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• W2074958345 abstract "‘Angiogenesis’ refers to the formation of new blood vessels, a tightly controlled process regulated by multiple factors in vivo. Proangiogenic molecules include VEGF, HIF-1a, PDGF, bFGF angiopoietins and IL-8 (reviewed in [1]). On the other hand, antiangiogenic molecules include thrombo spondin, angiostatin and collagen type XVIII (the precursor of endostatin; reviewed in [1]). Without the induction of angiogenesis, diffusion of nutrients and oxygen are thought to limit the survival of proliferating cells in growing tumors. Therefore, perturbation of physiological regulation of angiogenesis is hypothesized to be necessary to sustain tumor growth. This has sustained interest in exploitation of angiogenesis as a therapeutic target in cancer over the past few decades, including in lung cancer, which remains the most common cause of cancer-related death in the western world. Building on outcomes with VEGF pathway antagonist therapy, we discuss some strategies to further exploit the potential of antiangiogenic therapy in lung cancer. Evidence from two large Phase III trials suggests that in nonsquamous metastatic non-small-cell lung cancer (NSCLC), bevacizumab (a VEGF-A inhibitor) led to significantly increased response rates and improved progression-free survival (PFS) [2,3]. One of the trials reported improved overall survival (OS) [2]. While antiangiogenic therapy is less studied for small-cell lung cancer, a recent Phase II trial of bevacizumab in combination with chemotherapy for extensive disease smallcell lung cancer suggested prolonged PFS and OS compared with historical controls [4]. However, Phase III data are awaited. Overall, the bevacizumab trials have confirmed the safety and tolerability of VEGF inhibitor therapy in combination with chemotherapy for nonsquamous NSCLC. Despite concerns for squamous tumors, significant bleeding episodes were rare, even in patients on full-dose anticoagulant therapy who had nonsquamous tumors [5]. Allergies and proteinuria were rare, while hypertension was conveniently managed in the minority who developed this side effect [2,3]. Nevertheless, the median OS benefit for the addition of bevacizumab to chemo therapy was only 2 months [2]. The" @default.
• W2074958345 created "2016-06-24" @default.
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• W2074958345 date "2012-06-01" @default.
• W2074958345 modified "2023-09-27" @default.
• W2074958345 title "Angiogenesis inhibitors in lung cancer: beyond VEGF?" @default.
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• W2074958345 doi "https://doi.org/10.2217/lmt.12.2" @default.
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