Impact of intercellular induction of apoptosis on low-dose radiation carcinogenesis
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作者:
Kundrat, P.
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机构:
Helmholtz Zentrum Munchen, Inst Radiat Protect, German Res Ctr Environm Hlth, Neuherberg, GermanyHelmholtz Zentrum Munchen, Inst Radiat Protect, German Res Ctr Environm Hlth, Neuherberg, Germany
Kundrat, P.
[1
]
Friedland, W.
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机构:
Helmholtz Zentrum Munchen, Inst Radiat Protect, German Res Ctr Environm Hlth, Neuherberg, GermanyHelmholtz Zentrum Munchen, Inst Radiat Protect, German Res Ctr Environm Hlth, Neuherberg, Germany
Friedland, W.
[1
]
机构:
[1] Helmholtz Zentrum Munchen, Inst Radiat Protect, German Res Ctr Environm Hlth, Neuherberg, Germany
In vitro data indicate that selective removal of oncogenic transformed cells by apoptosis induced via signalling by neighbouring cells may represent an important anti-carcinogenic process. Mechanistic modelling supports this concept and predicts that the phenomenon can stop the growth of a transformed cell population, forming a dormant pre-neoplastic lesion, or even remove the transformed clone completely. Radiation has been shown to enhance the underpinning signalling and increase the extent and rate of apoptosis induction in precancerous cells. Implications for low-dose radiation carcinogenesis are discussed based on in vitro data and mechanistic modelling. The possibility is outlined for radiation to act in a pro-carcinogenic manner, i.e. to reduce rather than enhance the removal of transformed cells by apoptosis. The effects of radiation exposure during early or late carcinogenesis are discussed.