• Radiation Oncology Journal
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• v.15 no.4
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• pp.393-402
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• 1997

Purpose : When an x-ray beam of small field size is irradiated to target area containing an air cavity, such as larynx, the underdosing effect is observed in the region near the interfaces of air and soft tissue. With a larynx model, air cavity embedded in tissue-equivalent material, this study is intonded for examining Parameters, such as beam quality, field size, and cavity size, to affect the dose distribution near the air cavity. Materials and Methods : Three x-rar beams, 4-, 6- and 10-MV, were employed to Perform a measurement using a 2cm $(width){\times}L$ (length in cm, one side of x-ray field used 2cm (height) air cavity in the simulated larynx. A thin window parallel-plate chamber connected to an electrometer was used for a dosimetry system. A ratio of the dose at various distances from the cavity-tissue interface to the dose at the same points in a homogeneous Phantom (ebservedlexpected ratio, O/E) normalized buildup curves, and ratio of distal surface dose to dose at the maximum buildup depth were examined for various field sizes. Measurement for cavity size effect was performed by varying the height (Z) of the air cavity with the width kept constant for several field sizes. Results : No underdosing effect for 4-MV beam for fields larger than $5cm\times5cm$ was found For both 6- and 10-MV beams, the underdosing portion of the larynx at the distal surface was seen to occur for small fields, $4cm\times4cm\;and\;5cm\times5cm$. The underdosed tissue was increased in its volume with beam energy even for similar surface doses. The relative distal surface dose to maximum dose was changed to 0.99 from 0.95, 0.92, and 0.91 for 4-, 6-, and 10-MV, respectively, with increasing field size, $4cm\times4cm\;to\;8cm\times8cm$, For 6- and 10-MV beams, the dose at the surface of the cavity is measured less than the predicted by about two and three percent. respectively. but decrease was found for 4-MV beam for $5cm\times5cm$ field. For the $4cm\timesL\timesZ$ (height in cm). varying depth from 0.0 to 4.8cm, cavity, O/E> 1.0 was observed regardless of the cavity size for any field larger than about $8cm\times8cm$. Conclusion : The magnitude of underdosing depends on beam energy, field size. and cavity size for the larynx model. Based on the result of the study. caution must be used when a small field of a high quality x-ray beam is irradiated to regions including air cavities. and especially the region where the tumor extends to the surface. Low quality beam. such as. 4-MV x-ray, and larger fields can be used preferably to reduce the risk of underdosing, local failure. In the case of high quality beams such as 6- and 10-MV x-rays, however. an additional boost field is recommended to add for the compensation of the underdosing region when a typically used treatment field. $8cm\times8cm$, is employed.

• Journal of Life Science
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• v.23 no.10
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• pp.1230-1238
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• 2013

The regulatory effect of the tumor-suppressor protein p53 on the apoptogenic activity of $17{\alpha}$-estradiol ($17{\alpha}-E_2$) was compared between HCT116 ($p53^{+/+}$) and HCT116 ($p53^{-/-}$) cells. When the HCT116 ($p53^{+/+}$) and HCT116 ($p53^{-/-}$) cells were treated with $2.5{\sim}10{\mu}M$ $17{\alpha}-E_2$ for 48 h or with $10{\mu}M$for various time periods, cytotoxicity and an apoptotic sub-$G_1$ peak were induced in the HCT116 ($p53^{+/+}$) cells in a dose- and time-dependent manner. However, the HCT116 ($p53^{-/-}$) cells were much less sensitive to the apoptotic effect of $17{\alpha}-E_2$. Although $17{\alpha}-E_2$ induced aberrant mitotic spindle organization and incomplete chromosome congregation at the equatorial plate, $G_2/M$ arrest was induced to a similar extent in both cell types. In addition, $17{\alpha}-E_2$-induced activation of Bak and Bax, ${\Delta}{\Psi}m$ loss, and PARP degradation were more dominant in the HCT116 ($p53^{+/+}$) than in the HCT116 ($p53^{-/-}$) cells. In accordance with enhancement of p53 phosphorylation (Ser-15) and p53 levels, p21 and Bax levels were elevated in the HCT116 ($p53^{+/+}$) cells treated with $17{\alpha}-E_2$. The HCT116 ($p53^{-/-}$) cells exhibited barely or undetectable levels of p21 and Bax, regardless of $17{\alpha}-E_2$ treatment. On the other hand, although the level of Bcl-2 was slightly lower in the HCT116 ($p53^{+/+}$) than in the HCT116 ($p53^{-/-}$) cells, it remained relatively constant after the $17{\alpha}-E_2$ treatment. Together, these results show that among the components of the $17{\alpha}-E_2$-induced apoptotic-signaling pathway, which proceeds through mitotic spindle defects causing mitotic arrest, subsequent activation of Bak and Bax and the mitochondria-dependent caspase cascade, leading to PARP degradation, $17{\alpha}-E_2$-induced activation of Bak and Bax is the upstream target of proapoptotic action of p53.