Oncogenic transformation

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  • Oncogenic viruses are the known etiologic agents in 15% – 20% of all human cancers. Their impact on global health is signifi cant. The fi rst recognition that cancer can be caused by a virus dates back to observations of Rous sarcoma virus in chickens almost 100 years ago. However, it was not until the 1970s that the mechanistic basis for retroviral transformation became clearer. That era was marked by the discovery of many viral oncogenes and counterpart cellular proto - oncogenes.

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  • Cells respond to environmental cues through a complex and dynamic network of signaling pathways that normally maintain a critical balance between cellular proliferation, differentiation, senescence, and death. One current research challenge is to identify those aberrations in signal transduction that directly contribute to a loss of this division-limited equilibrium and the progression to malignant transformation. The study of cell-signaling molecules in this context is a central component of cancer research.

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  • The putative CLL precursor could be an antigen-experienced CD27+ B cell, expanded either in the course of a GC B-cell T-dependent or T-independent response by chronic antigen- stimulation through extrinsic or autoantigens. Over time, genetic abnormalities may accumulate in the genome of these chronically stimulated B cells and lead to the outgrow of clones with MBL phenotype. Additional genetic aberrations may be incorporated in the course of proliferation leading to the oncogenic hit that transform these precursor in bona fide CLL cells. ...

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  • Figure 80-6 Oncogene signaling pathways are activated during tumor progression and promote metastatic potential. This figure shows a cancer cell that has undergone epithelial to mesenchymal transition (EMT) under the influence of several environmental signals. Critical components include activated transforming growth factor beta (TGF-β) and the hepatocyte growth factor (HGF)/c-Met pathways, as well as changes in the expression of adhesion molecules that mediate cell-cell and cellextracellular matrix interactions.

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  • The ultimate goal of cancer research is the development of effective anticancer therapy. During the last several decades, the discovery of oncogenes, tumor suppressors, growth factors, signal transduction pathways has dramatically escalated our understanding of cancer cell biology and mechanisms of cell transformation.1-3 Hundreds of cellular proteins and pathways have been logically considered as molecular targets in a mechanism-based approaches of anticancer drug development.4-6 Yet, the progress in cancer treatment has not paralleled these dramatic achievements in basic research.

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