Open AccessRadiation‐induced concomitant overexpression of p53, p62 c‐fos and p21 N‐fas in mouse epidermis
Author(s) -
Leszczynski D.,
Servomaa K.,
Lang S.,
Kosmat V.M.,
Rytömaa T.
Publication year - 1994
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/j.1365-2184.1994.tb01489.x
Subject(s) - hairless , epidermis (zoology) , carcinogenesis , ionizing radiation , biology , polyclonal antibodies , in vivo , cancer research , p53 protein , gene , pathology , microbiology and biotechnology , irradiation , antibody , immunology , genetics , anatomy , medicine , physics , nuclear physics
. Early molecular events in radiation carcinogenesis in vivo are difficult to study, especially because it is usually impossible to know in advance the exact location of a radiation‐induced tumour. In the present study, we have attempted to overcome this difficulty by exposing a very small area of hairless mouse skin to high‐dose beta radiation (i.e. immobilized hot particles) on the reasonable assumption that a malignant tumour would subsequently develop and be found at the exposed site in a long‐term follow‐up. The results showed that at an exposed site, before the appearance of a visible or histologically detectable tumour, overexpression of the product of the tumour suppressor gene p53 was common (28% of the sites studied; tested with PAbl801, PAb421, PAb240 and a polyclonal antibody CM1) and that this change was regularly accompanied by overexpression of p62 c‐fos and p21 N‐ras . Expression of several other oncoproteins studied (p39 c‐jun , p21 K‐ras , p21 H‐ras ) was not altered at these sites. A similar pattern of changes was observed in a visible and histopathologically distinct tumour that was analyzed after its development at an exposed site. These results suggest a re'markably regular pattern of molecular changes, induced by ionizing radiation in mouse epidermis, which might be associated with carcinogenesis.