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Abstract Summary We introduce NRGSuite-Qt, a PyMOL plugin, that provides a comprehensive toolkit for macromolecular cavity detection, virtual screening, small-molecule docking, normal mode analysis, analyses of molecular interactions, and detection of binding-site similarities. This complete redesign of the original NRGSuite (restricted to cavity detection and small-molecule docking) integrates five new functionalities: protein–protein and protein–ligand interaction analysis using Surfaces, ultra-massive virtual screening with NRGRank, binding-site similarity detection with IsoMIF, normal mode analysis using NRGTEN, and mutational studies through integration with the Modeler Suite. By merging these advanced tools into a cohesive platform, NRGSuite-Qt simplifies visualization and streamlines complex workflows within a single interface. Additionally, we benchmark a newer version of the Elastic Network Contact Model (ENCoM) for normal mode analysis method, utilizing the same 40 atom-type pairwise interaction matrix that is used in all other software. This version outperforms the default model in multiple benchmarking tests. Avalilability and implementation The Installation guide and tutorial is available at https://nrg-qt.readthedocs.io/en/latest/index.html. The NRGSuite-Qt is implement in Python.

[This corrects the article DOI: 10.3389/fphar.2025.1676800.].

A novel electrochemiluminescence (ECL) method was developed for determination of protein kinase A (PKA) ultra-sensitively based on amidated nano-titanium (NH.sub.2-TiO.sub.2) embellished carbon dots (Mg@N-CDs) fluorescent probe, which integrated the target recognition and ECL signal enhancement. The Cys-labeled kemptides were employed to build a serine-rich synthetic substrate-heptapeptide (Cys-kemptide) on the Au-electrode surface. Then, the PKA-induced biosensor was triggered as a signal switch to introduce the large amounts of TiO.sub.2 decorated Mg@N-CD nanohybrid (Ti@NMg-CDs) into AuE/Cys-phosphopeptides for signal output. In particular, the presence of PKA could induce the formation of Cys-phosphopeptides by the catalytic reaction between specific substrate (kemptide) and PKA, which acts as an initiator to link the Ti@NMg-CDs according to the bridge interactions Ti-O-P. In this way, multiple Cys-phosphopeptides were adsorbed onto a single Ti@NMg-CDs, and the Ti@NMg-CDs not only provided high specific selectivity but also large surface area, as well as unprecedented high ECL efficiency. Using this PKA-induced enhanced sensor, the limit of detection of the PKA was 4.89 x 10.sup.-4 U/mL (S/N = 3). The proposed ECL biosensor was also universally applicable for the screening of PKA inhibitors and determining of other kinases activity. Our sensing system has excellent performance of specificity and the screening of kinase inhibitors, as well as it will inspire future effort in clinical diagnostics and new drug discovery. Graphical

[This corrects the article DOI: 10.3389/fphar.2025.1676800.].

A 37-year-old male presented with severe oral and genital mucosal ulcers, lichenoid eruption and twenty-nail dystrophy. Systemic examination was normal, except for anemia. On investigations, he was found to have persistently elevated peripheral eosinophilia, absolute eosinophil count >5000/mm 3 , bone marrow showing increased eosinophilic precursors, and infiltration by atypical cells. The serum vitamin B12 levels were grossly elevated, and Philadelphia chromosome study was negative. Thus, a diagnosis of chronic eosinophilic leukemia was made. The patient showed excellent response to imatinib mesylate. We are reporting a rare type of leukemia presenting with predominantly cutaneous manifestations.

Current antineoplastic agents present multiple disadvantages, driving an ongoing search for new and better compounds. Four lupane-type triterpenes, 3α,24-dihydroxylup-20(29)-en-28-oic acid (1), 3α,23-dihydroxy-30-oxo-lup-20(29)-en-28-oic acid (2), 3α,23-O-isopropylidenyl-3α,23-dihydroxylup-20(29)-en-28-oic acid (3), and 3α,23-dihydroxylup-20(29)-en-28-oic acid (4), previously isolated from Phoradendron wattii, were evaluated on two cell lines of chronic (K562) and acute (HL60) myeloid leukemia. Compounds 1, 2, and 4 decreased cell viability and inhibit proliferation, mainly in K562, and exhibited an apoptotic effect from 24 h of treatment. Of particular interest is compound 2, which caused arrest in active phases (G2/M) of the cell cycle, as shown by in silico study of the CDK1/Cyclin B/Csk2 complex by molecular docking. This compound [3α,23-dihydroxy-30-oxo-lup-20(29)-en-28-oic acid] s a promising candidate for incorporation into cancer treatments and deserves further study.

Every sixth person in the world dies due to cancer, making it the second leading severe cause of death after cardiovascular diseases. According to WHO, cancer claimed nearly 10 million deaths in 2020. The most common types of cancers reported have been breast (lung, colon and rectum, prostate cases), skin (non-melanoma) and stomach. In addition to surgery, the most widely used traditional types of anti-cancer treatment are radio- and chemotherapy. However, these do not distinguish between normal and malignant cells. Additional treatment methods have evolved over time for early detection and targeted therapy of cancer. However, each method has its limitations and the associated treatment costs are quite high with adverse effects on the quality of life of patients. Use of individual atoms or a cluster of atoms (nanoparticles) can cause a paradigm shift by virtue of providing point of sight sensing and diagnosis of cancer. Nanoparticles (1–100 nm in size) are 1000 times smaller in size than the human cell and endowed with safer relocation capability to attack mechanically and chemically at a precise location which is one avenue that can be used to destroy cancer cells precisely. This review summarises the extant understanding and the work done in this area to pave the way for physicians to accelerate the use of hybrid mode of treatments by leveraging the use of various nanoparticles.

In the ENESTnd study, with ≥10 years follow-up in patients with newly diagnosed chronic myeloid leukemia (CML) in chronic phase, nilotinib demonstrated higher cumulative molecular response rates, lower rates of disease progression and CML-related death, and increased eligibility for treatment-free remission (TFR). Cumulative 10-year rates of MMR and MR 4.5 were higher with nilotinib (300 mg twice daily [BID], 77.7% and 61.0%, respectively; 400 mg BID, 79.7% and 61.2%, respectively) than with imatinib (400 mg once daily [QD], 62.5% and 39.2%, respectively). Cumulative rates of TFR eligibility at 10 years were higher with nilotinib (300 mg BID, 48.6%; 400 mg BID, 47.3%) vs imatinib (29.7%). Estimated 10-year overall survival rates in nilotinib and imatinib arms were 87.6%, 90.3%, and 88.3%, respectively. Overall frequency of adverse events was similar with nilotinib and imatinib. By 10 years, higher cumulative rates of cardiovascular events were reported with nilotinib (300 mg BID, 16.5%; 400 mg BID, 23.5%) vs imatinib (3.6%), including in Framingham low-risk patients. Overall efficacy and safety results support the use of nilotinib 300 mg BID as frontline therapy for optimal long-term outcomes, especially in patients aiming for TFR. The benefit-risk profile in context of individual treatment goals should be carefully assessed.