TY - JOUR
T1 - Neurofibromatosis 2011
T2 - A report of the Children's Tumor Foundation Annual Meeting
AU - Kalamarides, Michel
AU - Acosta, Maria T.
AU - Babovic-Vuksanovic, Dusica
AU - Carpen, Olli
AU - Cichowski, Karen
AU - Gareth Evans, D.
AU - Giancotti, Filippo
AU - Oliver Hanemann, C.
AU - Ingram, David
AU - Lloyd, Alison C.
AU - Mayes, Debra A.
AU - Messiaen, Ludwine
AU - Morrison, Helen
AU - North, Kathryn
AU - Packer, Roger
AU - Pan, Duojia
AU - Stemmer-Rachamimov, Anat
AU - Upadhyaya, Meena
AU - Viskochil, David
AU - Wallace, Margret R.
AU - Hunter-Schaedle, Kim
AU - Ratner, Nancy
PY - 2012/3
Y1 - 2012/3
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84857917804&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84857917804&partnerID=8YFLogxK
U2 - 10.1007/s00401-011-0905-0
DO - 10.1007/s00401-011-0905-0
M3 - Article
C2 - 22083253
AN - SCOPUS:84857917804
SN - 0001-6322
VL - 123
SP - 369
EP - 380
JO - Acta neuropathologica
JF - Acta neuropathologica
IS - 3
ER -