PubMed · 11763105
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2002. Selected bibliography.. https://doi.org/10.1016/s0265-931x(01)00087-x
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A model for bifurcation regions of the human tracheo-bronchial tree was developed. Equations for the surfaces are given to enable calculations of doses from alpha-particles emitted in these regions. It has been found that a bifurcation region is well approximated by a quasi-ellipsoid. The absorbed fractions of alpha-particles emitted in bifurcation regions were calculated by the Monte Carlo method. The average absorbed fraction under the bifurcation geometry is close to that found under the cylindrical geometry in the bronchial region. In the bronchiolar region, the absorbed fractions under the bifurcation geometry are up to 20% larger than those under the cylindrical geometry.
In some cases, evidence exists that exogenous carcinogenic exposures contribute to the mutation spectrum of the TP53 gene (p53) in human cancers. Although the clearest examples come from dietary and environmental sources, only a restricted number of papers have concentrated specifically on TP53 mutations in tumors from workers exposed to occupational carcinogens. In populations exposed to dietary aflatoxin B1 with liver cancer (AFB1) and ultraviolet (UV)-radiation with skin cancer, a single specific-looking TP53 mutation has been described in some of the tumors. Whether these fingerprints in the TP53 gene can be used to reveal an occupational etiology remains to be shown. In other cases, although differences in the TP53 mutation spectrum exist, they are more diffuse and difficult to interpret at this point. For instance, cigarette smoking seems to induce long-lasting molecular footprints in TP53. However, their use to rule out other occupational exposures as etiological factors in occupational cancers is still very questionable, especially due to the putative synergistic effects of cigarette smoke with other carcinogens. Although interesting implications of possible typical mutation spectra among cancers with other occupational etiologies exist, the data are scanty and await further development of TP53 mutation databases.