angelique Levi ◽  
Kevin Schofield ◽  
Malini Harigopal ◽  
David Chhieng

2005 ◽  
Vol 86 (12) ◽  
pp. 3235-3241 ◽  
Author(s):  
Marc Fiedler ◽  
Sigrun Ressler ◽  
Beatriz Campo-Fernández ◽  
Andreas Laich ◽  
Lars Jansen ◽  
...  

E7 proteins are major oncoproteins of high-risk human papillomaviruses (HPVs), which play a key role in cervical carcinogenesis. These proteins have been shown to immortalize primary human cells. Due to the absence of antibodies with suitable sensitivity and specificity, little is known about expression of the E7 oncoproteins in naturally infected tissues. Recently, high-level expression of the E7 protein of HPV-16, the most prevalent oncogenic HPV type, was demonstrated in cervical carcinomas by immunohistochemistry; however, approximately 15 additional high-risk HPV types are known to be associated with cervical carcinoma. It is unknown whether the E7 oncoproteins of HPV-18 and -45, the second and third most prevalent HPV types, are expressed in cervical cancers. Using antibodies against HPV-18 and -45 E7 proteins, it is shown here for the first time that the HPV-18 and -45 E7 proteins can be detected in cervical carcinoma biopsies. Together with anti-HPV-16 E7 antibodies, this could create the possibility of detecting E7 oncoproteins in approximately 80 % of all cervical cancers.


BMJ ◽  
2019 ◽  
pp. l1207 ◽  
Author(s):  
Jiayao Lei ◽  
Bengt Andrae ◽  
Alexander Ploner ◽  
Camilla Lagheden ◽  
Carina Eklund ◽  
...  

Abstract Objectives To examine the association of cervical cytology screening with the risk of adenosquamous cell carcinoma (ASC) and rare histological types of invasive cervical carcinoma (RICC), using comprehensive registry data, and to assess tumour human papillomavirus status of ASC and RICC. Design Nationwide, population based, nested case-control study. Setting Sweden. Participants All cases of invasive cervical carcinoma in Sweden during 2002-11 (4254 confirmed cases after clinical and histopathological review). 338 cases were neither squamous cell carcinoma nor adenocarcinoma, including 164 cases of ASC and 174 cases of RICC (glassy cell carcinoma, clear cell carcinoma, small cell carcinoma, neuroendocrine cell carcinoma, large cell carcinoma, and undifferentiated carcinoma). 30 birth year matched controls from the general Swedish population were matched to each case by applying incidence density sampling. Main outcome measures Conditional logistic regression was used to calculate odds ratios, interpreted as incidence rate ratios, for risk of ASC and RICC in relation to screening status and screening history, adjusted for education. Human papillomavirus distribution of ASC and RICC was based on available archival tumour tissues from most Swedish pathology biobanks. Results Women with two screening tests in the previous two recommended screening intervals had a lower risk of ASC (incidence rate ratio 0.22, 95% confidence interval 0.14 to 0.34) and RICC (0.34, 0.21 to 0.55), compared with women without any test. High risk human papillomavirus was detected in 148/211 (70%) cases with valid human papillomavirus results from tumour tissues. The risk reduction among women with tumours that were positive (incidence rate ratio 0.28, 0.18 to 0.46) and negative (0.27, 0.13 to 0.59) for high risk human papillomavirus was similar, compared with women who did not attend any test. Conclusions Cervical screening is associated with reduced risk of ASC and RICC, and most ASC and RICC are positive for high risk human papillomavirus. This evidence provides a benchmark for evaluating future cervical screening strategies.


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