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Mazin Elsarrag, Parantap D. Patel, Ajay Chatrath, Davis Taylor, and John A. Jane Jr.

OBJECTIVE

Innovations in genomics, epigenomics, and transcriptomics now lay the groundwork for therapeutic interventions against neoplastic disease. In the past 30 years, the molecular pathogenesis of pituitary adenomas has been characterized. This enhanced understanding of the biology of pituitary tumors has potential to impact current treatment paradigms, and there exists significant translational potential for these results. In this review the authors summarize the results of genomics and molecular biology investigations into pituitary adenoma pathogenesis and behavior and discuss opportunities to translate basic science findings into clinical benefit.

METHODS

The authors searched the PubMed and MEDLINE databases by using combinations of the keywords “pituitary adenoma,” “genomics,” “pathogenesis,” and “epigenomics.” From the initial search, additional articles were individually evaluated and selected.

RESULTS

Pituitary adenoma growth is primarily driven by unrestrained cell cycle progression, deregulation of growth and proliferation pathways, and abnormal epigenetic regulation of gene expression. These pathways may be amenable to therapeutic intervention. A significant number of studies have attempted to establish links between gene mutations and tumor progression, but a thorough mechanistic understanding remains elusive.

CONCLUSIONS

Although not currently a prominent aspect in the clinical management of pituitary adenomas, genomics and epigenomic studies may become essential in refining patient care and developing novel pharmacological agents. Future basic science investigations should aim at elucidating mechanistic understandings unique to each pituitary adenoma subtype, which will facilitate rational drug design.

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Salma M. Bakr, Ajay Patel, Mohamed A. Zaazoue, Kathryn Wagner, Sandi K. Lam, Daniel J. Curry, and Jeffrey S. Raskin

OBJECTIVE

The grid-based orthogonal placement of depth electrodes (DEs), initially defined by Jean Talairach and Jean Bancaud, is known as stereo-electroencephalography (sEEG). Although acceptance in the United States was initially slow, advances in imaging and technology have spawned a proliferation of North American epilepsy centers offering sEEG. Despite publications highlighting minimal access techniques and varied indications, standard work for phase I targeted DE has not been defined. In this article, the authors propose the term “dynamic sEEG” and define standard work tools and related common data elements to promote uniformity in the field.

METHODS

A multidisciplinary approach from July to August 2016 resulted in the production of 4 standard work tools for dynamic sEEG using ROSA: 1) a 34-page illustrated manual depicting a detailed workflow; 2) a planning form to collocate all the phase I data; 3) a naming convention for DEs that encodes the data defining it; and 4) a reusable portable perioperative planning and documentation board. A retrospective review of sEEG case efficiency was performed comparing those using standard work tools (between July 2016 and April 2017) with historical controls (between March 2015 and June 2016). The standard work tools were then instituted at another epilepsy surgery center, and the results were recorded.

RESULTS

The process for dynamic sEEG was formally reviewed, including anesthesia, positioning, perioperative nursing guidelines, surgical steps, and postoperative care for the workflow using cranial fixation and ROSA-guided placement. There was a 40% improvement in time per electrode, from 44.7 ± 9.0 minutes to 26.9 ± 6.5 minutes (p = 0.0007) following the development and use of the manual, the naming convention, and the reusable portable perioperative planning and documentation board. This standardized protocol was implemented at another institution and yielded a time per electrode of 22.3 ± 4.4 minutes.

CONCLUSIONS

The authors propose the term dynamic sEEG for stereotactic depth electrodes placed according to phase I workup data with the intention of converting to ablation. This workflow efficiency can be optimized using the standard work tools presented. The authors also propose a novel naming convention that encodes critical data and allows portability among providers. Use of a planning form for common data elements optimizes research, and global adoption could facilitate multicenter studies correlating phase I modality and seizure onset zone identification.

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Sepehr Sani, Tibor Boco, Steven L. Lewis, Elizabeth Cochran, Ajay J. Patel, and Richard W. Byrne

Microfibrillar collagen hemostat, known by its trade name Avitene, has been used in neurosurgery for decades. Complications with this product have been documented in other surgical specialties and described as mostly immune-mediated foreign-body reactions that can lead to a granulomatous reaction. There has never been a case of disseminated encephalomyelitis associated with this topical hemostatic agent. In this report the authors present a case of postoperative acute disseminated encephalomyelitis after exposure to Avitene. Possible pathophysiological mechanisms are discussed and the pertinent literature is reviewed.

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Ahmed Mohyeldin, Clifton L. Dalgard, Huasheng Lu, Thomas Mcfate, A. Sasha Tait, Viral C. Patel, Kondi Wong, Elizabeth Rushing, Subhojit Roy, Geza Acs, and Ajay Verma

Object

The hypoxia-inducible pleiotropic hormone, erythropoietin (EPO), has recently been found to promote the development and survival of neurons and astrocytes. Since hypoxia has been implicated in the malignant progression of some human cancers, the authors investigated whether EPO signaling influenced the malignant properties of human astrocytoma cells.

Methods

Reverse transcriptase–polymerase chain reaction, Western blot analysis, and immunohistochemical studies were used to measure EPO and its receptor (EPOR). Cell viability, Matrigel invasion assays, metalloprotease assays, EPO neutralizing antibodies, and EPOR overexpression were used to study the biological actions of EPO.

Expression of both EPO and EPOR was observed in the hypoxic regions and invasive margins of glioma specimens obtained at biopsy, and expression of EPOR correlated with the stage of the tumor. The EPOR was also functionally upregulated by hypoxia in cultured glioblastoma multiforme (GBM) cells. Both hypoxia and EPO protected cultured GBM cells from cisplatin cytotoxicity and promoted the invasiveness of GBM cells through Matrigel by potentiating metalloprotease activity. Hypoxia-enhanced cell invasion was attenuated in cells that overexpressed a nonfunctional EPOR.

Conclusions

Hypoxia-inducible autocrine and paracrine EPO signaling participates in the malignant progression of GBMs.

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Oral Presentations

2010 AANS Annual Meeting Philadelphia, Pennsylvania May 1–5, 2010