Showing papers by "Barbara Fisher published in 2007"
TL;DR: A technique to create an IMAT plan that replicates Tomotherapy deliveries by applying IMAT specific segmentation and leaf-sequencing algorithms to Tomotherapy output sinograms is illustrated and two alternative segmentation techniques are proposed, a clustering method, and a bottom-up segmentation method (BUS).
Abstract: A common method in generating intensity modulated radiation therapy(IMRT) plans consists of a three step process: an optimized fluence intensity map (IM) for each beam is generated via inverse planning, this IM is then segmented into discrete levels, and finally, the segmented map is translated into a set of MLC apertures via a leaf sequencing algorithm. To date, limited work has been done on this approach as it pertains to intensity modulated arc therapy (IMAT), specifically in regards to the latter two steps. There are two determining factors that separate IMAT segmentation and leaf sequencing from their IMRT equivalents: (1) the intrinsic 3D nature of the intensity maps (standard 2D maps plus the angular component), and (2) that the dynamic multileaf collimator(MLC) constraints be met using a minimum number of arcs. In this work, we illustrate a technique to create an IMAT plan that replicates Tomotherapy deliveries by applying IMAT specific segmentation and leaf-sequencing algorithms to Tomotherapy output sinograms. We propose and compare two alternative segmentation techniques, a clustering method, and a bottom-up segmentation method (BUS). We also introduce a novel IMAT leaf-sequencing algorithm that explicitly takes leaf movement constraints into consideration. These algorithms were tested with 51 angular projections of the output leaf-open sinograms generated on the Hi-ART II treatment planning system (Tomotherapy Inc.). We present two geometric phantoms and 2 clinical scenarios as sample test cases. In each case 12 IMAT plans were created, ranging from 2 to 7 intensity levels. Half were generated using the BUS segmentation and half with the clustering method. We report on the number of arcs produced as well as differences between Tomotherapy output sinograms and segmented IMAT intensity maps. For each case one plan for each segmentation method is chosen for full Monte Carlo dose calculation (NumeriX LLC) and dose volume histograms (DVH) are calculated. In all cases, the BUS method outperformed the clustering, method. We recommend using the BUS algorithm and discuss potential improvements to the clustering algorithms.
28 citations
TL;DR: The samples analyzed support previously reported observations about the distribution of CYP3A4 *1B genotype by race, but race was not associated with poorer outcome, and patient numbers were limited, and selection bias cannot be completely ruled out.
Abstract: Purpose: Inherited genotypes may explain the inferior outcomes of African American (AA) men with prostate cancer. To understand how variation in CYP3A4 correlated with outcomes, a retrospective examination of the CYP3A4∗1B genotype was performed on men treated with Radiation Therapy Oncology Group (RTOG) 92-02. Methods and Materials: From 1,514 cases, we evaluated 56 (28.4%) of 197 AA and 54 (4.3%) of 1,274 European American (EA) patients. All patients received goserelin and flutamide for 2 months before and during RT (STAD-RT) ± 24 months of goserelin (long-term androgen deprivation plus radiation [LTAD-RT]). Events studied included overall survival and biochemical progression using American Society for Therapeutic Radiology and Oncology consensus guidelines. Results: There were no differences in outcome in patients in with or without CYP3A4 data. There was an association between race and CYP3A4 polymorphisms with 75% of EAs having the Wild Type compared to only 25% of AA men ( p Conclusions: The samples analyzed support previously reported observations about the distribution of CYP3A4∗1B genotype by race, but race was not associated with poorer outcome. However, patient numbers were limited, and selection bias cannot be completely ruled out.
22 citations
TL;DR: The patient is a previously healthy 19-month-old child who became symptomatic in October 1998 with right hand weakness and cessation of new words with progression of right sided weakness and decreased sensation over the next month.
Abstract: The patient is a previously healthy 19-month-old child who became symptomatic in October 1998 with right hand weakness and cessation of new words with progression of right sided weakness and decreased sensation over the next month. The computed tomography (CT) and magnetic resonance imaging (MRI) scans demonstrated a large, deep, left frontal periventricular enhancing mass with several cystic areas. A left frontoparietal craniotomy was performed and the tumour was grossly resected. The pathological diagnosis was AT/RT. Grossly, the tumour was composed of firm, pink-tan hemorrhagic tissue. Sections showed a densely cellular, infiltrating neoplasm with areas of necrosis (some calcified), fascicular and focal sheets of collagen, and a variable, often prominent reticulin network. There was no endothelial proliferation. Light microscopy with hematoxylin and eosin stain (Figure 1) revealed a varied tumour appearance predominantly composed of larger tumour cells, with randomly dispersed nests of small undifferentiated cells close to the interface of tumour and normal brain tissue. The larger cells had several growth patterns: some were loosely arranged bi- or multi-polar cells forming cords and acinar structures against a faintly basophilic mucinous background, some were elongated cells arranged in coarse follicles or other compact bundles, while others were arranged in sheets or nests with prominent, sometimes glassy eosinophilic and cytoplasmic inclusions and eccentric nuclei (rhabdoid cells). Larger cells had nuclei with vesicular chromatin and prominent nucleoli, and smaller cells had hyperchromatic nuclei. Mitoses were focally numerous with some atypical in form, and cytoplasmic glycogen was inconspicuous. Immunohistochemical studies revealed widespread staining for epithelial membrane antigen (EMA), vimentin (Figure 2), glial fibrillary acid protein (GFAP), groups of cells with membranous patterns of staining for CD99, regional staining for neuron-specific enolase (NSE), scattered staining for transthyretin, and rare staining for actin, cytokeratin, and synaptophysin. The tumour was positive for chromosome 22 monosomy. Electron microscopy showed polygonal cells arranged in ill-defined acini that formed inconspicuous, sometimes entwined short microvillus processes. Variable numbers of intermediate filaments were identified and some cells showed a rudimentary basal lamina. Desmosomes were not seen, and there was no evidence of neural differentiation.