Breast cancer (BCa) is the most frequently diagnosed malignant tumor in women and is also one of the leading causes of cancer-related death. Most breast tumors are hormone-dependent and estrogen signaling plays a critical role in promoting the survival and malignant behaviors of these cells. Estrogen signaling involves ligand-activated cytoplasmic estrogen receptors that translocate to the nucleus with various co-regulators, such as steroid receptor co-activator (SRC) family members, and bind to the promoters of target genes and regulate their expression. SRC-3 is a member of this family that interacts with, and enhances, the transcriptional activity of the ligand activated estrogen receptor. Although SRC-3 has important roles in normal homeostasis and developmental processes, it has been shown to be amplified and overexpressed in breast cancer and to promote malignancy. The malignancy-promoting potential of SRC-3 is diverse and involves both promoting malignant behavior of tumor cells and creating a tumor microenvironment that has an immunosuppressive phenotype. SRC-3 also inhibits the recruitment of tumor-infiltrating lymphocytes with effector function and promotes stemness. Furthermore, SRC-3 is also involved in the development of resistance to hormone therapy and immunotherapy during breast cancer treatment. The versatility of SRC-3 in promoting breast cancer malignancy in this way makes it a good target, and methodical targeting of SRC-3 probably will be important for the success of breast cancer treatment.

It has been previously shown that the aldehyde dehydrogenase (ALDH) family member ALDH1A1 has a significant association with acute myeloid leukemia (AML) patient risk group classification and that AML cells lacking ALDH1A1 expression can be readily killed via chemotherapy. In the past, however, a redundancy between the activities of subgroup members of the ALDH family has hampered the search for conclusive evidence to address the role of specific ALDH genes. Here, we describe the bioinformatics evaluation of all nineteen member genes of the ALDH family as prospective actionable targets for the development of methods aimed to improve AML treatment. We implicate ALDH1A1 in the development of recurrent AML, and we show that from the nineteen members of the ALDH family, ALDH1A1 and ALDH2 have the strongest association with AML patient risk group classification. Furthermore, we discover that the sum of the expression values for RNA from the genes, ALDH1A1 and ALDH2, has a stronger association with AML patient risk group classification and survival than either one gene alone does. In conclusion, we identify ALDH1A1 and ALDH2 as prospective actionable targets for the treatment of AML in high-risk patients. Substances that inhibit both enzymatic activities constitute potentially effective pharmaceutics.

This work is focused on the synthesis of leucyl-glycine-functionalized γ-Fe₂O₃ magnetic nanoparticles coated by polydioxanone (γ-Fe₂O₃-CA-Leu-Gly-PDX) as a polyethersulphone (PES) membrane for biotechnological applications. The physicochemical characteristics were investigated by FT-IR, SEM, XRD, a vibrating sample magnetometer (VSM), and ICP-OES. The present investigation also centered on the several biological activities of γ-Fe₂O₃-CA-Leu-Gly-PDX. The 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging and metal chelating activity was studied for evaluation of its antioxidant activity potential. It exhibited 100% DPPH radical scavenging and 93.33% metal chelating activity. With applicability to antimicrobial photodynamic therapy, DNA cleavage and antimicrobial activity, the cell viability of γ-Fe₂O₃-CA-Leu-Gly-PDX was investigated in detail. The γ-Fe₂O₃-CA-Leu-Gly-PDX demonstrated the significant biofilm inhibition activity as being 81.54% and 86.34% for P. aeruginosa and S. aureus, respectively. Moreover, a novel polyethersulphone nanocomposite membrane incorporated with γ-Fe₂O₃-CA-Leu-Gly-PDX was prepared. The performance of the γ-Fe₂O₃-CA-Leu-Gly-PDX-blended polyethersulphone (PES) membrane was investigated by measuring the antifouling and E. coli rejection. The nanocomposite membranes demonstrated remarkable antifouling properties in contrast with the pristine PES when BSA (bovine serum albumin) and E. coli were filtrated. A complete rejection was obtained by the composite membrane. After an application of the membrane study, the modified polyethersulphone (PES) membrane blended with γ-Fe₂O₃-CA-Leu-Gly-PDX removed 100% of the E. coli.

It has been previously shown that aldehyde dehydrogenase (ALDH) family member ALDH1A1 has a significant association with acute myeloid leukemia (AML) patient risk group classification, and that AML cells lacking ALDH1A1 expression can be readily killed by chemotherapy. In the past, however, a redundancy between the activities of subgroup members of the ALDH family has hampered conclusive evidence for addressing the role of specific ALDH genes. We here describe the bioinformatics evaluation of all nineteen member genes of the ALDH family as prospective actionable targets for the development of methods aimed to improve AML treatment. We implicate ALDH1A1 in the development of recurrent AML, and we show that from the nineteen members of the ALDH family, ALDH1A1 and ALDH2 have the strongest association with AML patient risk group classification. Furthermore, we discover that the sum of the expression values for RNA from the genes ALDH1A1 and ALDH2 has a stronger association with AML patient risk group classification and survival than either one gene alone. In conclusion, we identify ALDH1A1 and ALDH2 as prospective actionable targets for the treatment of AML in high risk patients. Substances that inhibit both enzymatic activities can constitute potentially effective pharmaceutics.

The mutagenicity and antimutagenicity of leaves and flower extract of Cynara syriaca Boiss were studied with Ames assay in Salmonella typhimurium TA98 and TA100 strains. While leaves extract did not show any mutagenic effects against all the tester strains with or without metabolic activation, the flower extract showed mutagenic effect against TA98 strain without metabolic activation. On the other hand, it has been observed that the extracts have antimutagenic activity against mutations induced by sodium azide and daunomycin. The antimicrobial activity of extracts was determined by disc diffusion and MIC value. Both of the extracts possess weak antimicrobial activity. Cupric reducing antioxidant capacity (CUPRAC), DPPH free radical scavenging activity, and ABTS radical cation decolorization methods were carried out to determine the antioxidant activity. Among the tested antioxidant methods, the highest antioxidant capacity was determined in ABTS radical cation decolorization assay in which both of the extracts exhibited the best effect. Flower extract exhibited higher activity also in DPPH free radical scavenging.

Breast cancer (BCa) is the most frequently diagnosed malignant tumor in women and is also one of the leading causes of cancer-related death. Most breast tumors are hormone-dependent and estrogen signaling plays a critical role in promoting the survival and malignant behaviors of these cells. Estrogen signaling involves ligand-activated cytoplasmic estrogen receptors that translocate to the nucleus with various co-regulators such as steroid receptor co-activator (SRC) family members, and bind to the promoters of target genes and regulate their expression. SRC-3 is a member of this family that interacts with, and enhances the transcriptional activity of the ligand activated estrogen receptor. Although SRC-3 has important roles in normal homeostasis and developmental processes, it has been shown to be amplified and overexpressed in breast cancer and to promote malignancy. The malignancy-promoting potential of SRC-3 is diverse and involves both promoting malignant behavior of tumor cells and creating a tumor microenvironment that has an immunosuppressive phenotype. SRC-3 also inhibits the recruitment of tumor-infiltrating lymphocytes with effector function and promotes stemness. Furthermore, SRC-3 is also involved in the development of resistance to hormone therapy and immunotherapy during breast cancer treatment. The versatility of SRC-3 in promoting breast cancer malignancy in this way makes it a good target, and methodical targeting of SRC-3 probably will be important for the success of breast cancer treatment.