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Venteicher, Andrew S

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Venteicher

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Andrew S

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Venteicher, Andrew S
Author's Publications: search.filters.isAuthorOfPublication.633ee626-b285-45f6-a75e-98b6106f6a50

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Now showing 1 - 5 of 5
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    Glioblastoma Mimicking an Arteriovenous Malformation
    (Frontiers Media S.A., 2013) Khanna, Arjun; Venteicher, Andrew S; Walcott, Brian; Kahle, Kristopher T.; Mordes, Daniel; William, Christopher M.; Ghogawala, Zoher; Ogilvy, Christopher
    Abnormal cerebral vasculature can be a manifestation of a vascular malformation or a neoplastic process. We report the case of a patient with angiography-negative subarachnoid hemorrhage (SAH) who re-presented 3 years later with a large intraparenchymal hemorrhage. Although imaging following the intraparenchymal hemorrhage was suggestive of arteriovenous malformation, the patient was ultimately found to have an extensive glioblastoma associated with abnormal tumor vasculature. The case emphasizes the need for magnetic resonance imaging to investigate angiography-negative SAH in suspicious cases to rule out occult etiologies, such as neoplasm. We also discuss diagnostic pitfalls when brain tumors are associated with hemorrhage and abnormal vasculature.
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    Rapid Intraoperative Molecular Characterization of Glioma
    (American Medical Association (AMA), 2015) Shankar, Ganesh; Francis, Joshua M.; Rinne, Mikael; Ramkissoon, Shakti H.; Huang, Franklin; Venteicher, Andrew S; Akama-Garren, Elliot H.; Kang, Yun Jee; Lelic, Nina; Kim, James C.; Brown, Loreal E.; Charbonneau, Sarah K; Golby, Alexandra; Sekhar Pedamallu, Chandra; Hoang, Mai; Sullivan, Ryan; Cherniack, Andrew D.; Garraway, Levi; Stemmer-Rachamimov, Anat; Reardon, David; Wen, Patrick; Brastianos, Priscilla; Curry, William; Barker, Frederick; Hahn, William; Nahed, Brian; Ligon, Keith; Louis, David; Cahill, Daniel; Meyerson, Matthew
    IMPORTANCE: Conclusive intraoperative pathologic confirmation of diffuse infiltrative glioma guides the decision to pursue definitive neurosurgical resection. Establishing the intraoperative diagnosis by histologic analysis can be difficult in low-cellularity infiltrative gliomas. Therefore, we developed a rapid and sensitive genotyping assay to detect somatic single-nucleotide variants in the telomerase reverse transcriptase (TERT) promoter and isocitrate dehydrogenase 1 (IDH1). OBSERVATIONS: This assay was applied to tissue samples from 190 patients with diffuse gliomas, including archived fixed and frozen specimens and tissue obtained intraoperatively. Results demonstrated 96% sensitivity (95% CI, 90%–99%) and 100% specificity (95% CI, 95%–100%) for World Health Organization grades II and III gliomas. In a series of live cases, glioma-defining mutations could be identified within 60 minutes, which could facilitate the diagnosis in an intraoperative timeframe. CONCLUSIONS AND RELEVANCE: The genotyping method described herein can establish the diagnosis of low-cellularity tumors like glioma and could be adapted to the point-of-care diagnosis of other lesions that are similarly defined by highly recurrent somatic mutations.
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    Insulator dysfunction and oncogene activation in IDH mutant gliomas
    (2015) Flavahan, William A.; Drier, Yotam; Liau, Brian; Gillespie, Shawn M.; Venteicher, Andrew S; Stemmer-Rachamimov, Anat; Suva, Mario; Bernstein, Bradley
    Gain-of-function IDH mutations are initiating events that define major clinical and prognostic classes of gliomas1,2. Mutant IDH protein produces a novel onco-metabolite, 2-hydroxyglutarate (2-HG), that interferes with iron-dependent hydroxylases, including the TET family of 5′-methylcytosine hydroxylases3–7. TET enzymes catalyze a key step in the removal of DNA methylation8,9. IDH mutant gliomas thus manifest a CpG island methylator phenotype (G-CIMP)10,11, though the functional significance of this altered epigenetic state remains unclear. Here we show that IDH mutant gliomas exhibit hyper-methylation at CTCF binding sites, compromising binding of this methylation-sensitive insulator protein. Reduced CTCF binding is associated with loss of insulation between topological domains and aberrant gene activation. We specifically demonstrate that loss of CTCF at a domain boundary permits a constitutive enhancer to aberrantly interact with the receptor tyrosine kinase gene PDGFRA, a prominent glioma oncogene. Treatment of IDH mutant gliomaspheres with demethylating agent partially restores insulator function and down-regulates PDGFRA. Conversely, CRISPR-mediated disruption of the CTCF motif in IDH wildtype gliomaspheres up-regulates PDGFRA and increases proliferation. Our study suggests that IDH mutations promote gliomagenesis by disrupting chromosomal topology and allowing aberrant regulatory interactions that induce oncogene expression.
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    Clinical features of brain metastasis from salivary gland tumors
    (Elsevier BV, 2013) Venteicher, Andrew S; Walcott, Brian; Sheth, Sameer A.; Snuderl, Matija; Patel, Anoop Premswaroop; Curry, William; Nahed, Brian
    Salivary gland tumors comprise a group of 24 tumor subtypes with a wide range of clinical behaviors and propensities for metastasis. Several prognostic factors have been identified that help predict the development of systemic metastases, most commonly to the lung, liver, or bone. Metastases to the brain are rare. To better understand the behavior of salivary gland tumors that metastasise to the brain, we performed a retrospective cohort analysis on a series of patients to highlight features of their medical and surgical management. From 2007 to 2011, a database of 4117 elective craniotomies were queried at a single institution to identify patients surgically treated for salivary gland metastases to the brain. Three patients were identified. Histologic subtypes included salivary duct carcinoma, poorly differentiated carcinoma, and papillary mucinous adenocarcinoma. They had all undergone previous treatment for their primary malignancy. The mean time to intracranial metastasis was 48 months from initial diagnosis (range, 14–91 months). Treatment for intracranial metastases included surgical resection, whole brain radiation, stereotactic radiosurgery, and chemotherapy. Intracranial metastases from salivary gland tumors are rare, present years after diagnosis of the primary tumor, and are treatable with multimodality therapy.
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    Decoupling genetics, lineages, and microenvironment in IDH-mutant gliomas by single-cell RNA-seq
    (American Association for the Advancement of Science (AAAS), 2017) Venteicher, Andrew S; Tirosh, Itay; Hebert, Christine; Yizhak, Keren; Neftel, Cyril Ralf Alexander; Filbin, Mariella; Hovestadt, Volker; Escalante, Leah; Shaw, McKenzie; Rodman, Christopher Jiahn-Leh; Gillespie, Shawn; Dionne, Danielle; Luo, Christina; Ravichandran, Hiranmayi; Mylvaganam, Ravindra; Mount, Christopher; Onozato, Maristela Lika; Nahed, Brian; Wakimoto, Hiroaki; Curry, William; Iafrate, Anthony; Rivera, Miguel; Frosch, Matthew; Golub, Todd; Brastianos, Priscilla; Getz, Gad; Patel, Anoop Premswaroop; Monje, Michelle; Cahill, Daniel; Rozenblatt-Rosen, Orit; Louis, David; Bernstein, Bradley; Regev, Aviv; Suva, Mario