Worldwide, breast cancer is the second leading cause of cancer death among women and the third most common cancer. Although our understanding of the molecular basis of this fatal disease has improved, this malignancy remains elusive. Melatonin (Mel), retinoic acid (RA) and Nigella sativa (NS) are substances with anticancer effects. To date, our understanding of the mechanisms of therapeutic effects of these products in mammary cancer is still marginal. To look at the preventive and therapeutic values of these products, we carried out this investigation. An animal model formed of 80 rats was established. The animals were divided into eight groups of 10 animals each: (a) control group injected with the same vehicle used for treatments in the relevant dosages and routes; (b) carcinogen group injected with the known carcinogenic substance 7,12-di-methylbenz(a)anthracene (DMBA) that induces mammary carcinoma; (c) three prophylactic (Pro) groups (Mel-Pro, RA-Pro and NS-Pro) injected with test substances (Mel, RA and NS, respectively) 14 days before the intake of the carcinogenic substance DMBA and then continued until the end of the experiments; and (d) three treated (Tr) groups (Mel-Tr, RA-Tr and NS-Tr) injected with the vehicles after the intake of DMBA. In both the Pro and Tr groups, the drugs were daily administered for 3 months. The animals were killed, and their serum and tissues were evaluated for (a) markers of tumorigenicity [serum levels of total sialic acid (TSA) and lipid-bound sialic acid (LSA)], (b) markers of endocrine derangement (serum prolactin, estradiol and progesterone levels), (c) apoptotic changes [serum tumour necrosis factor (TNF)-alpha, tissue caspase-3 activity, percentage of DNA fragmentation and ultrastructural features of apoptosis] and (d) markers of oxidative stress (tissue levels of lipid peroxides and nitric oxide). Carcinoma was absent both in the control and in the NS-Pro groups. Mammary carcinoma occurred in DMBA and other Pro and Tr groups. The frequency of mammary carcinoma was high in the carcinogen DMBA group (60%), followed by the Tr (56%) and finally the Pro groups (33%). These tumours included papillary, comedo and cribriform carcinomas. As compared with the control group, the development of carcinoma in the carcinogen DMBA group was associated with increased levels of (a) markers of tumorigenicity (77.0 +/- 3.3 vs. 209.0 +/- 5.6 and P < 0.05 for TSA; 28.7 +/- 1.7 vs. 41.8 +/- 1.2 and P < 0.01 for LSA), (b) markers of endocrine derangement (2.5 +/- 0.1 vs. 3.6 +/- 0.3 and P < 0.05 for prolactin; 39.6 +/- 1.3 vs. 24.8 +/- 2.1 and P < 0.01 for progesterone and 31.0 +/- 0.7 vs. 51.1 +/- 3.4 and P < 0.01 for estradiol) and (c) markers of oxidative stress (2.3 +/- 0.2 vs. 5.2 +/- 0.7 and P < 0.01 for lipid peroxides and 4.4 +/- 0.2 vs. 7.6 +/- 0.8 and P < 0.01 for nitric oxide). Also, it was associated with decreased levels of markers of apoptotic activity (20.8 +/- 1.1 vs. 13.4 +/- 0.7 and P < 0.01 for caspase-3; 29.0 +/- 1.7 vs. 20.9 +/- 1.3 and P < 0.05 for percentage of DNA fr...

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Background Post-variceal band ligation bleeding ulcer is a severe complication with considerable mortality. We tried evaluating self-expandable metallic stent (SEMS) with concern to the ulcer morphology not well studied. Results We did a retrospective analysis of patients with bleeding post-band ulcers and treated by SEMS with concern to control bleeding and 6 weeks survival. Twenty-eight patients studied had their age (mean ± S.D.) 57.8 ± 8.6 years, and 85.7% were males. The Child-Pugh score range was 5–12]. Control of bleeding by SEMS was achieved in 23 (82.1%) patients, and overall, 6-week survival was 75%. Both post-band ulcer types B (oozing blood and type C (active spurted) were a risk for 6 weeks mortality (P = 0.04, OR 1.58, CI 95% 1.12–2.23). Conclusion SEMS is considered an excellent choice to control esophageal post-banding ulcer bleeding and a definite treatment bridge.

Background: Phytic acid is an anti-neoplastic agent. We hypothesize that during mammary tumorigenesis, the administration of phytic acid is associated with biochemical changes including enhancement of apoptosis and inhibition of oxidative stress.Materials and methods: An animal model formed of 25 rats was established. The animals were divided into three groups: (1) a control group which received the same phytic acid treatment in the right route and amount; (2) a carcinogen group which received a carcinogenic substance DMBA that can induce proliferative changes in the mammary gland; (3) treated group which received phytic acid, 60 days after the intake of DMBA. The animals were sacrificed, serum and tissue were evaluated for markers of tumorigenicity (serum total sialic acid, TSA); apoptotic changes (tissue caspase-3 activity and % DNA Fragmentation) and oxidative stress (tissue level of nitric oxide, NO).Results: Following DMBA administration, benign proliferative breast changes occurred in all animals. However, these changes disappeared following phytic acid treatment. As compared to the control group, the development of these proliferative changes in DMBA group was associated with statistically significantly (p < 0.05) increased levels of TSA and NO and decreased apoptotic activity. When compared to DMBA group, the disappearance of the proliferative changes in phytic acid -treated group was associated with statistically significantly (p < 0.05) decreased levels of TSA and NO and increased apoptotic activity.Conclusions: Administration of phytic acid reversed the proliferative effects of DMBA, suggesting its protective role.

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