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Angiogenesis in Hematological Malignancies
Published in Gertjan J. L. Kaspers, Bertrand Coiffier, Michael C. Heinrich, Elihu Estey, Innovative Leukemia and Lymphoma Therapy, 2019
Alida C. Weidenaar, Hendrik J. M. de Jonge, Arja ter Elst, Evelina S. J. M. de Bont
The knowledge about increased tumor growth augmented by angiogenesis resulted directly in new antiangiogenic treatment strategies. Thalidomide was used as an antiangiogenic drug in MM and resulted in enhanced survival. Nowadays, it is demonstrated that the function of thalidomide seems not restricted to antiangiogenesis; surrounding bone marrow stromal cells as well as myeloma cells themselves seemed to be targets of thalidomide (90).
Radiolabeled Agents for Molecular Imaging and/or Therapy
Published in George C. Kagadis, Nancy L. Ford, Dimitrios N. Karnabatidis, George K. Loudos, Handbook of Small Animal Imaging, 2018
Dimitrios Psimadas, Eirini A. Fragogeorgi
This could provide essential information in the evaluation of anti-angiogenic therapy and could lead to better understanding and patient-tailored therapy. This could lead to a better understanding of the biology of these tumors and consequently could provide a more efficient evaluation of the anti-angiogenic treatment effects and new patient-tailored therapy options. In a recent study, 166Ho-bevacizumab was used for biodistribution evaluation and to acquire dosimetric aspects of the radiolabeled antibody in mice using SPECT (Khorami-Moghadam et al. 2013). 166Ho-bevacizumab imaging in wild-type rats showed distinct accumulation of the radiotracer in the chest region. Accumulation of the radiolabeled antibody in liver, spleen, kidney, bone, and other tissues as well as sufficient tumor uptake demonstrates a similar pattern to the majority of radiolabeled anti-VEGF immunoconjugates. 166Ho-bevacizumab can become a potential compound for diagnosis and treatment studies and follow-up of VEGF expression in oncology.
Biologically Targeted Agents in Head and Neck Cancers
Published in John C Watkinson, Raymond W Clarke, Terry M Jones, Vinidh Paleri, Nicholas White, Tim Woolford, Head & Neck Surgery Plastic Surgery, 2018
Kevin J. Harrington, Magnus T. Dillon
A number of EGFR-targeted MAB have been tested in the clinic. They differ in terms of their species of origin (murine, chimeric (part human/part murine) or fully human) and the part (epitope) of the EGFR protein that they target. Cetuximab (C225, Erbitux) is a human-murine chimeric MAB. In vitro studies showed anti-tumour activity through anti-proliferative effects, direct cytotoxicity and potentiation of the effects of chemotherapy or radiotherapy.15–18 In addition, in vivo experiments demonstrated anti-angiogenic effects.19 Early stage clinical trials confirmed the efficacy of cetuximab in combination with chemotherapy or radiotherapy.20–24
Production of a biosimilar version of aflibercept to improve VEGF blocker cytotoxicity on endothelial cells
Published in Growth Factors, 2023
Amin Ramezani, Mohammadrasul Zareinejad, Elham Mahmoudi Maymand, Elina Kaviani, Abbas Ghaderi
The 10-fold increase in cytotoxicity observed when LEN and SOR were co-treated with biosimilar-AFL may be due to a synergistic effect between these drugs. Lenvatinib is a multi-kinase inhibitor that targets VEGF and other receptors involved in tumor angiogenesis, while SOR inhibits the activity of VEGF and other growth factors receptors. Biosimilar-AFL, as a VEGF blocker, can work in conjunction with LEN and SOR to enhance their effectiveness by targeting VEGF from multiple angles, leading to a more potent inhibition of angiogenesis. Moreover, the combined treatment may lead to the suppression of various signaling pathways that are involved in the proliferation and survival of cancer cells. The combination of LEN and SOR with biosimilar-AFL may also lead to an increase in apoptosis, or programmed cell death, of cancer cells, thereby reducing their viability and proliferation. However, further studies are required to elucidate the exact mechanism behind the observed synergistic effect and to optimize the dosing and administration of these drugs for maximal efficacy and minimal toxicity. Finally, the observed 10-fold increase in cytotoxicity of LEN and SOR when co-treated with biosimilar-AFL is an exciting finding with great potential for improving cancer treatment outcomes. It highlights the importance of exploring the combination of different anti-angiogenic drugs for cancer therapy and may lead to the development of more effective and less toxic treatment regimens for cancer patients.
Nano-composite hydrogels of Cu-Apa micelles for anti-vasculogenic mimicry
Published in Journal of Drug Targeting, 2023
Rui Kang, Mengdi Song, Zhou Fang, Kehai Liu
Anti-angiogenic drugs are exclusively being used to treat VM currently. However, anti-angiogenic drugs were found to have adverse side effects during treatment, including coagulation disorders, gastrointestinal perforation, slow wound healing, and hypertension [8–14]. When used to treat angiogenesis in liver cancer, kidney cancer, colorectal cancer, non-small cell lung cancer, and gastric cancer [15, 16], kinase inhibitors (e.g. Gefitinib, Lapatinib, Apatinib) and monoclonal antibodies (e.g. Bevacizumab, Ramuciruma) were found to lead to cell hypoxia, which promoted the activation of the HIF-1 of the VEGF/PI3K/EphA2/AKT pathway, which reinduced tumour angiogenesis. Moreover, single anti-angiogenic drugs are less efficient in inhibiting VM. Gefitinib elicits a significant initial response in the treatment of patients with advanced non-small-cell lung cancer (NSCLC); however, tumours become resistant after 9–12 months [17]. Drug resistance also developed to Apatinib during the late stages of treatment of patients with NSCLC [18]. Based on these observations, a combination of drugs that target multiple pathways has been proposed to inhibit the formation of VM. Zhao et al. [19]. discovered that a direct thrombin inhibitor peptide (DTIP) and gefitinib combination was superior to gefitinib alone in the treatment of VM in NSCLC. In follow-up studies, these drugs were modified with metallic ions to inhibit VM. For example, copper sulfide-modified cetuximab and mononuclear copper (II) polypyridine complexes proved to be an effective strategy for the treatment of angiogenesis [20–23].
Molecular Mechanism of Curcumin and Its Analogs as Multifunctional Compounds against Pancreatic Cancer
Published in Nutrition and Cancer, 2022
Qun Huang, Ya Zhang, Yanlin Zheng, Hongjing Yang, Yang Yang, Ya Mo, Liuying Li, Hong Zhang
Angiogenesis is essential for tumor growth and metastasis (37). Proangiogenic factors such as vascular endothelial growth factor (VEGF), platelet-derived growth factor (PD-ECGF), angiopoietin, and tumor growth factor β (TGF-β) are frequently overexpressed in tumors (38, 39). Therefore, the development of anti-angiogenic drugs is an effective strategy for tumor treatment. Studies have demonstrated that curcumin could significantly inhibit the secretion of VEGF, angiopoietin 1, angiopoietin 2, PD-ECGF, and TGF-β in PC cell lines (39). Furthermore, curcumin could inhibit the expression of VEGF and vascular endothelial growth factor receptor 1 (VEGFR1) genes in PC cell lines (36, 40). The above evidence indicates that curcumin is a potential antiangiogenic drug for treating PC.