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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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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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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

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Ahmed J. Awad, Terry C. Burns, Ying Zhang and Roger Abounader

G lioblastoma multiforme (GBM; WHO Grade IV) is the most common and most lethal of all primary brain tumors. The incidence rate of GBM in the US is estimated to be 2.69 per 100,000 persons per year, comprising 12%–20% of all brain tumors. 21 , 54 Even with the standard triad of surgery, chemotherapy, and radiation therapy, life expectancy is still poor, with an average survival of approximately 14 months following initial diagnosis. 28 Hence, there is an urgent need for novel treatment strategies that inhibit proliferation and angiogenesis in high

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Matthew T. Harting, James E. Baumgartner, Laura L. Worth, Linda Ewing-Cobbs, Adrian P. Gee, Mary-Clare Day and Charles S. Cox Jr.

shown to be rich in MSCs. 63 Given the fact that these tissues are a readily available source of cells, they may prove a valuable niche for cell isolation. Cell Therapy: Possible Mechanisms of Action The interactions of transplanted cells and the recipient organism or specific tissue are poorly understood. Significant investigation into potential mechanisms of action that may lead to functional recovery is yielding valuable insight ( Table 1 ). Although recent skepticism has been expressed, differentiation into local–regional cell types and supporting cell

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Adam M. Sonabend, Ilya V. Ulasov, Yu Han and Maciej S. Lesniak

M alignant brain tumors remain refractory to current medical and/or surgical therapy. The characteristic resistance to treatment shown by high-grade gliomas resides in their biological behavior and their location within the CNS. As is true with most cancers, gliomas are subject to constant genotypic and phenotypic alterations that can generate treatment-resistant clones. These cell populations are selected once a therapy is administered. In addition, high-grade gliomas cannot be effectively targeted by systemic chemotherapy because the blood–brain barrier

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Bhargav Desai, Ying Hsu, Benjamin Schneller, Jonathan G. Hobbs, Ankit I. Mehta and Andreas Linninger

overproduction of CSF. In these forms of hydrocephalus where overproduction of CSF is implicated, inhibition of AQP4 may be therapeutically desired. It is important to understand the molecular mechanism of hydrocephalus to best design therapies to facilitate the clearance of fluid. Clearly, numerous studies have elucidated that a link exists between AQP4 channels, brain water balance, and hydrocephalus. The CSF cycle commences at AQP channels in the choroid (i.e., AQP1) and may have a terminus at the BBB interface linking capillary fluid exchange to interstitial fluid

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Robert H. Andres, Raphael Guzman, Angélique D. Ducray, Pasquale Mordasini, Atul Gera, Alain Barth, Hans R. Widmer and Gary K. Steinberg

survivors suffer from persistent, severe neurological deficits. It is estimated that 90% of surviving patients are dependent on a caregiver at 1 month, and 80% are dependent on a caregiver at 6 months after the insult. 7 , 8 , 19 The available therapy is mainly supportive, including maintenance of homeostasis and treatment of brain edema. Therapies that prevent hematoma expansion and continuous bleeding through the administration of hemostatic agents, such as recombinant activated factor VII, 79 are currently under investigation, but the results of a Phase III study