Author details

have revealed that the rate of apoptosis tends to increase from normal to preneoplastic to malignant cells [66]. Comparative studies with the rat bladder have also suggested that apoptosis is closely linked to chemically induced carcinogenesis [67]. Additional support for this transition comes from a variety of other models [7]. However, ultimately, tumor formation only seems to occur once the cancer cells have become resistant to apoptosis while continuing to proliferate. In fact, acquired resistance to apoptosis appears to be a pivotal

In summary, various laboratory studies on animals and certain human data [68] are suggestive that tumor formation requires at least two discrete events to take place in response to a carcinogen. The first involves an elevation of apoptosis in a particular tissue due to a genetic predisposition, stress, or mutation. The second confers resistance to apoptosis in that same tissue resulting in the formation of an abnormal growth due to a dysregulation of cell number homeostasis. Moreover, there is some evidence to suggest that both these events can be reversible when treated with a selective apoptotic agent and, hence, they may be either genetic

Thus, according to this new model, apoptosis becomes an important focus of study and key determinant of carcinogenic potential for any particular chemical or other complete carcinogen being studied, especially in normal, non-transformed cells derived from the target tissue [11]. In the microwave radiation exposure model, there are a number of cellular processes and responses that appear to lead to the endpoint of an increased rate of apoptosis in both animals and humans. These parameters include DNA damage, alterations in gene expression, metabolic perturbations in intracellular calcium levels, effects on the immune system involving decreases in natural killer cells and T lymphocytes, and bursts in ROS activity. All these biochemical effects represent early events that can trigger or are linked to apoptosis and, therefore, could be

Briefly, epidemiological data on the human effects of microwave radiation suggest a predominance of brain tumors and leukemia. In vivo and in vitro animal studies point to genotoxic effects that can trigger apoptosis and detrimental effects on the immune system. Human cell studies corroborate the genotoxic effects of microwave radiation and its ability to cause various kinds of DNA damage resulting in cell death. Possible immune effects are also recorded.

The induction of apoptosis by microwaves in human and rat neural cells and in human lymphocytes correlates well with the increased incidence of brain tumors and leukemia epidemiologically associated with the high-frequency radio waves emitted by cellphone towers. However, further studies need to be conducted on the apoptotic potential of microwaves in non-transformed neural and human lymphocytes at 1800–1900 MHz in order to test this

These results are in keeping with a two-stage apoptotic model of carcinogenesis [11].

involved in initiating an apoptotic model of carcinogenesis as described above.

event in cell immortalization and the transition to malignancy [65].

144 Current Understanding of Apoptosis - Programmed Cell Death

or epigenetic in nature.

6. Discussion

Chanda Siddoo-Atwal1,2,3,4

Address all correspondence to: moondustcosmetics@gmail.com

