Literature DB >> 21247933

Modelling of intercellular induction of apoptosis in oncogenic transformed cells and radiation effects on the phenomenon.

P Kundrát1, W Friedland, P Jacob.   

Abstract

The removal of transformed cells via induction of apoptosis through intercellular signalling by surrounding cells is supposed to represent an important control mechanism limiting carcinogenesis. Low doses of radiation influence the efficiency of this anti-carcinogenesis process, indicating possible beneficial effects of low doses of radiation mediated by intercellular communication ('non-targeted effects'). To quantitatively understand the signalling system involved and the effects of radiation and to assess the role of this phenomenon in radiation-induced carcinogenesis, multi-scale modelling studies have been started. The proposed kinetic model takes into account (i) triggering of the effector function in cells in the vicinity of transformed cells, (ii) intercellular signalling between effector and transformed cells and (iii) execution of apoptosis in attacked cells. The systems model without radiation perturbance is reviewed. First results accounting for radiation-induced modulations of the signalling schemes are presented.

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Year:  2011        PMID: 21247933     DOI: 10.1093/rpd/ncq521

Source DB:  PubMed          Journal:  Radiat Prot Dosimetry        ISSN: 0144-8420            Impact factor:   0.972


  2 in total

1.  Mechanistic modelling suggests that the size of preneoplastic lesions is limited by intercellular induction of apoptosis in oncogenically transformed cells.

Authors:  Pavel Kundrát; Georg Bauer; Peter Jacob; Werner Friedland
Journal:  Carcinogenesis       Date:  2011-10-31       Impact factor: 4.944

2.  Enhanced release of primary signals may render intercellular signalling ineffective due to spatial aspects.

Authors:  Pavel Kundrát; Werner Friedland
Journal:  Sci Rep       Date:  2016-09-20       Impact factor: 4.379

  2 in total

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