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Traduzione e revisione capitoli di 38, 39, 40, 43, 48 e 56 della 10a edizione 2007 Inglese Basic and Clinical Pharmacology McGraw-Hill - Katzung corrispondente alla 7a edizione 2009 Italiana Piccin
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Capitolo 37: Ormoni ipotalamici e ipofisari; Capitolo 38: Tiroide e farmaci antitiroidei; Capitolo 39: Gli steroidi corticosurrenalici e antagonisti; Capitolo 40§: Ormoni delle gonadi; Capitolo 43: Antibiotici beta-lattamici ed altri antibiotici attivi sulla parete o della membrana cellulari; Capitolo 48: Agenti antimicotici; Capitolo 55: Immunofarmacologia.
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Parte V- Farmaci per il trattamento di infezioni, tumori e malattie immunologiche; Capitoli: 49, Principi di chemioterapia antimicrobica; 50, Farmaci antibatterici; 51, Farmaci antivirali; 52, Farmaci antifungini; 53, Farmaci antiprotozoari; 54, Farmaci anti-elmintici; 55, Farmaci antitumorali. Farmacologia, VII edizione Italiana di Rang and Dale's Pharmacology (VII ed. Inglese); p.616-680.
No full textRisorse economiche, compatibilità cliniche, libertà prescrittiva. In: I farmaci e le sfide di una medicina a misura di paziente.
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Therapeutic implication of vascular endothelial growth factor receptor-1 (VEGFR-1) targeting in cancer cells and tumor microenvironment by competitive and non-competitive inhibitors
No full textThe vascular endothelial growth factor receptor-1 (VEGFR-1) is a tyrosine kinase receptor for VEGF-A, VEGF-B, and placental growth factor (PlGF) ligands that is expressed in endothelial, myelomonocytic and tumor cells. VEGF-B and PlGF exclusively bind to VEGFR-1, whereas VEGF-A also binds to VEGFR-2. At variance with VEGFR-2, VEGFR-1 does not play a relevant role in physiological angiogenesis in the adult, while it is important in tumor-associated angiogenesis. VEGFR-1 and PlGF are expressed in a variety of tumors, promote invasiveness and contribute to resistance to anti-VEGF-A therapy. The currently approved antiangiogenic therapies for the treatment of a variety of solid tumors hamper VEGF-A signaling mediated by both VEGFR-2 and VEGFR-1 [i.e., the monoclonal antibody (mAb) anti-VEGF-A bevacizumab, the chimeric molecule aflibercept and several small molecule tyrosine kinase inhibitors] or exclusively by VEGFR-2 (i.e., the mAb anti-VEGFR-2 ramucirumab). However, molecules that interfere with VEGF-A/VEGFR-2 signaling determine severe adverse effects due to inhibition of physiological angiogenesis and their efficacy is hampered by tumor infiltration of protumoral myeloid cells. Blockade of VEGFR-1 may exert anti-tumor activity by multiple mechanisms: a) inhibition of tumor-associated angiogenesis; b) reduction of myeloid progenitor mobilization and tumor infiltration by VEGFR-1 expressing M2 macrophages, which contribute to tumor progression and spreading; c) inhibition of invasiveness, vasculogenic mimicry and survival of VEGFR-1 positive tumor cells. As a consequence of these properties, molecules targeting VEGFR-1 are expected to produce less adverse effects and to counteract resistance towards anti-VEGF-A therapies. More interestingly, selective VEGFR-1 inhibition might enhance the efficacy of immunotherapy with immune checkpoint inhibitors. In this review, we will examine the experimental evidence available so far that supports targeting VEGFR-1 signal transduction pathway for cancer treatment by competitive inhibitors that prevent growth factor interaction with the receptor and non-competitive inhibitors that hamper receptor activation without affecting ligand binding
Capitoli 37, 38, 39, 55 di Farmacologia IX Ed. Italiana di Katzung B.G. Masters S.B. Trevor A.J. (XII Ed. Americana)
No full textApplication of multipoles expansion technique to two-dimensional nonlinear free-surface flows
No full textThe original idea by Rokhlin (1985) to rapidly solve the Laplace equation is applied here for studying nonlinear free-surface flows. The boundary integral equations for the velocity field are discretized through the Euler-McLaurin quadrature formula, which, in spite of its simplicity, displays spectral convergence properties for regular boundary data. In order to solve the discretized boundary integral equations, an iterative solver for algebraic systems is coupled to a fast summation technique based on the multipoles expansion of the influence coefficients. The resulting algorithm allows for a small size of the code (O(N)) and fast computation (O(Nlog N)) without affecting the original convergence properties. Typical long-time evolution and large-scale computations, which often arise in nonlinear free-surface flows, are discussed to show the effectiveness of the developed approach
Role of BRCA mutations in cancer treatment with poly(ADP-ribose) polymerase (PARP) inhibitors
Full text linkInhibition of poly(ADP-ribose) polymerase (PARP) activity induces synthetic lethality in mutated BRCA1/2 cancers by selectively targeting tumor cells that fail to repair DNA double strand breaks (DSBs). Clinical studies have confirmed the validity of the synthetic lethality approach and four different PARP inhibitors (PARPi; olaparib, rucaparib, niraparib and talazoparib) have been approved as monotherapies for BRCA-mutated or platinum-sensitive recurrent ovarian cancer and/or for BRCA-mutated HER2-negative metastatic breast cancer. PARPi therapeutic efficacy is higher against tumors harboring deleterious germline or somatic BRCA mutations than in BRCA wild-type tumors. BRCA mutations or intrinsic tumor sensitivity to platinum compounds are both regarded as indicators of deficiency in DSB repair by homologous recombination as well as of favorable response to PARPi. However, not all BRCA-mutated or platinum-responsive patients obtain clinical benefit from these agents. Conversely, a certain percentage of patients with wild-type BRCA or platinum-resistant tumors can still get benefit from PARPi. Thus, additional reliable markers need to be validated in clinical trials to select patients potentially eligible for PARPi-based therapies, in the absence of deleterious BRCA mutations or platinum sensitivity. In this review, we summarize the mechanisms of action of PARPi and the clinical evidence supporting their use as anticancer drugs as well as the additional synthetic lethal partners that might confer sensitivity to PARPi in patients with wild-type BRCA tumors
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