The expression of transcription factor BORIS and its association with the estrogen receptor beta (ER-ß) in cervical carcinogenesis.

BORIS is a transcription factor aberrantly expressed in human cancers that can regulate the expression of estrogen receptors in endometrial cancer and breast cancer. We evaluated the expression of BORIS and the estrogen receptors alpha (ER-α) and beta (ER-ß) in ten cell lines derived from cervical cancer using RT-PCR and Western-blot. We also evaluated 54 cervical tissues: normal epithelia, low-grade intraepithelial lesions (LSIL), high-grade intraepithelial lesions (HSIL), and invasive squamous carcinomas (SC) using immunohistochemistry. In the cell lines, BORIS mRNA and protein expressions are associated with ER-ß expression but not with ER-α expression. In the normal cervical epithelium, ER-α and ER-ß were expressed but the BORIS protein was not detected. In the LSIL samples, BORIS, ER-α and ER-ß were expressed; however, in the HSIL samples, only the BORIS and ER-ß expressions were detected, but ER-α expression was minimal or null. In the SC, only BORIS and ER-ß were detected. In summary, the results show that the expressions of BORIS and ER-ß increase while the expression of ER-α decreases according to the severity of the lesions. These results suggest synergistic roles for BORIS and ER-ß during cervical cancer progression with a possible regulation of the estrogen receptors by BORIS in the development of cervical cancer; however, more detailed studies are needed to confirm this suggestion and to determine the precise role of BORIS in cervical cancer.

Detection of apoptosis in pemphigus vulgaris by TUNEL technique.

BACKGROUND: Pemphigus is part of a group of blistering diseases that affect the skin and mucous membranes. Based on its autoimmune origin, autoantibodies develop in pemphigus that are directed toward cell surface components of keratinocytes. However, some data cannot be explained, such as the lack of a relationship between autoantibody levels and the severity of clinical manifestations, treatment resistance, the presence of inflammatory infiltrates and the potential occurrence of apoptosis as determinants of vesicle formation. OBJECTIVE: To examine the presence of apoptosis in pemphigus vulgaris by TUNEL technique. METHODS: In this cross-sectional study, we selected 15 paraffin-embedded tissues from subjects who were diagnosed with pemphigus vulgaris by hematoxylin and eosin staining. The samples were subjected to TUNEL assay and examined under an Olympus BX61 fluorescence microscope. Positivity was categorized dichotomously, and the statistical analysis was performed using the X2 test. RESULTS: Positivity was observed in basal layer cells in 14 (93.3%) cases. In 13 (86.7%) of the positive cases, we noted espinosum and granular layers that formed the blister roof, and in 12 cases (80%), positive acantholytic cells were observed. CONCLUSIONS: TUNEL positivity was observed in pemphigus vulgaris, implicating apoptosis in the pathophysiology of this condition, which can help guide the development of apoptotic blockers as therapeutics.

Detection of apoptosis in pemphigus vulgaris by TUNEL technique

Abstract: Background: Pemphigus is part of a group of blistering diseases that affect the skin and mucous membranes. Based on its autoimmune origin, autoantibodies develop in pemphigus that are directed toward cell surface components of keratinocytes. However, some data cannot be explained, such as the lack of a relationship between autoantibody levels and the severity of clinical manifestations, treatment resistance, the presence of inflammatory infiltrates and the potential occurrence of apoptosis as determinants of vesicle formation. Objective: To examine the presence of apoptosis in pemphigus vulgaris by TUNEL technique. Methods: In this cross-sectional study, we selected 15 paraffin-embedded tissues from subjects who were diagnosed with pemphigus vulgaris by hematoxylin and eosin staining. The samples were subjected to TUNEL assay and examined under an Olympus BX61 fluorescence microscope. Positivity was categorized dichotomously, and the statistical analysis was performed using the X2 test. Results: Positivity was observed in basal layer cells in 14 (93.3%) cases. In 13 (86.7%) of the positive cases, we noted espinosum and granular layers that formed the blister roof, and in 12 cases (80%), positive acantholytic cells were observed. Conclusions: TUNEL positivity was observed in pemphigus vulgaris, implicating apoptosis in the pathophysiology of this condition, which can help guide the development of apoptotic blockers as therapeutics.

Is there a causal relationship between HSV-1 and pemphigus vulgaris?

BACKGROUND: Pemphigus vulgaris is a chronic autoimmune bullous disease, the initiation of autoimmunity has been linked to viral infections. In 1974, Krain first reported the association between herpes simplex virus and pemphigus vulgaris, since then, there have been few such studies, prompting us to examine this link. FINDINGS: We randomly selected 15 cases of PV, the diagnosis was confirmed using hematoxylin and eosin (H&E)-stained slides-2-micron sections were deparaffinized and rehydrated to be processed by immunohistochemistry, antigen retrieval was performed with 0.1 % sodium citrate, pH 6.2, endogenous peroxidase was inactivated with 0.9 % H2O2, and washes were performed with distilled water. Finally the slides were allowed to stand for 5 min in phosphate-buffered saline (PBS). The tissues were incubated for 45 min with polyclonal anti-HSV-I, (1:150, Dako Corporation, Carpinteria, CA). The MACH 1 system was applied for 15 min to visualize the reaction using 3,3'-diaminobenzidine-H2O2 (both from Biocare Medical) as substrate under a microscope. The tissues were counterstained with Lillie-Mayer's hematoxylin (Biocare Medical). We failed to observe positivity for HSV-1 in any of the 15 PV cases that were processed. CONCLUSIONS: It is not possible to determine whether HSV-PV is a causal relationship; most studies are case reports. Thus, we propose research studies with greater methodological weight to determine the involvement of HSV in the pathogenesis of PV and demonstrate that the relationship between HSV-1 and PV is a trigger at the beginning of the disease and has an etiologic function in its pathogenesis or that it is merely a coinfection due to the immunosuppression of patients with PV.