Abusing AAS is starting to become a public health concern that implies the need to implement educational programmes, which will educate and warn adolescents and mentors about the negative side effects of AAS abuse on the health of users.
2DG causes cytotoxicity in cancer cells by disrupting thiol metabolism while Doxorubicin (DOX) induces cytotoxicity in tumor cells by generating reactive oxygen species (ROS). Here we examined the combined cytotoxic action of 2DG and DOX in rapidly dividing T47D breast cancer cells vs. slowly growing MCF-7 breast cancer cells. T47D cells exposed to the combination of 2DG/DOX significantly decreased cell survival compared to controls, while 2DG/DOX had no effect on MCF-7 cells. 2DG/DOX also disrupted the oxidant status of T47D treated cells, decreased intracellular total glutathione and increased glutathione disulfide (%GSSG) compared to MCF-7 cells. Lipid peroxidation increased in T47D cells treated with 2DG and/or DOX, but not in MCF-7 cells. T47D cells were significantly protected by NAC, indicating that the combined treatment exerts its action by increasing ROS production and disrupting antioxidant stores. When we inhibited glutathione synthesis with BSO, T47D cells became more sensitive to 2DG/DOX-induced cytotoxicity, but NAC significantly reversed this cytotoxic effect. Finally, 2DG/DOX, and BSO significantly increased the %GSSG in T47D cells, an effect which was also reversed by NAC. Our results suggest that exposure of rapidly dividing breast cancer cells to 2DG/DOX enhances cytotoxicity via oxidative stress and via disruptions to thiol metabolism.
Targeted disruption of E2f2 in mice causes T-cell hyperactivation and a disproportionate cell cycle entry upon stimulation. However, E2f2−/− mice do not develop a lymphoproliferative condition. We report that E2f2 plays a Fas-dependent anti-apoptotic function in vitro and in vivo. TCR-stimulated murine E2f2−/− T cells overexpress the proapoptotic genes Fas and FasL and exhibit enhanced apoptosis, which is prevented by treatment with neutralizing anti-FasL antibodies. p53 pathway is activated in TCR-stimulated E2f2−/− lymphocytes, but targeted disruption of p53 in E2f2−/− mice does not abrogate Fas/FasL expression or apoptosis, implying a p53-independent apoptotic mechanism. We show that E2f2 is recruited to Fas and FasL gene promoters to repress their expression. in vivo, E2f2−/− mice are prone to develop immune-mediated liver injury owing to an aberrant lymphoid Fas/FasL activation. Taken together, our results suggest that E2f2-dependent inhibition of Fas/FasL pathway may play a direct role in limiting the development of immune-mediated pathologies.
Introduction: The term "gestational trophoblastic neoplasia" (GTN) refers to abnormal proliferation of trophoblastic tissue and occurs during pregnancy. It includes hydatiform mole, invasive mole, choriocarcinoma, placental site trophoblastic tumour and epitheliod trophoblastic tumour. Patients and Methods: This retrospective study was conducted at the Department of radiology, Peoples Medical College, Hospital, Nawabshah, Shaheed Benazirabad, Sindh; the clinical & ultrasonographic records of biopsy-proven cases of gestational trophoblastic disease registered in the department from January 1, 2019, to December 31, 2020 was evaluated and analysed through SPSS. Results: Total of 137 patients of biopsy proven gestational trophoblastic tumor was registered during the period. The age of the patient ranges between 15 to 50 years, the disease is most common in 21 to 30 years of age. Majority of patients belong to the rural areas (73%) in comparsion to urban area (26%).The most common tumor was hydatiform mole (76% ) followed by choriocarcinoma Conclusion: Gestational trophoblastic neoplasia are common disease in females of 21 to 30 years of age and hydatiform mole is the most frequent tumor type Keywords: Gestational trophoblastic disease, Hydatiform Mole, Malignancy, Ultrasound.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.