Surface modification of a screen-printed electrode with a flower-like nanostructure to fabricate a guanine DNA-based electrochemical biosensor to determine the anticancer drug pemigatinib.

The present study developed a DNA biosensor to determine pemigatinib for the first time. Three-dimensional carnation flower-like Eu3+:ß-MnO2 nanostructures (3D CF-L Eu3+:ß-MnO2 NSs) and a screen-printed electrode (SPE) modified with polyaniline (PA) were employed. The double-stranded DNA was also immobilized completely on the PA/3D CF-L Eu3+:ß-MnO2 NSs/SPE. Then, electrochemical techniques were used for characterizing the modified electrode. After that, the interaction between pemigatinib and DNA was shown by a reduction in the oxidation current of guanine using differential pulse voltammetry (DPV). According to the analysis, the dynamic range of pemigatinib was between 0.001 and 180.0 µM, indicating the new electrode has a low limit of detection (LOD = 0.23 nM) for pemigatinib. Afterwards, pemigatinib in real samples was measured using the PA/3D CF-L Eu3+:ß-MnO2 NSs/SPE loaded with ds-DNA. The proposed DNA biosensor showed good selectivity toward pemigatinib in the presence of other interference analytes, such as other ions, structurally related pharmaceuticals, and plasma proteins. In addition, the interaction site of pemigatinib with DNA was predicted by molecular docking, which showed the interaction of pemigatinib with the guanine bases of DNA through a groove binding mode. Finally, we employed the t-test to verify the capability of the ds-DNA/PA/3D CF-L Eu3+:ß-MnO2 NSs/SPE for analyzing pemigatinib in real samples.

Breast cancer vaccines; A comprehensive and updated review.

According to the International Agency for Research on Cancer, breast cancer is more common than lung cancer globally. By 2040, mortality from breast cancer will rise by 50% and 40%, respectively. Despite advances in chemotherapy, endocrine therapy, and HER2-targeted therapy, breast cancer metastases and recurrences remain challenging to treat. Cancer vaccines are an effective treatment option because they stimulate a long-lasting immune response that will eliminate tumor cells. In studies on the breast cancer vaccine, no appreciable advantages were discovered. A recent study claims that immune checkpoint inhibitors or anti-HER2 monoclonal antibodies may be used in vaccinations. This vaccination strengthens the immune system to fight off breast cancer cells. Clinical trials have been conducted on DNA, dendritic cells, and peptide-based breast cancer vaccines. Studies on the breast cancer vaccine have employed subcutaneous, intramuscular, and intradermal injections. Clinical studies have shown that these efforts have not been successful. Several factors might have slowed the development of a breast cancer vaccine. The complexity of the immune system makes it challenging to create cancer vaccines. Given the heterogeneity of breast cancer, there may be a need for different vaccination strategies. Despite these obstacles, research into breast cancer vaccines continues. Effective methods for creating vaccines include immune checkpoint inhibition and anti-HER2 monoclonal antibodies. Research is also being done on specialized tumor vaccinations.

Oxidative stress affects the beginning of the growth of cancer cells through a variety of routes.

Oxidative stress is a physiological condition that occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the cell's antioxidant defense system. ROS are highly reactive molecules that can cause damage to cellular structures such as DNA, proteins, and lipids. the regulation of ROS levels and the antioxidant defense system is crucial for cancer prevention and treatment. Strategies to enhance antioxidant defenses or induce oxidative stress selectively in cancer cells are being developed as potential therapeutic approaches. targeting oxidative stress in cancer treatment is an active area of research with several potential therapeutic approaches being investigated. Developing selective and effective therapies that target oxidative stress in cancer cells while sparing normal cells will be crucial for improving cancer treatment outcomes.

Investigation of catalytic activity of metal doped nanocages (Ni-C72 and Ni-Al36P36) for ozone decomposition to oxygen molecules.

CONTEXT: The potential of Ni-C72 and Ni-Al36P36 as effective catalysts for O3 decomposition is examined by LH and ER mechanisms. The activation barrier energy and Gibbs free energy of reaction steps for O3 decomposition on Ni-C72 and Ni-Al36P36 are calculated. The ∆Eformation of Ni-C72 and Ni-Al36P36 are negative values and these structures are stable nano-catalysts. The Ni atoms are catalytic positions to adsorb the O3 and other important species of O3 decomposition by LH and ER mechanisms. The Ni-Al36P36 for O3 decomposition has lower Eacivation and more negative ∆Greaction than Ni-C72. The Eacivation value of rate-determining step for O3 decomposition by LH mechanism is lower than ER mechanism. The Ni-C72 and Ni-Al36P36 can catalyze the reaction steps of O3 decomposition by LH and ER mechanisms. METHODS: The structures of Ni-C72 and Ni-Al36P36 nanocages and their complexes with O3 and other important species of are optimized by PW91PW91/6-311 + G (2d, 2p) model and M06-2X/cc-pVQZ model in GAMESS software. The strcutures of nanocages and their complexes with important species of O3 decomposition by LH and ER mechanisms are optimized and their frequencies are calculated in order to demonstrate that these structures are real minima on the potential energy surface.

LncRNA-miRNA interaction is involved in colorectal cancer pathogenesis by modulating diverse signaling pathways.

LncRNAs function as molecular sponges for miRNAs to control their availability for targeting mRNA molecules. This procedure indirectly regulates the expression of cancer-related genes. Some lncRNAs also directly interact with miRNAs, leading to their degradation or sequestration, which can negatively impact gene expression. miRNAs, on the other hand, play a critical role in controlling the expression of genes, including oncogenes and tumor suppressor genes. Multiple types of cancer have been linked to the onset and progression of miRNA dysregulation. Even though there is a lot of potential for treating CRC by targeting the LncRNA-miRNA axis, several challenges remain to be overcome. The specificity of the targeting approach, delivery methods, resistance, safety, and cost-effectiveness are critical research areas that must be addressed to advance this field and improve treatment outcomes for people with CRC.

LncRNA PVT1: as a therapeutic target for breast cancer.

A significant number of women are identified with breast cancer (BC) every year, making it among the most prevalent malignancies and one of the leading causes of mortality globally. Despite significant progress in understanding BC pathogenesis and treatment options, there is still a need to identify new therapeutic targets and develop more effective treatments. LncRNAs have been discovered as biomarkers and a promising target for various cancers, including BC. PVT1 is a particular one of these lncRNAs, and research has indicated that it has a significant impact on the appearance and progression of BC.PVT1 is an attractive therapeutic target for BC due to its role in promoting cancer cell growth, metastasis and invasion. In addition to its potential as a treatment strategy, PVT1 may also have diagnostic value in BC. In this article, we will discuss targeting PVT1 as a treatment strategy for BC.