Objective Arsenic trioxide (ATO) is a drug commonly used for the treatment of acute promyelocytic leukemia (APL). Although ATO has been shown to cause significant improvement in patients, it is associated with serious side effects, which sometimes lead to the patient's death. In this review paper, we examine the reports of ATO‐induced cardiotoxicity in APL patients and evaluate the strategies to reduce the incidence of such toxicity. Methods The key search terms were “arsenic trioxide,” “acute promyelocytic leukemia,” “cardiotoxicity,” “molecular pathway,” and “biomarker.” Results Studies have indicated the involvement of several molecular pathways in ATO‐induced cardiotoxicity. These pathways increase the production of reactive oxygen species by interfering with intracellular calcium homeostasis as well as impairing the transfer of calcium into endoplasmic reticulum and mitochondria. On the other hand, increasing or decreasing expressions of some microRNAs (miRs) have been shown to play a role in cardiotoxicity. Conclusion Finally, it can be stated that given the essential role of molecular pathways in cardiotoxicity and considering the fact these pathways impair the regulation of miRs expression, identification of molecular pathways involved in ATO‐induced cardiotoxicity aimed at targeting miRs could be a new therapeutic strategy to prevent cardiotoxicity.

Background Cardiomyopathic manifestations induced by continuous blood transfusion are the leading cause of death among patients with thalassemia major (TM). Despite introduction of chelation therapy, heart failure after cardiomyopathic manifestations is still a major threat to patients. Methods We performed a search of relevant English-language literature, retrieving publications from the PubMed database and the Google Scholar search engine (2005–2018). We used “thalassemia major”, “cardiomyopathy”, “iron overload”, “cardiac magnetic resonance T2” “chelation therapy”, and “iron burden” as keywords. Results The results of the studies we found suggest that cardiac hepcidin is a major regulator of iron homeostasis in cardiac tissue. Unlike previous assumptions, the heart appears to have a limited regeneration capability, originating from a small population of hypoxic cardiomyocytes. Conclusions Oxygen levels determine cardiomyocyte gene-expression patterns. Upregulation of cardiac hepcidin in hypoxia preserves cardiomyocytes from forming out of reactive oxygen species catalyzed by free cellular iron in cardiomyocytes. Using the limited regeneration capacity of cardiac cells and gaining further understanding of the cellular aspects of cardiomyopathic manifestations may help health care professionals to develop new therapeutic strategies.

Colorectal cancer is the third most common cancer. The activity of the Sonic hedgehog pathway is increased in patients with colorectal cancer. bFGF and Cyclopamine could act as Shh pathway inhibitors. But, by considering the dual role of bFGF on the growth of cancer cells, this study aimed to evaluate the simultaneous effect of bFGF and Cyclopamine, on apoptosis in the HT-29 cell line. Cell viability was performed using MTT assay. The apoptosis rate was measured using Annexin V-FITC/PI flow cytometry. Clonogenic assay was performed. The gene expression was investigated using Real-Time PCR method. The bFGF decreased the expression of apoptotic genes. But, the Cyclopamine increased the expression of apoptotic genes and decreased the colony formation ability. Simultaneous treatment with bFGF and Cyclopamine was associated with decreased expression of anti-apoptotic genes and decreased colony formation ability. Despite the anti-apoptotic effect of bFGF on cancer cells, it increased the anti-cancer effect of Cyclopamine, which can be due to the existence of a less-known signaling pathway between bFGF and Shh to inhibit growth, so it is important to investigate its exact mechanisms.

Background: Breast cancer and cervix cancer are the prevalent and deadly types of solid tumors around the world. According to the importance of cancer, it is necessary to understand predisposing factors that affect cancer risk. In this regard, previous studies suggest that blood types particularly ABO and Rh-Hr Blood-Group System could play roles in the risk and different features of cancers. In the present study, we aimed to evaluate the potential of ABO and Rh blood groups as risk factors for breast cancer and cervix cancer. Materials and Methods: A retrospective study included 109 and 14 patients diagnosed with breast cancer and cervix cancer, respectively with known ABO and Rh blood types, between 2018 and 2020 in Khuzestan province, Iran. For compression of ABO blood groups distribution between the cancer patients group and the healthy population, we used data from a large-scale study that report the distribution of ABO blood groups in 29,922 blood donors in Khuzestan province. Results: Based on obtained results the most frequent blood group is O followed by B, A, and AB in breast cancer and followed by A, B, and AB in cervix cancer. Results showed no significant association between ABO and Rh and the risk of breast and cervix cancer. Moreover, there is no relationship between blood types and clinic pathological features of breast cancer.   Conclusion:  Based on our data, ABO and in this regard, previous studies suggest that blood types particularly ABO and Rh-Hr Blood-Group System could play roles in the risk and different features of cancers. In the present study, we aimed to evaluate the potential of ABO and Rh blood groups as risk factors for breast cancer and cervix cancer do have not any association with the risk of breast and cervix cancer and their characteristics.