Whole-pelvic volumetric-modulated arc therapy for high-risk prostate cancer: treatment planning and acute toxicity

The objectives of this study were to evaluate dosimetric quality and acute toxicity of volumetric-modulated arc therapy (VMAT) and daily image guidance in high-risk prostate cancer patients. A total of 100 consecutive high-risk prostate cancer patients treated with definitive VMAT with prophylactic whole-pelvic radiotherapy (WPRT) were enrolled. All patients were treated with a double-arc VMAT plan delivering 52 Gy to the prostate planning target volume (PTV), while simultaneously delivering 46.8 Gy to the pelvic nodal PTV in 26 fractions, followed by a single-arc VMAT plan delivering 26 Gy to the prostate PTV in 13 fractions. Image-guided RT was performed with daily cone-beam computed tomography. Dose–volume parameters for the PTV and the organs at risk (OARs), total number of monitor units (MUs) and treatment time were evaluated. Acute toxicity was assessed using the Common Terminology Criteria for Adverse Events, version 4.0. All dosimetric parameters met the present plan acceptance criteria. Mean MU and treatment time were 471 and 146 s for double-arc VMAT, respectively, and were 520 and 76 s for single-arc VMAT, respectively. No Grade 3 or higher acute toxicity was reported. Acute Grade 2 proctitis, diarrhea, and genitourinary toxicity occurred in 12 patients (12%), 6 patients (6%) and 13 patients (13%), respectively. The present study demonstrated that VMAT for WPRT in prostate cancer results in favorable PTV coverage and OAR sparing with short treatment time and an acceptable rate of acute toxicity. These findings support the use of VMAT for delivering WPRT to high-risk prostate cancer patients.     

Spatial and topologic distribution of verapamil-sensitive atrial tachycardia originating from the vicinity of the atrioventricular node

BACKGROUND: Little information exists regarding the precise distribution of verapamil-sensitive atrial tachycardia originating from the vicinity of the atrioventricular node (V-AT). METHODS: In 12 patients with V-AT, we examined the spatial and topologic distribution of tachycardia origin relative to the His bundle (HB) site. The V-AT origin was divided into six areas: anterior (A-HB), posterior (P-HB), superior (S-HB), inferior (I-HB), lateral (L-HB), and septal (SP-HB) portion of HB catheter. Three dimensional distance between the distal pair of the electrodes of HB catheter and that of V-AT origin (DIS) was obtained by calculating the distances on the right and left anterior fluoroscopic images. Topologic distribution was expressed as the interval between the onset of the atrial electrogram of V-AT origin and that of HB catheter (INT). RESULTS: The tachycardia origin was observed at the P-HB in four, S-HB in two, I-HB in two, SP-HB in three, and L-HB in one patient. The tachycardia cycle length, DIS, and INT were 369 +/- 67 ms, 12 +/- 3 mm, and -12 +/- 8 ms, respectively. After successful ablation of initial V-AT (1st V-AT), V-AT with a different origin (2nd V-AT) was induced in five patients. The tachycardia origin, tachycardia cycle length, DIS, and INT of the 2nd V-AT (P-HB in three, S-HB in one, and SP-HB in one patient; 333 +/- 66 ms, 8 +/- 3 mm, and -11 +/- 4 ms, respectively) were not different from those of 1st V-AT. CONCLUSIONS: V-AT often shows a shift in tachycardia origin to another site where the spatial and topologic distributions are similar to those of 1st V-AT.     

Thyroid hormone regulation of apoptosis induced by retinoic acid in promyeloleukemic HL-60 cells: studies with retinoic acid receptor-specific and retinoid x receptor-specific ligands.

3,5,3'-Triiodo-L-thyronine (T3) potentiates apoptosis during the all-trans-retinoic acid-induced differentiation of promyeloleukemic HL-60 cells. We examined whether the retinoid receptor-specific thyroid hormone action is present during differentiation of HL-60 cells in this study. We used two distinct retinoid receptor agonists. T3 potentiates G1 arrest induced by Am80, a retinoic acid receptor (RAR)-specific agonist, but had no effect on G1 arrest induced by HX600, a retinoid x receptor (RXR)-specific agonist. Am80 alone induces the apoptosis, and T3 enhances it. Although HX600 alone fails to increase the apoptotic fraction, T3 enables the compounds to induce apoptosis. Am80-induced expression of CD11b, a marker for the differentiation, is enhanced by T3. However, T3 or HX600 or both do not affect the expression of CD11b. T3 does not alter the amount of mRNAs of various members of the bcl-2 family. T3, however, enhances the Am80-induced expression of bfl-1 and suppression of bcl-2. In contrast, T3 does not alter either bfl-1 and bcl-2 expression in the presence of HX600. Our observations suggest that cooperative action of T3 with an RXR-specific ligand is different from that with an RAR ligand in cellular apoptotic regulation and that thyroid hormone may be available as a chemotherapeutic agent in acute leukemia.