ASSESSMENT OF PCXMC MONTE CARLO SIMULATIONS IN SLOT-SCANNING-BASED EXAMINATIONS: COMPARISON WITH IN-PHANTOM THERMOLUMINESCENT DOSIMETRY.

Slot-scanning technology is nowadays a valid solution for the follow-up of chronic musculoskeletal disorders on children and adolescent patients, but there is no commercial software designed for simulating this X-ray beam geometry. PC Program for X-ray Monte Carlo (PCXMC) is a widespread Monte Carlo software developed for dose computation in projection radiography. In this study, experimental measurements were performed to evaluate its applicability in examinations with a slit-beam device. Physical phantoms corresponding to an adult and a 5-y-old child with calibrated thermoluminescent dosemeters were used for experiments. Different simulation approaches were investigated. Differences between measured and calculated organ doses ranged from -95 to 67% and were statistically significant for almost all organs. For both patients, PCXMC underestimated the effective dose of about 25%. This study suggests that PCXMC is not suited for organ dose evaluation in examinations with slot-scanning devices. It is still a useful tool for effective dose estimation when a proper correction factor is applied.

Analysis of gene expression identifies PLAB as a mediator of the apoptotic activity of fenretinide in human ovarian cancer cells.

Fenretinide (4-HPR) is a synthetic retinoid with antitumor activity, which induces apoptosis in cancer cell lines of different histotypes. To identify genes contributing to its apoptotic activity in ovarian cancer cells, we monitored, by cDNA arrays, gene expression changes after 4-HPR exposure in A2780, a human ovarian carcinoma cell line sensitive to the retinoid. Among the differentially expressed transcripts, PLAcental Bone morphogenetic protein (PLAB), a proapoptotic gene, was the most highly induced. In a panel of ovarian carcinoma cell lines with different 4-HPR sensitivities, PLAB upregulation was associated with cellular response to 4-HPR, its overexpression increased basal apoptosis and its silencing by small interfering RNA decreased the ability of 4-HPR to induce apoptosis. PLAB induction by 4-HPR was p53- and EGR-1 independent and was regulated, at least in part, by increased stability of PLAB mRNA. PLAB up-modulation by 4-HPR also occurred in vivo: in ascitic cells collected from patients with ovarian cancer before and after 4-HPR treatment, PLAB was upmodulated in 2/4 patients. Our results in certain ovarian cancer cell lines indicate a role for PLAB as a mediator of 4-HPR-induced apoptosis. The correlation of increased PLAB in vivo with antitumor activity remains to be established.