Scopus Research — Mohammed Sami Hasan

Focus of this study is on the use of the hydrazone compound (3) (N-(4-bromobenzylidene)-4-(1H-indol-3-yl) butane hydrazide), which was previously prepared from the reaction of the compound p-bromobenzaldehyde with the corresponding hydrazide (2), as an intermediate compound for the synthesis of azetidine, thiazolidine, tetrazole, oxadiazole and phthalazine heterocyclic compounds through its reaction with some cyclic reagents and catalysts such as chloro acetyl chloride, thioglycolic acid, sodium-azid, lead dioxide and Hydrogen chloride gas. The prepared compounds were characterized using physical properties and also spectroscopic methods such as infrared spectroscopy, nuclear magnetic resonance spectra of the proton and the isotope of carbon13 as well as mass spectrometry, which accurately identified the proposed structures of the prepared compounds. The identity of the prepared compounds was determined using physical and spectroscopic properties, where infrared and 1HNMR spectroscopy of the proton as well as carbon13 were used in addition to using mass spectrometry to verify the validity of the prepared structures. Conclusions: Also, the biological antibacterial evaluation of the compounds (4–8) was conducted and it gave a good result compared to the drug (8) used as a reference for the control, The MTT test was performed on the healthy and cancerous cells of the compounds (4,5,8) and gave an excellent result for the compound (8). © 2024 The Author(s)

Background: Tamoxifen (TAM) is often recommended as a first-line treatment for estrogen receptor-positive breast cancer (BC). However, TAM resistance continues to be a medical challenge for BC with hormone receptor positivity. The function of macro-autophagy and autophagy has recently been identified to be altered in BC, which suggests a potential mechanism for TAM resistance. Autophagy is a cellular stress-induced response to preserve cellular homeostasis. Also, therapy-induced autophagy, which is typically cytoprotective and activated in tumor cells, could sometimes be non-protective, cytostatic, or cytotoxic depending on how it is regulated. Objective: This review explored the literature on the connections between hormonal therapies and autophagy. We investigated how autophagy could develop drug resistance in BC cells. Methods: Scopus, Science Direct, PubMed, and Google Scholar were used to search articles for this study. Results: The results demonstrated that protein kinases such as pAMPK, BAX, and p-p70S6K could be a sign of autophagy in developing TAM resistance. According to the study's findings, autophagy plays an important role in BC patients' TAM resistance. Conclusion: Therefore, by overcoming endocrine resistance in estrogen receptor-positive breast tumors, autophagy inhibition may improve the therapeutic efficacy of TAM. © 2023 Société Française de Pharmacologie et de Thérapeutique.