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Background: This study evaluated and compared the quantitative expression of Multidrug Resistance-associated Protein 1 (MRP1) and ATP Binding Cassette subfamily G member 2 ( ABCG2), two Multidrug Resistance (MDR) related genes, in 30 CML patients and 27 normal subjects. Methods: Total RNA was extracted from peripheral blood Mononuclear cells (MNCs) using the Trizol method. Then cDNAs were synthesized. Gene expression was quantified with Real-Time PCR System. Relative expression of target genes was calculated using the 2-ΔΔCt method. Results: High expression of MRP1 and ABCG2 mRNAs were detected in the patient's group. Intra-group comparisons also revealed increased expression of ABCG2 in Accelerated Phase (AP)-Blastic Crisis (BC) patients compared to Chronic Phase (CP) patients. Whereas, increased expression of MRP1 in AP-BC patients was not statistically significant. Conclusion: Considering the wide spectrum of (ATP Binding Cassette) ABC transporter superfamily substrates, they can play an important role in cell fate determination. High expression of MRP1 and ABCG2 genes can result in the efflux of therapeutic agents, and subsequent reduction in their intracellular concentration. This mechanism finally protects the cells from the therapeutic effects of medications. On the other hand, these transporters are able to export growth factors out of the cell. Such exported molecules may have a growth-inducing effect on adjacent cells. These are the possible mechanisms for the participation of MRP1 and ABCG2 genes in conferring drug resistance to CML cells.

Background: According to the World Health Organization, the high prevalence of breast cancer mortality in the least developed countries is because breast cancer is diagnosed at late stages. Accordingly, cost-effective breast cancer screening plans are the most effective methods to control this cancer and also increase women's survival.Methods: This retrospective cross-sectional study was conducted to evaluate the performance of the breast cancer screening program based on the guidelines of the Ministry of Health on 14,493 eligible women in rural areas of the Rudsar city in 2018-19. Providing target coverage, identification of the at-risk population, early diagnosis, referral index, and other statistical indices were calculated, analyzed and quantified using the relevant scales and SPSS 22 software.Results: The target population coverage was estimated at 48%. The results showed that 0.4% of the cases (27 cases) were identified as high-risk group according to national guidelines with referral to a specialist of 100%. All cases identified at the first stage of screening were found with BIRADS (Breast Imaging Reporting and Data System)4 and 5 based on biopsy specimens. Conclusion: The low target population coverage, as well as the cases with advanced breast cancer, indicated the need for more attention and consideration in implementing programs and policies for preventable cancer by all organizations. In this regard, there is a need for relevant interventions and follow-up by health authorities.

Background: Metastasis of cancer cells is the primary responsible for death in patients with colorectal cancer (CRC). Transforming growth factor-β (TGF-β)-induced matrix metalloproteinases (MMPs) are essential for the metastasis process. Silibinin is a natural compound extracted from the Silybum marianum that exhibits anti-neoplastic activity in cancer cell lines. In this study, we evaluated the effects of silibinin on MMP-2 and MMP-9 induced by TGF-β in human HT-29 CRC cell line and the potential mechanism underlying the effects. Methods: The present in vitro study was done on the HT-29 cell line. The HT-29 cell line was cultured in RPMI1640 and exposed to TGF- β (5 ng/ml) in the absence and presence of different concentrations of silibinin (10, 25, 50, and 100 μM). The effect of silibinin on HT-29 cell viability was measured with the MTT assay. A real-time polymerase chain reaction (Real-Time PCR) determined the relative mRNA expression of MMP-2 and MMP-9. Western blotting was employed to examine MMP-2 and MMP 9 protein expression and Smad2 phosphorylation. Results: Silibinin inhibits cell viability of HT-29 cell line at 24 hours in a dose-dependent manner. TGF-β increased the mRNA and protein expression of MMP-2, MMP-9, and phosphorylated Smad2 compared to controls. Pharmacological inhibition with silibinin markedly blocked TGF-β–induced MMP-2 and MMP-9 mRNA and protein expression and Smad2 phosphorylation. Conclusion: Silibinin decreased the cell viability of HT-29 cancer cells in a dose-dependent manner. Silibinin also inhibited TGF-β-stimulated MMP-2 and MMP-9 expression in HT-29 cells, possibly mediated with the Smad2 signaling pathway.

Background: Cervical cancer is known to be a preventable cancer in which various risk factors play role in increasing the risk of the disease. In this study, we have assessed different risk factors involved in invasive cervical cancer in Northeast of Iran. Methods: In a case control study, 100 patients with advanced cervical cancer were compared to 100 healthy, normal women. In addition, 100 cases of prisoner women who had a high risk profile for cervical cancer were also investigated. Cervical risk factors for these groups were documented using a questionnaire and available medical notes. Univariate analysis was done for each risk factor followed by a multivariate regression analysis to evaluate the most powerful risk factors after adjustment. Result: Age of first intercourse ≤16 (P<0.001)[OR= 4.18, 95% CI (2.32-7.54)], sexually transmitted diseases (STD) (P<0.001) [OR=8.59,95% CI (4.25-17.37)], passive smoking (P<0.01) [OR= 2.35, 95% CI (1.17-4.72)], smoking (P<0.01) [OR=10.33, 95% CI (2.32-46.17)], age of first pregnancy ≤17 years (P<0.001) [OR= 3.37, 95% CI (1.79-6.33)] were strongly related to the occurrence of cervical cancer. However, STD remained statistically significant (P<0.01) after adjustment. 

Several epidemiological studies have reported that regular use of opium can be associated with an increased risk of developing cancers, including oesophageal, laryngeal, bladder, lung, and gastric cancer. In this systematic review, we aimed at investigating whether experimental studies support this finding and, if yes, how opium consumption can cause cancer. Most of the articles that have studied opium or its derivatives have found it as a carcinogen. However, due to the complex composition, different forms, and various ways of opium use, further comprehensive experimental studies are required. Using modern genomic and epigenomic methods seems to help determine the molecular mechanisms underlying opium carcinogenicity.