title: Neurofibromatosis 2011: a report of the Children's Tumor Foundation annual meeting.
abstract: The 2011 annual meeting of the Children's Tumor Foundation, the annual gathering of the neurofibromatosis (NF) research and clinical communities, was attended by 330 participants who discussed integration of new signaling pathways into NF research, the appreciation for NF mutations in sporadic cancers, and an expanding pre-clinical and clinical agenda. NF1, NF2, and schwannomatosis collectively affect approximately 100,000 persons in US, and result from mutations in different genes. Benign tumors of NF1 (neurofibroma and optic pathway glioma) and NF2 (schwannoma, ependymoma, and meningioma) and schwannomatosis (schwannoma) can cause significant morbidity, and there are no proven drug treatments for any form of NF. Each disorder is associated with additional manifestations causing morbidity. The research presentations described in this review covered basic science, preclinical testing, and results from clinical trials, and demonstrate the remarkable strides being taken toward understanding of and progress toward treatments for these disorders based on the close interaction among scientists and clinicians.
authors.affiliation: Hôpital Beaujon, Inserm U674, Universite Paris 7, Paris, France. michel.kalamarides@bjn.aphp.fr
authors.forename: Michel
authors.initials: M
authors.lastname: Kalamarides
authors.forename: Maria T
authors.initials: MT
authors.lastname: Acosta
authors.forename: Dusica
authors.initials: D
authors.lastname: Babovic-Vuksanovic
authors.forename: Olli
authors.initials: O
authors.lastname: Carpen
authors.forename: Karen
authors.initials: K
authors.lastname: Cichowski
authors.forename: D Gareth
authors.initials: DG
authors.lastname: Evans
authors.forename: Filippo
authors.initials: F
authors.lastname: Giancotti
authors.forename: C Oliver
authors.initials: CO
authors.lastname: Hanemann
authors.forename: David
authors.initials: D
authors.lastname: Ingram
authors.forename: Alison C
authors.initials: AC
authors.lastname: Lloyd
authors.forename: Debra A
authors.initials: DA
authors.lastname: Mayes
authors.forename: Ludwine
authors.initials: L
authors.lastname: Messiaen
authors.forename: Helen
authors.initials: H
authors.lastname: Morrison
authors.forename: Kathryn
authors.initials: K
authors.lastname: North
authors.forename: Roger
authors.initials: R
authors.lastname: Packer
authors.forename: Duojia
authors.initials: D
authors.lastname: Pan
authors.forename: Anat
authors.initials: A
authors.lastname: Stemmer-Rachamimov
authors.forename: Meena
authors.initials: M
authors.lastname: Upadhyaya
authors.forename: David
authors.initials: D
authors.lastname: Viskochil
authors.forename: Margret R
authors.initials: MR
authors.lastname: Wallace
authors.forename: Kim
authors.initials: K
authors.lastname: Hunter-Schaedle
authors.forename: Nancy
authors.initials: N
authors.lastname: Ratner
mesh_terms: D002648:Child; D016514:Genes, Neurofibromatosis 1; D016515:Genes, Neurofibromatosis 2; D006801:Humans; D008579:Meningioma / Q000235:genetics / Q000473:pathology; D009442:Neurilemmoma / Q000235:genetics / Q000473:pathology; D009456:Neurofibromatosis 1 / Q000235:genetics / Q000473:pathology*; D016518:Neurofibromatosis 2 / Q000235:genetics / Q000473:pathology*
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