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Jennifer Kosty and Timothy W. Vogel

sutures following surgery may lead to suboptimal cosmetic results, decreased intracranial volumes, and ultimately, neurological comorbidities prompting a surgical revision. In this article, we review the current literature on the molecular mechanisms related to the development of craniosynostosis and discuss the most promising candidates for translational therapies ( Table 1 ). TABLE 1. Molecular genetics of craniosynostosis and potential translational approaches Signaling Molecule Type of Molecule Associated Disorders Translational

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Zoe E. Teton, Daniel Blatt, Amr AlBakry, James Obayashi, Gulsah Ozturk, Vural Hamzaoglu, Philippe Magown, Nathan R. Selden, Kim J. Burchiel and Ahmed M. Raslan

therapies depends on the particular technology used, the indication for therapy, and the practical difficulties of maintaining a working system that sustains therapeutic benefit. Analysis of device survival and therapy survival together, therefore, presents an opportunity to evaluate treatment effectiveness in a novel way. Device and therapy survival data are necessary to guide accurate, patient-centered counseling when deciding whether or not to institute neuromodulatory therapy. Presenting this information side by side in language that patients can understand is

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Thomas Graillon, David Romano, Céline Defilles, Alexandru Saveanu, Amira Mohamed, Dominique Figarella-Branger, Pierre-Hugues Roche, Stéphane Fuentes, Olivier Chinot, Henry Dufour and Anne Barlier

have analyzed octreotide efficacy in patients with meningioma, yet their conclusions remain disputed and are sometimes undefined. 10 , 17 , 18 , 21 , 23 , 38 , 40 , 42 , 45 Moreover, the results of octreotide treatment in meningioma cells in vitro have been contradictory. 4 , 26 Therefore, should we reject octreotide for meningioma therapy? To clarify the direct antitumor effects of octreotide, we conducted an in vitro study using a large set of human meningiomas that included all histological subtypes and World Health Organization (WHO) Grade I, II, and III tumors

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Hector E. James and John S. Bradley

C erebrospinal fluid shunts are commonly placed to treat hydrocephalus and other conditions, and the most frequent complications are malfunction and infection. The incidence of shunt infection reported in the literature is 1.5–41%, 44 and multiple treatment modalities are currently in use. 1 , 9 , 20 , 36 , 43 , 44 Most authors agree that antibiotic therapy should be administered intravenously to obtain high concentrations of the same in the CSF, but there is very limited consensus as to the duration of therapy, the need for and manner of administration

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Brain-tumor therapy

Quantitative analysis using a model system

Mark L. Rosenblum, Kathy D. Knebel, Dolores A. Vasquez and Charles B. Wilson

months of additional lifespan. In one recent study, 32 radiotherapy alone or in combination with BCNU appeared to be more efficacious than BCNU alone; but again, the best treatment falls far short of cure. More effective treatment of this devastating disease, affecting about 5000 patients in the United States annually, 28 is dependent on a better understanding of the biological behavior of tumors and the effects of therapy. Characteristics of a drug for brain-tumor chemotherapy have been described by Rall and Zubrod, 18 and include the appropriate combination of

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Andrew D. Norden, Jan Drappatz and Patrick Y. Wen

microarray studies showed that losses on chromosomes 10 and 14 in high-grade meningiomas were associated with distinct expression profiles including increased expression of several genes related to the IGF ( IGF-2, IGFBP3, and AKT3 ) or wingless (WNT; CTNNB1 , CDK5R1 , ENC1 , and CCND1 ) pathways. 138 Pro-teomic analysis may also help to elucidate the molecular events that underlie the transition from benign to atypical or malignant meningiomas. 101 In this review, the treatment of meningiomas with targeted molecular therapies will be discussed. Current

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Erin N. Kiehna and Thomas E. Merchant

morbidity and mortality associated with such attempts may be avoided by using a multimodality approach. In 1961, Kramer et al. 18 at the Royal Marsden Hospital became the first group to publish a report on limited surgery and radiation therapy for pediatric craniopharyngioma. They recognized that with fenestration alone, symptomatic regrowth of the cystic portion of the tumor could be expected within 3–6 months. 14 By combining bur-hole aspiration with external-beam radiation therapy to 5000–6550 R, disease control was achieved in all 6 children who were reported to

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Mandeep S. Tamber, Paul Klimo Jr., Catherine A. Mazzola and Ann Marie Flannery

C erebrospinal fluid shunt infection is one of the most common and serious complications of CSF shunt therapy. Infection admissions number approximately 2300 per year in the United States and, in aggregate, account for more than 50,000 hospital days. 29 Total hospital charges related to the management of CSF shunt infection were nearly $250 million in 2003 adjusted dollars. 29 Within 24 months after insertion, infections complicate approximately 11% of initial CSF shunt placements. 28 Despite the high incidence of this complication, the optimal

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Pantelis Stavrinou, Aristotelis Kalyvas, Stefan Grau, Christina Hamisch, Norbert Galldiks, Sotirios Katsigiannis, Christoph Kabbasch, Marco Timmer, Roland Goldbrunner and George Stranjalis

a combination of resection, reirradiation, and alkylating chemotherapy. However, evidence for the efficacy of these therapies is rather limited and inconclusive. 4 , 7 , 16 , 18 Furthermore, it is still unclear whether second-line treatment of GBM at first progression achieves better survival than supportive care alone. The very few studies that address this question usually compare cohorts generated from a single institution after certain selection criteria are met (based on competing comorbidities, performance status, or resectability of the tumor at baseline

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Claire D. Clelland, Roger A. Barker and Colin Watts

in treating HD. Disease-modifying therapies—for example, small interfering RNA, pharmacological intervention, and modulation of autophagy—target pathogenic pathways, whereas cell replacement therapies attempt to replace dysfunctional or dying cells primarily through transplantation ( Fig. 2 ). Cell therapy strategies in HD have traditionally been aimed at replacing or protecting cells lost during the course of the disease and thereby preventing or retarding disease progression. Current work in HD cell therapy is broadly classified into 1 of 3 aims: 1) to harness