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cervical intraepithelial neoplasia/protease

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Страница 1 от 18 полученные результаты

HIV protease inhibitors to prevent progression of cervical intraepithelial neoplasia to cervical cancer: therapeutic opportunities and challenges.

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Expression patterns of seprase, a membrane serine protease, in cervical carcinoma and cervical intraepithelial neoplasm.

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BACKGROUND Seprase is a membrane-bound serine proteinase with gelatinase activity, which may be involved in cancer invasion and metastasis. METHODS We examined the seprase expression patterns in invasive or preinvasive squamous epithelial lesions. CONCLUSIONS No seprase immunoreactivity was found in

Ritonavir or saquinavir impairs the invasion of cervical intraepithelial neoplasia cells via a reduction of MMP expression and activity.

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OBJECTIVE Treatment of human immunodeficiency virus (HIV)-infected women with the highly active antiretroviral therapy (HAART) has reduced the onset of uterine cervical intraepithelial neoplasia (CIN), and halted its progression to cervical carcinoma. We and others demonstrated that the HIV protease

The Impact of Human Papilloma Viruses, Matrix Metallo-Proteinases and HIV Protease Inhibitors on the Onset and Progression of Uterine Cervix Epithelial Tumors: A Review of Preclinical and Clinical Studies.

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Infection of uterine cervix epithelial cells by the Human Papilloma Viruses (HPV) is associated with the development of dysplastic/hyperplastic lesions, termed cervical intraepithelial neoplasia (CIN). CIN lesions may regress, persist or progress to invasive cervical carcinoma (CC), a leading cause

Granzyme B as a prognostic marker of cervical intraepithelial neoplasia.

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Granzyme B (GrB) is a serine protease synthesized in T lympocytes (CTL), released after T-cell activation resulting from exogenous stimulation. With perforin, GrB discharges apoptotic signals to a target cell and therefore constitutes a marker to identify activated CTL. We aimed to quantify GrB

Effect of excisional therapy and highly active antiretroviral therapy on cervical intraepithelial neoplasia in women infected with human immunodeficiency virus.

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OBJECTIVE Our purpose was to determine the rates of recurrence, persistence, and progression of cervical intraepithelial neoplasia in women who were seropositive for human immunodeficiency virus after excisional therapy with and without highly active antiretroviral therapy. METHODS The records of

Inhibition of MMP-9 expression by ritonavir or saquinavir is associated with inactivation of the AKT/Fra-1 pathway in cervical intraepithelial neoplasia cells.

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A reduced incidence and decreased clinical progression of uterine cervical intraepithelial neoplasia (CIN) has been observed in women infected with human immunodeficiency virus (HIV) treated with HIV-protease inhibitors (PIs). The HIV-PIs saquinavir (SQV) and ritonavir (RTV) have been demonstrated

Cervical intraepithelial neoplasia is associated with genital tract mucosal inflammation.

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BACKGROUND Clinical studies demonstrate increased prevalence of human papillomavirus (HPV)-associated disease in HIV-infected individuals and an increased risk of HIV acquisition in HPV-infected individuals. The mechanisms underlying this synergy are not defined. We hypothesize that women with

MASP-1 and MASP-2 Serum Levels Are Associated With Worse Prognostic in Cervical Cancer Progression.

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Background: MBL-associated serine proteases (MASP-1, MASP-2, MASP-3, MAp-44, and MAp-19) are key factors in the activation of the lectin pathway of complement. Serum levels of these components have been associated with recurrence and poor survival of some types of cancer, such as colorectal

The fluorescent location of abnormal cervical cells employing the principle of differential competitive inhibition.

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The screening of cervical smears is concerned with the detection of abnormal epithelial cells which may be indicative of cervical intraepithelial neoplasia (CIN). Several types of cells in cervical smears possess a cell surface protease where isoenzymic forms of this enzyme can be differentially

Up-regulation of plasminogen activator inhibitor-2 is associated with high-risk HPV and grade of cervical lesion at baseline but does not predict outcomes of high-risk HPV infections or incident CIN.

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Protease inhibitor serpin-B2 (plasminogen activator inhibitor-2 [PAI-2]) protects pRb from degradation in human papillomavirus (HPV)-18+ HeLa cells. Our objective was to assess whether the pRb-mediated HPV-suppressive effect of PAI-2 in cancer cell lines has implications in the outcome of HPV

Cidofovir in the treatment of HPV-associated lesions.

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The acyclic nucleoside phosphonate cidofovir (CDV) has proved efficacious in the treatment of different clinical manifestations of HPV-induced epithelial cell proliferation. Local intratumor injections of CDV in an immunocompetent patient with hypopharyngeal/esophageal papillomatous lesions,

Expression and localization of maspin in cervical cancer and its role in tumor progression and lymphangiogenesis.

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OBJECTIVE Cervical cancer is the most common malignant tumor in female reproductive tract and primarily metastasizes through the lymphatic system that will affect prognosis of patients. Maspin, a member of the serine protease inhibitors (serpins) super family, has recently been indicated as a tumor

Prognostic role of maspin expression in patients with cervical dysplasia and cervical cancer.

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Mammary serine protease inhibitor (maspin) acts as a tumor suppressor through the inhibition of cancer cell invasion and metastasis. Paradoxically, maspin levels are increased in some types of malignant cells. The aim of this study was to investigate the maspin expression in cervical

Maspin expression in CIN 3, microinvasive squamous cell carcinoma, and invasive squamous cell carcinoma of the uterine cervix.

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Maspin is a serine protease inhibitor with tumor suppression activity. It is expressed in normal breast and prostate tissue but is downregulated or absent in breast and prostate tumors. Recent reports have shown that decreased expression is associated with a greater propensity for metastasis in oral
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