ABSTRACT
Cancer constitutes a diverse class of diseases which differ widely in their origin and development, but which share the characteristic acquired ability of cells to grow in an uncontrolled fashion, and at a later stage to invade adjacent tissues and spread further throughout the rest of the body through blood and the lymph. According to the World Health Organization, cancer is the leading cause of death worldwide, accounting for 7.9 million deaths in 2007, a fi gure expected to increase to reach 12 million by 2030. Six major alterations in the physiology of cancer cells, have been recognized to contribute to malignant cell growth. These features are commonly referred to as cancer hallmarks: (1) the acquisition of self-suffi ciency in growth signals, (2) the loss of sensitivity to growth inhibitory signals, (3) the loss of ability to undergo apoptosis, (4) the acquisition of limitless replicative potential, i.e. the loss of ability to senescence, thereby allowing for uncontrolled growth and unlimited proliferation (immortality), (5) the development of sustained angiogenesis, and (6) the ability to invade tissues and metastasize at distant sites (Hanahan and Weinberg 2000). In addition, cancer cells present a characteristic lack of surveillance and repair mechanisms, develop means of avoiding the immune system, and display a signifi cantly different metabolic activity from healthy cells (Kroemer and Pouyssegur 2008), as schematized in Fig. 6.1.
