Please use this identifier to cite or link to this item: https://doi.org/10.18632/oncotarget.2194
Title: The NF1 gene revisited -from bench to bedside
Authors: Yap, Y.-S 
McPherson, J.R 
Ong, C.-K 
Rozen, S.G 
Teh, B.-T 
Lee, A.S.G 
Callen, D.F
Keywords: 2 (2 chloro 4 iodoanilino) n cyclopropylmethoxy 3,4 difluorobenzamide
alisertib
alpha2a interferon
erlotinib
everolimus
imatinib
isotretinoin
n (2,3 dihydroxypropoxy) 3,4 difluoro 2 (2 fluoro 4 iodoanilino)benzamide
neurofibromin
pirfenidone
placebo
rapamycin
retaspimycin
selumetinib
sorafenib
thalidomide
tipifarnib
neurofibromin
article
brain tumor
breast tumor
cancer inhibition
colorectal carcinoma
down regulation
drug potentiation
drug targeting
epigenetics
gene deletion
gene mutation
gene sequence
genetic association
genetic procedures
hematologic malignancy
human
lung cancer
malignant peripheral nerve sheath tumor
melanoma
molecular diagnosis
neurofibroma
neurofibromatosis
next generation sequencing
NF1 gene
nonhuman
ovary carcinoma
phase 1 clinical trial (topic)
phase 2 clinical trial (topic)
protein function
somatic mutation
tumor suppressor gene
animal
genetics
neoplasm
tumor suppressor gene
Animals
Genes, Neurofibromatosis 1
Humans
Neoplasms
Neurofibromin 1
Issue Date: 2014
Publisher: Impact Journals LLC
Citation: Yap, Y.-S, McPherson, J.R, Ong, C.-K, Rozen, S.G, Teh, B.-T, Lee, A.S.G, Callen, D.F (2014). The NF1 gene revisited -from bench to bedside. Oncotarget 5 (15) : 5873-5892. ScholarBank@NUS Repository. https://doi.org/10.18632/oncotarget.2194
Abstract: Neurofibromatosis type 1 (NF1) is a relatively common tumour predisposition syndrome related to germline aberrations of NF1, a tumour suppressor gene. The gene product neurofibromin is a negative regulator of the Ras cellular proliferation pathway, and also exerts tumour suppression via other mechanisms. Recent next-generation sequencing projects have revealed somatic NF1 aberrations in various sporadic tumours. NF1 plays a critical role in a wide range of tumours. NF1 alterations appear to be associated with resistance to therapy and adverse outcomes in several tumour types. Identification of a patient's germline or somatic NF1 aberrations can be challenging, as NF1 is one of the largest human genes, with a myriad of possible mutations. Epigenetic factors may also also contribute to inadequate levels of neurofibromin in cancer cells. Clinical trials of NF1-based therapeutic approaches are currently limited. Preclinical studies on neurofibromin-deficient malignancies have mainly been on malignant peripheral nerve sheath tumour cell lines or xenografts derived from NF1 patients. However, the emerging recognition of the role of NF1 in sporadic cancers may lead to the development of NF1-based treatments for other tumour types. Improved understanding of the implications of NF1 aberrations is critical for the development of novel therapeutic strategies.
Source Title: Oncotarget
URI: https://scholarbank.nus.edu.sg/handle/10635/174999
ISSN: 19492553
DOI: 10.18632/oncotarget.2194
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