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.
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.
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. ...
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.
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
Yet, the progress in cancer treatment has not paralleled these dramatic achievements
in basic research.