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Articles by E. Azizi
Total Records ( 3 ) for E. Azizi
  S. Fouladdel , E. Azizi , H.R. Rahimi and S.N. Ostad
  Genetic differences among tumor cells of breast cancer patients are the main reasons for therapeutic failure. COX-2 and aromatase proteins have been determined to be important in breast cancers as potential targets for prevention and can also be a part of the therapeutic regimen of these cancers. Consequently, we decided to determine the expression of these proteins in human breast cancer T47D cells and its established tamoxifen resistant subline, namely T47D/TAMR-6 cells. Immunocytochemical technique was employed using primary antibodies for each protein followed by visualization of results with LSAB2 detection kit under the microscope. Our data showed that expression of COX-2 was relatively the same in parent and resistant T47D cells in the presence and absence of Tamoxifen (1 uM). Unlike tamoxifen, celecoxib could dramatically decrease the expression level of COX-2 in both cell types. Aromatase protein expression seems to be absent or is expressed at very low levels in both cell types and under all experimental conditions. Our data indicates no significant difference between studied cell types with respect to expression of aromatase and COX-2 enzymes. Therefore, these data suggest different possible outcomes for specific inhibitors of these enzymes alone or in combination with tamoxifen in the therapeutic regimen of breast cancer patients.
  S. Kaabinejadian , Sh. Fouladdel , M. Ramezani and E. Azizi
  Numerous mutated genes have been shown to be involved in breast cancer. The p53, a well-known tumor suppressor gene, is the most commonly mutated gene that plays an important role in directing cells with DNA damage into apoptosis. On the other hand, Estrogen Receptor (ER), an important prognostic factor is differentially expressed in breast cancer cells. Therefore, we decided to study the p53 gene and its protein in MCF7, T47D and MDA-MB-468 breast cancer cell lines with different ER status following exposure to Adriamycin (ADR). Cytotoxicity of ADR on these cell lines was determined using MTT assay. The mRNA and protein levels were also analyzed in cell lines using RT-PCR and immunocytochemistry (ICC) assays, respectively. ADR cytotoxicity was highest on ER negative MDA-MB-468 cells and lowest on ER positive MCF7 cells. The p53 mRNA level was highest before or after treatment with ADR in MDA-MB-468 and lowest in T47D cells. It is noteworthy to mention that the p53 mRNA level slightly increased in T47D cells but decreased in other two cell lines after ADR treatment. Interestingly, higher level of p53 protein expression was detected after ADR exposure in all three cell lines. In conclusion, these three cell lines with different ER status showed differential molecular responses to Adriamycin that is important in tumor-targeted cancer therapy.
  M. Mohseni , T. Ohe , M.R. Fazeli , S.N. Ostad , M. Hamedi , H. Jamalifar and E. Azizi
  In this study, mutagenic potential of red florets of Iranian Safflowers IL 111 was evaluated by Ames test using Salmonella typhimurium TA98 and TA100 strains. Florets collected and dried in two conditions, dried on shade and dried on the bolls by sun. Extractions have been done with 70% hydro-ethanolic solution and also boiling water. Solvents were then evaporated from extracts by freeze drier. Different dilutions of extracts were prepared in either distilled water or DMSO to be evaluated in the presence and absence of S9 bioactivation. Test and control plates were prepared according to the plate incorporation method and incubated for 48 h at 37°C. Then the number of reverted colonies was counted to determine the Mutation Ratio (MR) for each test concentration. The MR for test samples was far less than positive controls to be considered mutagen. There was also no significant difference in MR of extracts before and after S9 bioactivation at studied concentrations. Therefore, it can be concluded that Safflower extracts have no mutagenic activities under different preparatory and assay conditions using Ames mutagenicity assay.
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