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1 PDGFRA amplification and 1q gain occurred at significant
2 PDGFRA intragenic deletion of exons 8 and 9 were previou
3 PDGFRA mutations and KIT exon 11 insertion or duplicatio
4 PDGFRA mutations can explain response and sensitivity to
5 PDGFRA was the predominant target of focal amplification
6 PDGFRA, a receptor whose activity is required for cell m
7 PDGFRA/NG2 cells generated very few GFAP(+)-reactive ast
8 FIP1L1-PDGFRA-myeloid neoplasm (FP; n =12), PDGFRA-negative HES with >/=4 criteria suggestive of a m
9 4 astrocytomas and included the MDM4 (1q32), PDGFRA (4q12), MET (7q21), CMYC (8q24), PVT1 (8q24), WNT
10 tation, 43 (12.6%) had GISTs that harbored a PDGFRA mutation, and 24 (7.0%) had GISTs that were wild
15 r platelet-derived growth factor receptor A (PDGFRA) mutations respond to treatment with targeted KIT
17 either wild-type or constitutively activated PDGFRA (platelet-derived growth factor receptor-alpha) u
18 ding of rearranged, constitutively activated PDGFRA/B identifies patients who are eminently treatable
20 ed by copy number analysis, we sequenced all PDGFRA coding exons from a cohort of pediatric HGGs.
23 of the Fip1-like 1 (FIP1L1) and PDGFR alpha (PDGFRA) genes has been identified as a therapeutic targe
24 atelet-derived growth factor receptor alpha (PDGFRA) (F/P) fusion gene has been identified as a cause
26 atelet-derived growth factor receptor alpha (PDGFRA) and epidermal growth factor receptor (EGFR).
27 atelet derived growth factor receptor alpha (PDGFRA) and type 3 fibroblast growth factor receptor (FG
28 atelet derived growth factor receptor alpha (PDGFRA) antibodies have been associated with extensive c
29 at either IGF-1R or the PDGF receptor alpha (PDGFRA) can mediate intrinsic resistance to rapamycin.
30 atelet-derived growth factor receptor alpha (PDGFRA) fusion was also documented in enriched eosinophi
31 atelet-derived growth factor receptor alpha (PDGFRA) have been reported in a subset of gastrointestin
32 atelet-derived growth factor receptor alpha (PDGFRA) in prostate cells and indirectly influences the
33 atelet-derived growth factor receptor alpha (PDGFRA) is the most frequent target of focal amplificati
35 atelet-derived growth factor receptor alpha (PDGFRA) mutations in contrast to a mutation rate of 80%
37 atelet-derived growth factor receptor alpha (PDGFRA) overexpression is concomitant with a loss of cyc
38 atelet-derived growth factor receptor alpha (PDGFRA) receptor tyrosine kinase proteins, and these kin
39 atelet-derived growth factor receptor alpha (PDGFRA) that are potential therapeutic targets for imati
41 atelet-derived growth factor receptor alpha (PDGFRA), and fibroblast growth factor receptor 1 (FGFR1)
42 atelet derived growth factor receptor alpha (PDGFRA), and the most common of these mutations is resis
43 KIT-related kinase gene PDGF receptor alpha (PDGFRA), which occurred in either exon 18 (5.6%) or 12 (
45 atelet-derived growth factor receptor-alpha (PDGFRA) gene rearrangement in these tumors is unknown.
46 atelet-derived growth factor receptor-alpha (PDGFRA), as evident from the expression of myogenic mark
47 atelet-derived growth factor receptor-alpha (PDGFRA), has been invariably associated with a primary e
48 latelet-derived growth factor receptor alpha(PDGFRA), which can be therapeutically targeted by tyrosi
50 rongly influenced by the balance of EGFR and PDGFRA activation in individual cells, which is heteroge
51 was performed on eight samples with EGFR and PDGFRA amplification, revealing distinct tumor cell subp
52 K activation levels correlated with EGFR and PDGFRA expression, and p-FAK and EGFR expression co-loca
55 most commonly amplified RTK genes, EGFR and PDGFRA, were found to be present in variable proportions
57 ted with the mTORC1 inhibitor everolimus and PDGFRA inhibitor imatinib mesylate confirmed that this d
58 n, the role of mutation screening in KIT and PDGFRA as a diagnostic and prognostic aid is emphasized
59 expressed minimal to null levels of KIT and PDGFRA but expressed levels of PDGFRB that are comparabl
60 l stromal tumors (GISTs), which lack KIT and PDGFRA gene mutations, are the primary form of GIST in c
61 racteristic somatic mutations in the KIT and PDGFRA genes in GIST tumors may similarly be mutational
69 nt of GIST harboring the most common KIT and PDGFRA mutations, optimal management of other genotypic
71 zed GISTs with mutation analysis for KIT and PDGFRA performed centrally using conventional sequencing
73 echanisms of genetic progression and KIT and PDGFRA transforming roles in pediatric GIST might facili
75 disorder, and at least two genes (c-kit and PDGFRA) with pathogenetically relevant mutations have be
81 K27M expression synergizes with p53 loss and PDGFRA activation in neural progenitor cells derived fro
84 ng caused by overexpression of genes such as PDGFRA is responsible for robust glioma growth and cell
86 as well as in chronic myeloid leukemia (BCR-PDGFRA translocation), and sunitinib can yield clinical
92 T, although the reduced sensitivity of D842V-PDGFRA probably limits the potential of nilotinib monoth
95 ng skeletal muscle defects, the hESC-derived PDGFRA(+) cells exhibit significant in vitro expansion w
97 , and hallmark copy number variations (EGFR, PDGFRA, MDM4, and CDK4 amplification; PTEN, CDKN2A, NF1,
98 on, integrin expression was enriched in EGFR/PDGFRA-overexpressing areas but was more regionally conf
99 we detected mutations in ERBB2, EGFR, FGFR1, PDGFRA, and MAP2K1 as potential mechanisms of primary re
106 chieved at least a 3-log reduction in FIP1L1-PDGFRA fusion transcripts relative to the pretreatment l
108 row mast cell infiltration pattern in FIP1L1-PDGFRA(+) SMCD-eos was distinctly diffuse with loose tum
112 In 2003, a karyotypically-occult FIP1L1-PDGFRA was reported in a subset of patients with blood e
113 aken in patients with a high level of FIP1L1-PDGFRA expression prior to initiation of imatinib (100 m
115 abnormality, whereas the incidence of FIP1L1-PDGFRA in the remaining 81 patients with primary eosinop
116 a rational basis for the treatment of FIP1L1-PDGFRA positive chronic eosinophilic leukemia and mastoc
118 as an in vitro model for the study of FIP1L1-PDGFRA-positive chronic eosinophilic leukemia and for th
121 S and CEL and the implications of the FIP1L1-PDGFRA discovery on their diagnosis, classification, and
128 the exception of the presence of the FIP1L1-PDGFRA fusion gene, little is known about predictors of
135 These observations suggest that the FIP1L1-PDGFRA rearrangement occurs in an early hematopoietic pr
138 s clearly the treatment of choice for FIP1L1/PDGFRA-positive chronic eosinophilic leukemia (CEL), lit
139 imination of the clonal population in FIP1L1/PDGFRA-positive CEL and suggest that molecular monitorin
140 le-blind, placebo-controlled study of FIP1L1/PDGFRA-negative, corticosteroid-responsive subjects with
143 ress these questions, 5 patients with FIP1L1/PDGFRA-positive CEL with documented clinical, hematologi
145 Lu et al. describe a phenotypic switch from PDGFRA-enriched "proneural" to EGFR-enriched "classical"
147 t-derived growth factor receptor-alpha gene (PDGFRA) to an uncharacterized human gene FIP1-like-1 (FI
151 B/p14ARF as early events, and aberrations in PDGFRA and PTEN as later events during cancer progressio
159 may aid in the diagnosis of GISTs, including PDGFRA mutants that fail to express KIT antigen, and lea
163 Tumor expression of total and activated KIT, PDGFRA, and PDGFRB were assessed using immunohistochemis
164 tive investigational inhibitor of FLT3, KIT, PDGFRA, PDGFRB and RET; evolution of AC220-resistant sub
170 RA-mutant GIST, similar progress against KIT/PDGFRA wild-type GIST, including mutant BRAF-driven tumo
171 ansporter type 4 (GLUT4) expression, and KIT/PDGFRA mutation status in patients with gastrointestinal
172 ies of 20 cases originally classified as KIT/PDGFRA wild-type GIST revealed that 17 (85.0%) harbored
173 We assessed the relationship between KIT/PDGFRA mutations and select deletions or single nucleoti
174 argeting is expected to be selective for KIT/PDGFRA and a subset of other HSP90 clients, and thereby
175 ing strategy for inactivating the myriad KIT/PDGFRA oncoproteins in TKI-resistant GIST patients.
176 te clinical advances in the treatment of KIT/PDGFRA-mutant GIST, similar progress against KIT/PDGFRA
177 linical resistance to imatinib and other KIT/PDGFRA kinase inhibitors and there is an urgent need to
178 tions respond to treatment with targeted KIT/PDGFRA inhibitors such as imatinib mesylate, these treat
179 testinal stromal tumors (GISTs), and the KIT/PDGFRA kinase inhibitor, imatinib, is standard of care f
181 ning mutations that confer resistance to KIT/PDGFRA kinase inhibitors.Oncogene advance online publica
185 nib-sensitive adenosquamous NSCLC cell line, PDGFRA expression was associated with focal PFGRA gene a
186 ly in a human FASD genome-wide dataset links PDGFRA to craniofacial phenotypes in FASD, prompting a m
187 T oncoproteins, suggesting that KIT-mediated PDGFRA phosphorylation is an efficient and biologically
188 tumors, rare tumors that show PDGFC-mediated PDGFRA activation may also be clinically responsive to p
192 in promoting transformation than the mutant PDGFRA, which is important because 78% of human MPNSTs
193 in promoting transformation than the mutant PDGFRA, which is important because ~78% of human MPNSTs
195 tion or point mutation, KIT exon 9 mutation, PDGFRA mutation, or wild-type tumor, although some of th
196 luding BLNK, DGKH, FGFR1, IL2RB, LYN, NTRK3, PDGFRA, PTK2B, TYK2, and the RAS signaling pathway.
197 s with PDGFRA amplification: overall, 43% of PDGFRA-amplified GBM were found to have amplification of
198 lasms with eosinophilia and abnormalities of PDGFRA, PDGFRB, or FGFR1') and undefined (chronic eosino
199 b and test the hypothesis that abrogation of PDGFRA signaling can ameliorate the manifestations of cG
202 GFRII) and the PDGFRA gene, and six cases of PDGFRA(Delta8, 9), an intragenic deletion rearrangement.
210 lupus nephritis, intra-renal mRNA levels of PDGFRA and associated pathway members showed significant
212 lasms with eosinophilia and rearrangement of PDGFRA, PDGFRB, or FGFR1, or with PCM1-JAK2" In addition
214 ll KIT mutant isoforms, but only a subset of PDGFRA mutant isoforms, were sensitive to imatinib, in v
215 d evidence for functional transactivation of PDGFRA by EGFR and EGF-induced receptor heterodimerizati
219 tivating mutations in either KIT (75-80%) or PDGFRA (5-10%), two closely related receptor tyrosine ki
223 have somatic mutations in either the KIT or PDGFRA gene, but there are no known inherited genetic ri
224 mutation or no detectable mutation of KIT or PDGFRA had PR rates of 47.8% (P =.0006) and 0.0% (P <.00
225 stinal stromal tumors (GISTs) contain KIT or PDGFRA kinase gain-of-function mutations, and therefore
229 is activated in GIST, irrespective of KIT or PDGFRA mutational status, and is expressed at levels unp
230 eutic targets in GISTs containing the KIT or PDGFRA mutational types with which they are associated.
232 l stromal tumors (WT-GISTs) that lack KIT or PDGFRA mutations represent a unique subtype of GIST that
235 s require oncogenic activation of the KIT or PDGFRA receptor tyrosine kinase proteins, and the genomi
236 GISTs express oncogenic forms of the KIT or PDGFRA receptor tyrosine kinase proteins, which serve as
238 which are known to have key roles in KIT or PDGFRA signaling, and which might therefore contribute t
242 ations of the genes encoding the RTK KIT (or PDGFRA in a minority of cases) result in constitutive ki
243 r with known WT GIST (no mutations in KIT or PDGFRA) were recruited; 116 patients with WT GIST were e
246 Fip1-like 1 (FIP1L1) gene to the PDGFRalpha (PDGFRA) gene generated by an interstitial deletion on ch
251 ies of the PDGF receptor, alpha polypeptide (PDGFRA) isoforms (V561D; D842V and delta842-845) carryin
252 and subtype implementation, including PTEN, PDGFRA, RB1, VEGFA, STAT3, and RUNX1, suggesting that th
253 and included markers localized to 4q11-q13 (PDGFRA, GSX2; P=4.5x10(-7)), 16p12 (SLC5A11; P=5.1x10(-7
254 atelet-derived growth factor alpha receptor (PDGFRA)/NG2-expressing glia are distributed throughout t
255 eoplasm (MHES; n =10), or steroid-refractory PDGFRA-negative HES with <4 myeloid criteria (SR; n = 5)
256 d nilotinib, and imatinib, on 2 GIST-related PDGFRA mutants, V561D and D842V, which possess different
257 Including our cases, there are 289 reported PDGFRA-mutant GISTs, of which 181 (62.6%) had the imatin
260 igand PDGFC was also detected, and silencing PDGFRA or PDGFC expression by RNA interference inhibited
261 Through generation of hepatocyte-specific PDGFRA knockout (KO) mice that lack an overt phenotype,
263 ling of clinical tumor samples revealed that PDGFRA was the most highly expressed kinase gene among s
264 al sarcoma disease subtypes, suggesting that PDGFRA may be uniquely significant for synovial sarcomas
267 sert domain receptor (KDR) (VEGFRII) and the PDGFRA gene, and six cases of PDGFRA(Delta8, 9), an intr
268 A subset of cardiac FAPs, identified by the PDGFRA(pos):Lin(neg):THY1(neg):DDR2(neg) signature, expr
272 I1 reexpression also resulted in loss of the PDGFRA and EGFR proteins, suggesting a rapid turnover of
273 T to imatinib depends on the location of the PDGFRA mutation; for example, the V561D juxtamembrane do
275 no or limited efficacy in patients with the PDGFRA D842V mutation or patients with GIST lacking KIT
276 e results suggest the possibility that these PDGFRA mutants behave as oncogenes in this subset of gli
279 esults indicate that the fusion of FIP1L1 to PDGFRA occurs rarely in leukemia cell lines, but they id
280 escribed in gastrointestinal stromal tumors (PDGFRA mutations) as well as in chronic myeloid leukemia
281 a model in which overexpression of wild-type PDGFRA associated with NF1 deficiency leads to aberrant
283 terestingly, overexpression of the wild-type PDGFRA was even more potent in promoting transformation
284 terestingly, overexpression of the wild-type PDGFRA was even more potent in promoting transformation
285 of human MPNSTs have expression of wild-type PDGFRA, whereas only 5% harbor activating mutations of t
286 of human MPNSTs have expression of wild-type PDGFRA, whereas only 5% harbor activating mutations of t
287 os overexpressing mutant, but not wild-type, PDGFRA, suggesting a mechanism through which the oncogen
289 of nilotinib as a treatment option for V561D-PDGFRA-associated GIST, although the reduced sensitivity
290 d potent activity in vitro against the V561D-PDGFRA mutant but were significantly less efficacious ag
294 with hypereosinophilic MPNs associated with PDGFRA and PDGFRB fusion genes are responsive to imatini
297 ggest that more than one third of GISTs with PDGFRA mutations may respond to imatinib and that mutati
298 sphorylated KIT oncoproteins interacted with PDGFRA, PDGFRB, phosphatidylinositol 3-kinase (PI3-K) an
299 menon is especially common among tumors with PDGFRA amplification: overall, 43% of PDGFRA-amplified G
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