scholarly journals PERIANAL SQUAMOUS CELL CARCINOMA WITH HIGH-GRADE ANAL INTRAEPITHELIAL NEOPLASIA IN AN HIV-NEGATIVE PATIENT

2013 ◽  
Vol 18 (1-2) ◽  
Author(s):  
E. A. R. Dobao ◽  
L. A. Afonso ◽  
C. Pires ◽  
B. Kawa Kac ◽  
L. D. V. Fonseca ◽  
...  
2003 ◽  
Vol 5 (4) ◽  
pp. 353-357 ◽  
Author(s):  
J. Mullerat ◽  
L. F. Wong Te Fong ◽  
S. E. Davies ◽  
M. C. Winslet ◽  
C. W. Perrett

2012 ◽  
Vol 136 (11) ◽  
pp. 1359-1365 ◽  
Author(s):  
Alfred Wellenhofer ◽  
Hermann Brustmann

Context.—Human telomerase reverse transcriptase (hTERT), an enzyme that enables cells to overcome replicative senescence and to divide indefinitely, is overexpressed in many cancers and their precursor lesions. Objective.—To test whether hTERT expression is related to neoplastic progression and resistance to apoptosis in vulvar epithelia. Design.—Immunoexpression of hTERT was evaluated in 101 formalin-fixed, paraffin-embedded archival vulvar epithelia consisting of normal squamous vulvar epithelia (n  =  25), lichen sclerosus (n  =  10), high-grade classic vulvar intraepithelial neoplasia (n  =  16), differentiated vulvar intraepithelial neoplasia (n  =  18), and vulvar invasive keratinizing squamous cell carcinoma (n  =  32) and related to survivin and p53 expression. Immunostaining for all factors was scored for moderate and strong intensities with regard to quantity to determine upregulation and overexpression (score 0, 0% immunoreactive cells; score 1+, <5% immunoreactive cells; score 2+, 5% to 50% immunoreactive cells; score 3+, >50% immunoreactive cells). Score 3+ was considered as overexpression. Results.—Nuclear hTERT immunoexpression was closely related to survivin reactivity, increased from normal vulvar squamous epithelia to lichen sclerosus and to high-grade classic vulvar intraepithelial neoplasia, differentiated vulvar intraepithelial neoplasia, and invasive keratinizing squamous cell carcinoma (P < .001), and followed the morphologic distribution of atypical squamous epithelial cells. Overexpression of hTERT was comparable to that seen for p53 in invasive keratinizing squamous cell carcinoma (P  =  .62); significant differences were calculated for differentiated vulvar intraepithelial neoplasia (P  =  .003) and high-grade classic vulvar intraepithelial neoplasia (P  =  .001). Conclusion.—Human telomerase reverse transcriptase is upregulated in vulvar intraepithelial neoplasia and invasive keratinizing squamous cell carcinoma compared with nonneoplastic squamous epithelia of the vulva as an apparently early and preinvasive event in the neoplastic transformation, with development of cellular longevity and resistance to apoptosis by survivin activation as associated features, independent of the etiology of vulvar intraepithelial neoplasia.


2018 ◽  
Vol 31 (06) ◽  
pp. 368-378 ◽  
Author(s):  
Kurt Davis ◽  
Guy Orangio

AbstractDespite the progress made in the reduction of squamous cell carcinoma of the cervix, the incidence of anal squamous cell carcinoma (ASCC) has been increasing since 1992. While it remains an uncommon disease, the prevalence is climbing steadily. Among human immunodeficiency virus (HIV)-infected adults, especially men who have sex with men, ASCC is one of the more common non-AIDS-defining malignancies. The precursor lesion, anal intraepithelial neoplasia (AIN), is prevalent in the HIV-infected population. More than 90% of ASCCs are related to human papilloma virus (HPV), oncogenic types (HPV 16, 18). While the biology of HPV-related intraepithelial neoplasia is consistent in the anogenital area, the natural history of AIN is poorly understood and is not identical to cervical intraepithelial neoplasia (CIN). CIN is also considered an AIDS-defining malignancy, and the methods for screening and prevention of AIN are derived from the CIN literature. This article will discuss the epidemiology of ASCC and its association with HPV and the life cycle of the HPV, and the molecular changes that lead to clearance, productive infection, latency, and persistence. The immunology of HPV infection will discuss natural immunity, humoral and cellular immunity, and how the HPV virus evades and interferes with these mechanisms. We will also discuss high-risk factors for developing AIN in high-risk patient populations with relation to infections (HIV, HPV, and chlamydia infections), prolonged immunocompromised people, and sexual behavior and tobacco abuse. We will also discuss the pre- and post-HAART era and its effect on AINs and ASCC. Finally, we will discuss the importance of anal cytology and high-resolution anoscopy with and without biopsy in this high-risk population.


2020 ◽  
Vol 7 (10) ◽  
pp. A502-508
Author(s):  
Niharika Rawat ◽  
Shivapriya Rajan

Background: Cervical cancer is the major cause of cancer deaths among women. Globally, around 5,70,000 new cases of cervical cancer and 3,11,000 deaths occurred in the year 2018. In India, Cervical cancer is a leading cause of cancer related mortality among women and the number of deaths is 60,000 per year among 97,000 diagnosed patients, especially those from lower socioeconomic group. Human Papilloma Virus (HPV) plays a crucial role in causing cervical dysplasia. This is done by upregulating p16INK4A, a cyclin dependent kinase inhibitor through interaction with cellular regulatory proteins. Hence p16INK4A can be used as a biomarker, since it is directly related variable for the presence of HPV. This study was conducted to evaluate the expression of p16INK4A in benign, premalignant and malignant cervical lesions and to assess its utility in diagnosing and grading cervical lesions. Methods: A total of 80 cervical specimens categorized histopathologically into nonspecific cervicitis, low grade squamous intraepithelial neoplasia (LSIL), high grade squamous intraepithelial neoplasia (HSIL) and squamous cell carcinoma cervix were included in this prospective study of one-year duration. Immunohistochemical study of p16INK4A were interpreted qualitatively and semi-quantitatively by Allred scoring system (0 to 8 points) which measures the proportion of stained cells and intensity of staining of cells. The collected data were statistically analyzed by ANOVA and chi square test. Result: Qualitative method showed absence of p16INK4A expression in all nonspecific cervicitis. 16.7% (2/12) LSIL, 100% (12/12) HSIL and 100% (28/28) squamous cell carcinoma cases showed p16INK4A positivity. Allred scoring of p16INK4A showed 66% (8/12) HSIL and 85.7% (24/28) squamous cell carcinoma cases with score 3 positivity. Hence high-grade lesions showed higher expression of this marker. Conclusion: IHC expression of p16INK4A showed increasing degree of expression from benign to premalignant and malignant lesions suggesting its diagnostic and prognostic value in the cervical cancer management


2014 ◽  
Vol 12 (1) ◽  
Author(s):  
Maria Lina Tornesello ◽  
Clorinda Annunziata ◽  
Luigi Buonaguro ◽  
Simona Losito ◽  
Stefano Greggi ◽  
...  

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