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  1. Harwansh RK, Hamid JA, Wal P, Deshmukh R, Patra PK, Gasmi A
    Curr Pharm Des, 2025 Feb 27.
    PMID: 40017252 DOI: 10.2174/0113816128334659241223113743
    OBJECTIVE OF THE STUDY: This review aims to critically analyze the scope for targeting drugs towards the treatment of improving outcomes in PDAC, focusing on DNA repair inhibitors, antiangiogenic therapy, inhibitors of the KRAS pathway, anti-stromal, and nanoparticle-based therapy.

    MATERIALS AND METHODS: A critical review of preclinical and clinical studies was conducted to summarize the therapeutic interventions that target specific mutations in PDAC, components of the tumor microenvironment, and drug delivery systems, especially nanotechnology, to enhance targeting and efficacy.

    RESULTS: Inhibitors and nanotechnology-based targeted therapies have reported promise in preclinical models: drug delivery is enhanced with the loss of PDAC resistance mechanisms. Formulations and combinations targeting KRAS as well as other pathways point toward improved drug delivery over 'orthodox' treatment approaches.

    CONCLUSION: This review concludes that although improvement in therapies for PDAC has incrementally been proven in recent literature, however, more research is expected to enhance these approaches so that they can be applied appropriately at the clinical stage. In future studies, it is expected to optimize treatment combinations, address mechanisms of resistance, and improve the delivery of drugs.

  2. Sharma A, Sharma C, Sharma L, Wal P, Mishra P, Sachdeva N, et al.
    Can J Physiol Pharmacol, 2024 May 01;102(5):305-317.
    PMID: 38334084 DOI: 10.1139/cjpp-2023-0259
    Mostly, cardiovascular diseases are blamed for casualties in rheumatoid arthritis (RA) patients. Customarily, dyslipidemia is probably the most prevalent underlying cause of untimely demise in people suffering from RA as it hastens the expansion of atherosclerosis. The engagement of inflammatory cytokines like tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), interleukin-6 (IL-6), etc., is crucial in the progression and proliferation of both RA and abnormal lipid parameters. Thus, lipid abnormalities should be monitored frequently in patients with both primary and advanced RA stages. An advanced lipid profile examination, i.e., direct role of apolipoproteins associated with various lipid molecules is a more dependable approach for better understanding of the disease and selecting suitable therapeutic targets. Therefore, studying their apolipoproteins is more relevant than assessing RA patients' altered lipid profile levels. Among the various apolipoprotein classes, Apo A1 and Apo B are primarily being focused. In addition, it also addresses how calculating Apo B:Apo A1 ratio can aid in analyzing the disease's risk. The marketed therapies available to control lipid abnormalities are associated with many other risk factors. Hence, directly targeting Apo A1 and Apo B would provide a better and safer option.
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