Expert review of anticancer therapy
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Lung cancer remains the leading cause of malignancy-related deaths in the USA, regardless of advances in therapeutic agents. Non-small-cell lung cancer demonstrates great molecular heterogeneity in which several pathways are simultaneously active leading to tumorigenesis. Novel agents targeting specific pathways associated with apoptosis, cell proliferation, angiogenesis and other mechanisms have emerged as a separate and unique therapeutic class delivering promising results in a vast number of malignancies. ⋯ Most of these agents have been shown to be 'cytostatic', inducing more stable disease rather than objective responses. Thus, the entrance of these novel agents into our drug armamentarium seems to be more attractive in combination with conventional chemotherapy agents based on additive or synergistic response seen with this combined approach. Herein, we review the most relevant clinical data using these novel targeted agents either alone or in combination with chemotherapy in non-small-cell lung cancer.
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Expert Rev Anticancer Ther · Oct 2007
ReviewInflammation and lung carcinogenesis: applying findings in prevention and treatment.
Lung carcinogenesis is a complex process requiring the acquisition of genetic mutations that confer the malignant phenotype as well as epigenetic alterations that may be manipulated in the course of therapy. Inflammatory signals in the lung cancer microenvironment can promote apoptosis resistance, proliferation, invasion, metastasis, and secretion of proangiogenic and immunosuppressive factors. Here, we discuss several prototypical inflammatory mediators controlling the malignant phenotype in lung cancer. ⋯ Inflammatory mediators within the tumor microenvironment are derived from neoplastic cells as well as stromal and inflammatory cells; thus, lung cancer develops in a host environment in which the deregulated inflammatory response promotes tumor progression. Inflammation-related metabolic and catabolic enzymes (prostaglandin E(2) synthase, prostaglandin I(2) synthase and 15-hydroxyprostaglandin dehydrogenase), cell-surface receptors (E-type prostaglandin receptors) and transcription factors (ZEB1, SNAIL, PPARs, STATs and NF-kappaB) are differentially expressed in lung cancer cells compared with normal lung epithelial cells and, thus, may contribute to tumor initiation and progression. These newly discovered molecular mechanisms in the pathogenesis of lung cancer provide novel opportunities for targeted therapy and prevention in lung cancer.