We present an approach for unsupervised segmentation of natural and textural images based on active contour, differential geometry and information theoretical concept. More precisely, we propose a new texture descriptor which intrinsically defines the geometry of textural regions using the shape operator borrowed from differential geometry. Then, we use the popular Kullback-Leibler distance to define an active contour model which distinguishes the background and textural objects of interest represented by the probability density functions of our new texture descriptor. We prove the existence of a solution to the proposed segmentation model. Finally, a fast and easy to implement texture segmentation algorithm is introduced to extract meaningful objects. We present promising synthetic and real-world results and compare our algorithm to other state-of-the-art techniques.
Abstract-In this paper, we present the segmentation of the head and neck lymph node regions using a new active contour-based atlas registration model. We propose to segment the lymph node regions without directly including them in the atlas registration process; instead, they are segmented using the dense deformation field computed from the registration of the atlas structures with distinct boundaries. This approach results in robust and accurate segmentation of the lymph node regions even in the presence of significant anatomical variations between the atlas-image and the patient's image to be segmented. We also present a quantitative evaluation of lymph node regions segmentation using various statistical as well as geometrical metrics: sensitivity, specificity, dice similarity coefficient and Hausdorff distance. A comparison of the proposed method with two other state of the art methods is presented. The robustness of the proposed method to the atlas selection, in segmenting the lymph node regions, is also evaluated.Index Terms-Atlas-based segmentation, head and neck, IMRT, lymph node regions, non-rigid registration, radiotherapy.
One of the key mechanisms linking cell signaling and control of gene expression is reversible phosphorylation of transcription factors. FOXC2 is a forkhead transcription factor that is mutated in the human vascular disease lymphedema-distichiasis and plays an essential role in lymphatic vascular development. However, the mechanisms regulating FOXC2 transcriptional activity are not well understood. We report here that FOXC2 is phosphorylated on eight evolutionarily conserved proline-directed serine/threonine residues. Loss of phosphorylation at these sites triggers substantial changes in the FOXC2 transcriptional program. Through genome-wide location analysis in lymphatic endothelial cells, we demonstrate that the changes are due to selective inhibition of FOXC2 recruitment to chromatin. The extent of the inhibition varied between individual binding sites, suggesting a novel rheostat-like mechanism by which expression of specific genes can be differentially regulated by FOXC2 phosphorylation. Furthermore, unlike the wild-type protein, the phosphorylation-deficient mutant of FOXC2 failed to induce vascular remodeling in vivo. Collectively, our results point to the pivotal role of phosphorylation in the regulation of FOXC2-mediated transcription in lymphatic endothelial cells and underscore the importance of FOXC2 phosphorylation in vascular development. Forkhead box (Fox) proteins are a family of transcription factors (TFs) that play an important role in development, cell cycle regulation, and other key biological processes (1). In mammals, more than 40 forkhead family members have been identified, all sharing the evolutionarily conserved forkhead DNA binding domain. Despite the similarity in their DNA-binding domains, different members of the forkhead family have evolved distinct functional roles. The forkhead transcription factor FOXC2 was first demonstrated to play a role in the morphogenesis of the cardiovascular system during embryonic development (2, 3). Subsequent studies revealed that FOXC2 is also implicated in lymphatic vascular development and disease. Mutations in FOXC2 cause lymphedema-distichiasis (LD; OMIM 153400) characterized by lymphedema and double rows of eyelashes (4). In both humans and mice, FOXC2 is highly expressed in the developing lymphatic vessels, as well as in the adult lymphatic valves (5, 6). The critical role of FOXC2 in lymphatic vascular development has been underscored by the demonstration of abnormal lymphatic patterning and failure to form lymphatic valves in Foxc2-deficient mice (5,7,8). LD patients develop similar defects characterized by lymph and venous reflux, indicating failure or absence of lymphatic and venous valves (9, 10). On a mechanistic level, FOXC2 genomic binding sites are enriched in NFATC1 consensus sequences, and the two transcription factors cooperate in vivo during lymphatic vascular morphogenesis (8).Phosphorylation of transcription factors represents a rapid and reversible mechanism for dynamic regulation of transcriptional networks (11). Most of the Fox...
Purpose There is growing evidence that interaction between stromal and tumor cells is pivotal in breast cancer progression and response to therapy. Based on earlier research suggesting that during breast cancer progression, striking changes occur in CD10+ stromal cells, we aimed to better characterize this cell population and its clinical relevance. Experimental Design We developed a CD10+ stroma gene expression signature (using HG U133 Plus 2.0) on the basis of the comparison of CD10 cells isolated from tumoral (n = 28) and normal (n = 3) breast tissue. We further characterized the CD10+ cells by coculture experiments of representative breast cancer cell lines with the different CD10+ stromal cell types (fibroblasts, myoepithelial, and mesenchymal stem cells). We then evaluated its clinical relevance in terms of in situ to invasive progression, invasive breast cancer prognosis, and prediction of efficacy of chemotherapy using publicly available data sets. Results This 12-gene CD10+ stroma signature includes, among others, genes involved in matrix remodeling (MMP11, MMP13, and COL10A1) and genes related to osteoblast differentiation (periostin). The coculture experiments showed that all 3 CD10+ cell types contribute to the CD10+ stroma signature, although mesenchymal stem cells have the highest CD10+ stroma signature score. Of interest, this signature showed an important role in differentiating in situ from invasive breast cancer, in prognosis of the HER2+ subpopulation of breast cancer only, and potentially in nonresponse to chemotherapy for those patients. Conclusions Our results highlight the importance of CD10+ cells in breast cancer prognosis and efficacy of chemotherapy, particularly within the HER2+ breast cancer disease.
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