reported (Soliman et al., 2001). Since, more than half of the Egyptian population is younger than 50 years, a mounting public health problem of CRC among young adults in Egypt should be highly considered (Silla et al., 2014).Despite extensive CRC-focused research over the past 20 years, the clinical outcome of CRC is still very

BackgroundStudies about cytotoxicity and genotoxicity in rheumatoid arthritis (RA) are limited and the toxicity of Disease Modifying Anti-Rheumatic Drugs (DMARDs) commonly used in treatment is still a concern.Objectivesto assess cytotoxicity and genotoxicity in RA and the possible cyto and genotoxic effects of some DMARDs used in treatment.MethodsThe study included 30 female RA patients divided according to treatment into three groups and ten healthy controls. Two groups received DMARDs for at least 3 months period: methotrexate (MTX) only group (n=12 patients), MTX with SSZ (sulphasalazine) group (n=8) and ten DMARDs naieve RA who received only Non Steroidal Anti-Inflammatory Drugs (NSAIDs). The MTX dose was 15–20 mg/wk, SSZ dose was 1.5–2 gm daily. All RA on DMARDs received concomitant daily folic acid dose of 0.5 mg.Peripheral blood samples were taken to assess the cytotoxicity by chromosomal analysis (karyotyping) using solid Giemsa stain and GTG-banding according to the International System for Human Chromosome Nomenclature. Genotoxicity and DNA damage was assessed by the miconucleustest usin g cytochalasin –B.ResultsCompared to controls, RA patients had significantly higher chromosomal aberrations (CAs) in the form of breaks, satellite association, endoreduplication, aneuploidy, double minute, and other aberrations. There was also a statistically significant increase in the markers of genotoxicity in RA patients compared to controls: micronuclei (MN), nucleoplasmic bridges (NPB) and necrotic and/or apoptotic cells (Table1). CAs were found in all RA groups, those receiving DMARDs as well as the DMARD naieve group. CAs were significantly higher in MTX and in MTX-SSZ group when compared to RA on NSAIDs only. Meanwhile, there was no significant difference between the CAs in the MTX and the MTX-SSZ groups. In addition, the number of binucleated (BN) cells with MN, NPB, and the necrotic and/or apoptotic cells was statistically higher in MTX-RA and MTX-SSZ-RA compared to the NSAIDs group. Whereas, no statistical difference was found between the two DMARDs groups.RA patients who were on DMARDs for a longer duration (>5 years) showed a statistically significant increase in all cytotoxicity and genotoxicity markers than those for shorter duration (<5 years).Markers of cyto/genotoxicityControl (n=10)Total RA (n=30)PMean ± SDMean ± SDBreaks0.6±1.0714.77±11.58<0.001*Satellite association6.2±6.4938.16 ±14.77<0.05*Double minute0.0±0.02.03±4.77<0.05*Endo- reduplication0.0±0.09.7±8.31<0.05*Aneuploidy0.0±0.05.3±4.5<0.05*Other aberrations0.0±0.00.70±0.51<0.05*BN cells with MN1.5±1.221.73±12.38<0.01*BN cells with NPB0.8±1.013.27±9.96<0.01*Necrotic and/or apoptotic cells2.3±1.829.93±12.10<0.001**P is significant at values ≤0.05.ConclusionsRA patients show significantly increased markers of cytotoxicity and genotoxicity, regardless the type of medications received, sugggesting them to represent underestimated disease features which could provide new insights into its pathogenesis. MTX further aggrevates the cyto- and genotoxicity...

No abstract

No abstract

This study was conducted to estimate the frequency of BRCA1 (185delAG) mutation among Egyptian female patients with breast cancer. Forty selected female patients with breast cancer, 80 of their female relatives and 10 healthy females as a control group were included in this study. Result: The age of onset of breast cancer was below 40 years in 25 (62.5%) patients and above 40 years in 15 (37.5%) patients. There were significant differences among the patients regarding the age at menarche before 13 years (p=0.011, p<0.05), onset of breast cancer (p=0.000, p<0.001), parity (p=0.000, p<0.001), first delivery before 30 years of age (p=0.04, p<0.05), breast feeding (p=0.002, p<0.05), and positive family history (p=0.000, p<0.001). The frequency of BRCA1 (185delAG) mutation was found among 10% of the patients' group. Eight percent of patients with early onset below 40 years and 13.5% of patients with onset after 40 years were heterozygotes for the mutation. Three percent of patients with unilateral breast cancer, 40% of patients with bilateral breast cancer and 50% of patients with breast ovarian cancer were carrying the mutation. Our results indicated that breast ovarian cancer and bilateral breast cancer patients were likely to have BRCA1 (185delAG) mutation than in unilateral breast cancer.