Relation between Vitamin D Level and Cyclin-Dependent Kinase-1 Gene Expression in Egyptian Patients with Lupus Nephritis and their Impact on Disease Activity.

INTRODUCTION: Lupus nephritis (LN) is a common complication of systemic lupus erythematosus. Vitamin D and cycline-dependent kinase-1 (CDK1) have been implicated in its pathogenesis. The aim of this study was to determine the relation between vitamin D level and CDK-1 in lupus nephritis patients and their impact on disease activity. PATIENTS AND METHODS: The current study was conducted on 50 LN patients and 20 control subjects from Egyptian population using ELISA to assess vitamin D level in serum and TaqMan assay for CDK1 gene expression. RESULTS: Serum vitamin D level was significantly lower in LN patients and CDK-1 gene was down expressed in the majority of LN patients. A significant inverse correlation was found between vitamin D level and 24 h protein in urine, ANA, anti-dsDNA, CRP, with a significant positive correlation with renal biopsy indices, eGFR. There was a non-significant inverse correlation between vitamin D and CDK-1 (before RO-3306 addition) and a positive correlation after RO-3306. A significant positive correlation was found between CDK-1 gene expressions with urinary albumin/creatinine ratio. However, a significant positive correlation was found between CDK-1 (after RO-3306 addition) and proteinuria. While a significant positive correlation was found between CDK-1 expression (after RO-3306 addition) and ANA, a significant positive correlation was found between CDK-1 expression (before RO-3306 addition) and anti-dsDNA but CDK-1 is not associated with renal biopsy indices nor with activity indices of SLE. There was a positive correlation between CDK-1 gene expression and CRP before and after RO-3306 addition. CONCLUSIONS: Vitamin D deficiency acts as a risk factor for developing LN. CDK-1 may have an association with the diagnosis of LN but its association with the progression of staging of LN is still confusing.

NY-BR-1 Antigen Expression and anti-NY-BR-1 IgG in Egyptian Breast Cancer Patients: Clinicopathological and Prognostic Significance.

Breast cancer is the most common gynecological malignancy in the world. In Egypt, it ranks the first among female malignancies with incidence of 37.7%. Over the last decades, the integration of prognostic and predictive markers in treatment decisions has led to more individualized and optimized therapy. NY-BR-1 antigen has been shown to be frequently expressed in breast cancers. The study aimed to assess the tissue expression of NY-BR-1 antigen and serum IgG antibody to this antigen in Egyptian breast cancer females. The study was conducted on 60 females (10 healthy, 10 having benign breast lesions, 40 with malignant breast cancer). NY-BR-1 Ag expression was evaluated by immunohistochemistry and anti-NY-BR-1 IgG was assessed by ELISA. Results revealed a significant difference in NY-BR-1 Ag expression between benign and malignant breast cancer patients. There was a significant correlation between NY-BR-1 antigen expression and estrogen receptor's status (P = 0.019), stage of the disease (P = 0.008), menopausal status (P = 0.008), lymph node involvement (P = 0.022) and anti-NY-BR-1 IgG (P = 0.032) among the studied individuals. In addition, there was a statistically significant increase in anti-NY-BR-1 IgG O.D. results among malignant breast cancer group. It is correlated with tumor type (P < 0.001) and progesterone receptor status (P = 0.038). In conclusion, our work may represent a step towards identification of a new prognostic marker specific for breast cancer.

Effect of murine exposure to gamma rays on the interplay between Th1 and Th2 lymphocytes.

Gamma radiation radiotherapy is one of the widely used treatments for cancer. There is an accumulating evidence that adaptive immunity is significantly contributes to the efficacy of radiotherapy. This study is carried out to investigate the effect of gamma rays on the interplay between Th1/Th2 response, splenocyte lymphoproliferative response to polyclonal mitogenic activators and lymphocytic capacity to produce IL-12 and IL-10 in mice. Results showed that exposure of intact spleens to different doses of γ-rays (5, 10, 20 Gy) caused spontaneous and dose-dependent immune stimulation manifested by enhanced cell proliferation and elevated IL-12 production with decreased IL-10 release (i.e., Th1 bias). While exposure of splenocytes suspension to different doses of γ-rays (5, 10, 20 Gy) showed activation in splenocytes stimulated by PWM at 5 Gy then a state of conventional immune suppression that is characterized by being dose-dependent and is manifested by decreased cell proliferation and IL-12 release accompanied by increase in IL-10 production (i.e., Th2 bias). In addition, we investigated the exposure of whole murine bodies to different doses of γ-rays and found that the exposure to low dose γ-rays (0.2 Gy) caused a state of immune stimulation terminated by a remarkable tendency for immune suppression. Exposure to 5 or 10 Gy of γ-rays resulted in a state of immune stimulation (Th1 bias), but exposure to 20 Gy showed a standard state of immune suppression (Th2 bias). The results indicated that apparently we can control the immune response by controlling the dose of γ-rays.