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Hepatocellular carcinoma (HCC) is the sixth most common type of cancer in the world. It is also the third most common cause of cancer-related mortality. In addition, the incidence of HCC has risen in many countries over the past decade. The greatest risk factor associated with the development of HCC is hepatitis B and C virus infection. Hepatitis infection is considered to increase the risk of developing HCC by 20 fold and is the major etiological factor in over 80% of HCC cases. Other main risk factors include excessive alcohol consumption, non-alcoholic steatohepatitis, exposure to environmental toxins such as aflatoxin B, cirrhosis, hemochromatosis, diabetes and obesity.
Hepatocarcinogenesis is a complex and multi-step process resulting from a combination of epigenetic and genetic alterations. In recent decades, much effort has been made to identify key molecules involved in the development and progression of HCC. Multiple signaling pathways that affect angiogenesis, cell proliferation, invasion, and metastasis are de-regulated in HCC. Among these, the most frequently reported pathways involve growth factors, such as insulin-like growth factor (IGF), platelet-derived growth factor (PDGF), epidermal growth factor (EGF), hepatocyte growth factor (HGF), and vascular endothelial growth factor (VEGF).
IGF signaling is important for the regulation of growth and development, and has been shown to be involved in the pathogenesis of several malignancies, including HCC. Alterations of this pathway include allelic losses of the IGFR2 receptor (80%) and overexpression of the IGF2 ligand (16–40%). Moreover, selective blockade of IGF signaling had antitumoral effects in experimental models of HCC. Various components of the HGF/MET pathway have been suggested to contribute to HCC progression. EGFR signaling has also been shown to be present, with overexpression at both mRNA and protein levels. De-regulation of EGF in cirrhotic tissue seems to impact HCC development, as shown in a gene signature able to predict prognosis in surgically resected HCC patients. In addition, high serum levels of VEGF have been associated with aggressive cancer behavior and poor prognosis. Finally, there has been increasing interest in anti-fibroblast growth factor (FGF) therapy in HCC, based on evidence indicating the importance of this system both in HCC progression and in acquired resistance to anti-VEGF therapy.
In recent years, tremendous progress has been made toward better understanding the molecular mechanisms of oncogenic processes. Many cell signaling pathways involved in tumor pathogenesis have been identified, resulting in the identification of new molecular targets for therapeutic development. Unlike conventional chemotherapy that utilizes broad spectrum cytotoxic agents, targeted therapy acts directly and specifically on the components that regulate tumorigenesis. Various strategies targeting these pathways have been explored and have shown varying degrees of success in the clinic. Additional novel strategies are being investigated and raise the hope that more effective therapies may be on the horizon.
Creative Biogene, as a leading biotechnology company, is able to offer various liver cancer pathway related products including stable cell lines, viral particles and clones for your drug discovery projects.