Metformin and Aspirin: Anticancer effects on A549 and PC3 cancer cells and the mechanisms of action.

Metformin exerts its anticancer effect through two mechanisms, directly affecting the tumor and indirectly reducing systemic insulin levels. The anticancer effects of aspirin occur by inhibiting Cyclooxygenase (COX)-2. COX-2 is absent in many cell types under normal conditions and increases under pathological conditions such as cancer. This study aims to investigate the effect of metformin and aspirin and their combination of them on A549 and PC3 cell lines. Metformin and aspirin were investigated separately and in combination on two cancer cell lines, A549 and PC3. The examined groups include the negative control of untreated cells and the positive control of cisplatin and drugs at concentrations of 15, 10, and 20 µg/ mL to investigate the mechanism of oxidative stress factors (reactive oxygen species, lipid peroxidation, Glutathione (GSH)) and apoptosis (lactate dehydrogenase). The results showed that aspirin, metformin, and their combination could affect cancer cell growth by damaging mitochondria, releasing reactive oxygen species, and activating the oxidative stress pathway. Also, these two drugs show the activation of the apoptotic pathway in cancer cells by increasing the lactate dehydrogenase factor and releasing it from the cells. By disrupting the balance of oxidants and antioxidants in the cell, metformin and aspirin cause an increase in the level of reactive oxygen species and a decrease in the level of glutathione reserves, followed by an increase in the level of lipid peroxidation and a decrease in cell viability. Unlike common chemotherapy drugs, these drugs have no known severe side effects; Therefore, in the not-so-distant future, these drugs can also be used as anticancer drugs. Highlights: Metformin and aspirin, commonly used drugs for diabetes and inflammation, inhibit the growth of cancer cell lines, A549 and PC3.Metformin and aspirin, either separately or in combination, can potentially impede cancer cell growth by disrupting mitochondrial function, inducing the release of reactive oxygen species (ROS), and activating oxidative stress pathways.Furthermore, these drugs can trigger apoptosis, a programmed cell death mechanism, in cancer cells by increasing lactate dehydrogenase (LDH) levels and facilitating its release from the cells.

Autologous stem cell transplantation as treatment modality in a patient with relapsed pancreatoblastoma.

Pancreatoblastoma (PB) is a rare malignant neoplasm of the pancreas, which occurs mostly during childhood. Presently, the optimal treatment strategy is neither clear nor uniform for patients in advanced stages, in particular those with metastasis, inoperable, or recurrent tumors. To our knowledge, until now, only one patient with PB has been treated with hematopoietic stem cell transplantation (HSCT) following aggressive chemotherapy and surgical resection. Here we report the second case of PB who was treated with aggressive chemotherapy combined with autologous peripheral blood stem cell transplantation.

First report of successful stem cell transplantation in a patient with sickle cell hemoglobin D disease.

Sickle cell hemoglobin D disease is a rare variant of sickle cell disease. Affected patients suffer from episodes of acute exacerbation of clinical course with a wide range of manifestations such as acute chest syndrome, stroke, painful vaso-occlusive crises, acute sequestration crises, joint necrosis, organ failure, infections, and temporary aplastic crises, collectively called sickling crises. Conventional treatments for patients with sickle cell disease include hydroxyurea therapy and prophylactic red blood cell transfusion. However, morbidity and mortality rates remain high with these remedies. In this article, we report hematopoietic stem cell transplantation as an alternative treatment in children with high-risk factors. According to our knowledge and an extensive review of the literature, stem cell transplantation in sickle cell hemoglobin D disease previously has not been reported in any published study and our patient is the first case.

Severe hypochromic microcytic anemia in a patient with congenital atransferrinemia.

Congenital atransferrinemia or hypotransferrinemia is a very rare autosomal recessive disorder, characterized by a deficiency of transferrin, resulting in hypochromic, microcytic anemia and hemosiderosis. The authors describe a 10-year-old Iranian girl with hypochromic microcytic anemia. The age presentation of anemia was 3 months. Further evaluations indicate severe hypochromic microcytic anemia with decreased serum levels of iron, TIBC, and increased serum level of ferritin in this patient. The serum level of transferrin was decreased. The diagnosis of atransferrinemia was confirmed. Although atransferrinemia is a rare condition, it should be considered in the cases with hypochromic microcytic anemia, decreased serum levels of iron, TIBC, and increased serum level of ferritin.