ABSTRACT
Over the last century cancer research has produced data leading to a composite picture where gene mutations and epigenetic phenomena strictly relate and overlap. This complexity has repercussions on the anti-cancer therapeutical strategies. The therapeutic pathway paved by the kochian one-cause/one disease principle fails in front of a multigenic multiphenomena disease like cancer. We still do not know what target(s) to hit/modify in order to prevent/stop the carcinogenic progression. On the light of cancer statistics 2005, we discuss the need of exactly defining the cancer targets in order to exploit the high potential of gene therapy.
Subject(s)
Genetic Therapy , Neoplasms/therapy , Chromosome Aberrations , Humans , Mutation , Neoplasms/etiology , Neoplasms/geneticsABSTRACT
Cell death and the subsequent post-mortem changes, called necrosis, are integral parts of normal development and maturation cycle. Despite the importance of this process, the mechanisms underlying cell death are still poorly understood. In the recent literature, cell death is said to occur by two alternative, opposite modes: apoptosis, a programmed, managed form of cell death, and necrosis, an unordered and accidental form of cellular dying. The incorrect consequence is the overlapping of: a) the process whereby cells die, cell death; and b) the changes that the cells and tissues undergo after the cells die. Only the latter process can be referred to as necrosis and represents a