Four distribution patterns in the cleft area were identified in both sets of dentition. Our findings of distribution patterns in UCLP patients support the hypothesis that there may be two odontogenic origins for maxillary lateral incisors. Clinicians involved in managing the dentition of UCLP patients should consider the high frequency of numerical variation both in and outside the cleft area before starting dental treatment.

Objective To investigate the distribution patterns of primary and permanent teeth in the cleft area and the numerical variation in teeth in unilateral complete cleft lip and palate (UCLP) patients. Design A survey of the dentition in UCLP patients. Setting Craniofacial Center, Chang Gung Memorial Hospital, Taipei, Taiwan. Patients 137 UCLP patients who met the following criteria: (1) have had at least one panoramic film taken, (2) the first panoramic film illustrates either primary or early mixed dentition. Evaluation of both permanent and primary dentition was available in 91 cases. Main Outcome Measures Two evaluators performed independent evaluations of number and distribution of teeth in UCLP patients. The hypothesis that there are two odontogenic origins for maxillary lateral incisors was proposed to explain the occurrence of distribution patterns of dentition in the cleft area and to explain differences between primary and permanent dentition in UCLP patients. Results Four distribution patterns in the cleft area were identified in both the primary and the permanent dentition. In the primary dentition, placement of the lateral incisor distal to the alveolar cleft was the predominant pattern (pattern y, 82.4%), followed by absence of the cleft side maxillary lateral incisor (pattern ab, 9.9%), presence of one tooth on each side of the alveolar cleft (pattern xy, 5.5%), and placement of the lateral incisor mesial to the alveolar cleft (pattern x, 2.2%). In the permanent dentition, the most common pattern was the absence of the maxillary lateral incisor on the cleft side (pattern AB, 51.8%), followed by lateral incisor placement distal to the alveolar cleft (pattern Y, 46%), lateral incisor placement mesial to the alveolar cleft (pattern X, 1.5%) and the presence of one tooth on each side of the alveolar cleft (pattern XY, 0.7%). The discrepancy between the distribution patterns of primary dentition and permanent dentition successors is 57.1%. Variations in tooth number in both primary and permanent dentition of UCLP patients occurred most often in the cleft area. Abnormalities in the number of teeth (hypodontia or hyper-dontia) outside the cleft area were more common in the permanent dentition than in the primary dentition (24.1% versus 4.4%). Conclusions Four distribution patterns in the cleft area were identified in both sets of dentition. Our findings of distribution patterns in UCLP patients support the hypothesis that there may be two odontogenic origins for maxillary lateral incisors. Clinicians involved in managing the dentition of UCLP patients should consider the high frequency of numerical variation both in and outside the cleft area before starting dental treatment.

The early removal of an unerupted mesiodens before the age of 5 years would seem to reduce complications and the need for orthodontic treatment. With the help of general anesthesia and evaluation by CT imaging, concerns regarding the child's cooperation and the possibility of damage to adjacent permanent teeth during early surgical intervention can be minimized.

Breast cancer amplified sequence 2 (BCAS2) was reported previously as a transcriptional coactivator of estrogen receptor. Here, we report that BCAS2 directly interacts with p53 to reduce p53 transcriptional activity by mildly but consistently decreasing p53 protein in the absence of DNA damage. However, in the presence of DNA damage, BCAS2 prominently reduces p53 protein and provides protection against chemotherapeutic agent such as doxorubicin. Deprivation of BCAS2 induces apoptosis in p53 wild-type cells but causes G 2 -M arrest in p53-null or p53 mutant cells. There are at least two apoptosis mechanisms induced by silencing BCAS2 in wildtype p53-containing cells. Firstly, it increases p53 retention in nucleus that triggers the expression of apoptosis-related genes. Secondly, it increases p53 transcriptional activity by raising p53 phosphorylation at Ser 46 and decreases p53 protein degradation by reducing p53 phosphorylation at Ser 315 . We show for the first time that BCAS2, a small nuclear protein (26 kDa), is a novel negative regulator of p53 and hence a potential molecular target for cancer therapy. [Cancer Res 2009;69(23):8877-85]

and the ¶Department of Ophthalmology, Mackay Memorial Hospital, Taipei 104, Taiwan Transcriptional regulation by members of the nuclear hormone receptor superfamily is a modular process requiring the mediation of distinct subclasses of coregulators. In this study, we isolated a novel WD40 repeatcontaining gene, human nuclear receptor interaction protein (NRIP). We found NRIP interacts with either androgen or glucocorticoid receptors from in vitro and in vivo pulldown assays. Subsequently, transient transfection and luciferase activity assays suggested that NRIP was a ligand-dependent coactivator of steroid receptors (androgen and glucocorticoid) in distinct promoters. To further clarify the function of NRIP, we found an RNA interference-3-targeted NRIP gene sequence (5-GATGATACAGCACGAGAAC-3) that could efficiently and specifically knock down endogenous and exogenous NRIP gene expression and that significantly diminished cell proliferation in prostate (LNCaP) and cervical (C33A) cells. Therefore, NRIP may play a role in enhancing the transcriptional activity of nuclear receptors and may be a critical target for developing therapeutic agents against nuclear receptor-mediated progression of prostate and cervical cancers.Steroid hormone receptors, such as androgen receptor (AR), 1 estrogen receptor, progesterone receptor, and glucocorticoid receptor (GR) etc., are known as type I nuclear receptors (1). Nuclear receptor family members function as ligand-inducible transcription factors (2). The binding of growth hormone to nuclear receptor induces receptor dimerization, facilitating the ability of the nuclear receptor to bind to its cognate response element and recruit coregulators to promote the expression of target genes (3). In the past decade, several coactivators have been cloned and characterized that associate with steroid receptors and enhance their ability to transactivate target genes (4). Well studied coactivators include the p160 family proteins (SRC-1, TIF-2/GRIP-1, ACTR/-CIP) (5), the p300/cAMP response element-binding protein-binding protein family (6), Ubc9 (7), ARA70 (8), ARA55 (9), TIP60 (10), and protein arginine methyltransferases (11). Some cofactors act through functional modification of other activators or coactivators (12), resulting in efficient recruitment of coactivators by the nuclear receptor to the target gene and/or the stabilization of general initiation factors that form pre-initiation complexes on common core promoter elements (13). Some coactivators contain intrinsic histone acetyltransferase or methyltransferase activities, suggesting that they modify chromatin and integrating stimuli into an appropriate transcription response at a wide variety of promoters (14 -16). In addition, a class of coregulators serves as bridges mediating interactions between the coactivators and other general transcription factors at post-chromatin-remodeling steps (17).In this study, we isolated a novel gene named nuclear receptor interaction protein (NRIP) by using the yeast two-hybrid system. From am...

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Human papillomavirus type 16 (HPV-16) E5 protein, along with the more publicized E6 and E7 proteins of this virus, has been found to be oncogenic. E5 is a highly hydrophobic membrane-bound protein of 83 amino acids associated with the Golgi apparatus, endoplasmic reticulum, and nuclear membrane in infected cells. E5 can activate epidermal growth factor receptor (EGFR) through binding to the 16 kD subunit of protein pump ATPase leading to a reduced downregulation of EGFR receptors. The activation of EGFR can initiate biochemical cascades that lead to overexpression of a variety of protooncogenes and stimulate rapid cell growth. Moreover, E5 can inhibit the expression of tumor suppressor gene p21((WafI/SdiI/CipI)) and impair the control of cell cycle checkpoint. E5 protein has been identified as a potential tumor vaccine target antigen.

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