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1 tizer for the clinical treatment of alveolar rhabdomyosarcoma.
2 rognosis for invasive or metastatic alveolar rhabdomyosarcoma.
3 essential component of therapy for alveolar rhabdomyosarcoma.
4 therapeutic targets for high-risk embryonal rhabdomyosarcoma.
5 fusion gene status to risk stratify alveolar rhabdomyosarcoma.
6 ation of dystrophies to the childhood cancer rhabdomyosarcoma.
7 anisation of the fused landscape in alveolar rhabdomyosarcoma.
8 ites and associated target genes in alveolar rhabdomyosarcoma.
9 evaluation of agents against this aggressive rhabdomyosarcoma.
10 expressed myogenic markers, consistent with rhabdomyosarcoma.
11 associated with the development of alveolar rhabdomyosarcoma.
12 ll leukemia, pancreatic cancer, melanoma and rhabdomyosarcoma.
13 m his father for the treatment of metastatic rhabdomyosarcoma.
14 the pediatric solid tumors, osteosarcoma and rhabdomyosarcoma.
15 lls from a common pediatric cancer, alveolar rhabdomyosarcoma.
16 PDGFR-A as a therapeutic target in alveolar rhabdomyosarcoma.
17 veloped tumors including medulloblastoma and rhabdomyosarcoma.
18 nd irinotecan is highly active in metastatic rhabdomyosarcoma.
19 subtype of the human skeletal muscle tumor, rhabdomyosarcoma.
20 ric patients with newly diagnosed metastatic rhabdomyosarcoma.
21 rk with critical therapeutic implications in rhabdomyosarcoma.
22 converted to a tumorigenic state that mimics rhabdomyosarcoma.
23 r testing in intermediate risk patients with rhabdomyosarcoma.
24 a new strategy to control the metastasis of rhabdomyosarcoma.
25 ved significantly, especially for metastatic rhabdomyosarcoma.
26 06B-BRAF), and a novel PAX3-GLI2 fusion in a rhabdomyosarcoma.
27 samples also confirmed their specificity to rhabdomyosarcoma.
28 and tumor and bone marrow biopsies disclosed rhabdomyosarcoma.
29 d and proliferative phenotypes for embryonal rhabdomyosarcoma.
30 ' tumour, Ewing's sarcoma, osteosarcoma, and rhabdomyosarcoma.
31 cause cancer, for example, breast cancer or rhabdomyosarcoma.
32 histopathology concluded the tissue to be a rhabdomyosarcoma.
33 ncers, but little is known about its role in rhabdomyosarcoma.
34 holds promise for the treatment of alveolar rhabdomyosarcoma.
35 contributes to the differentiation defect in rhabdomyosarcomas.
36 he contribution of two microRNAs (miRNAs) in rhabdomyosarcomas.
37 role for these miRNAs in the development of rhabdomyosarcomas.
38 rs that resembled the human form of alveolar rhabdomyosarcoma, a cancer associated with poor prognosi
40 y tumour (head and neck anaplastic embryonal rhabdomyosarcoma), all patients were alive at the time o
41 KCiota is functionally important in alveolar rhabdomyosarcoma anchorage-independent growth and tumor-
42 as single agents in both zebrafish embryonal rhabdomyosarcoma and a human cell line of rhabdomyosarco
43 fic and tissue-restricted gene expression in rhabdomyosarcoma and a second comprising a novel RAS-ind
44 evant distinction in PDGF signaling in human rhabdomyosarcoma and also suggests continued exploration
45 atients with first relapse or progression of rhabdomyosarcoma and an unfavorable prognosis were rando
46 ul reagent for studies of myasthenia gravis, rhabdomyosarcoma and arthrogryposis multiplex congenita
48 cell lines, independent of lineage (alveolar rhabdomyosarcoma and embryonal rhabdomyosarcoma), are pa
49 ced complete remissions in one model each of rhabdomyosarcoma and EWS, and in three of four osteosarc
50 med whole-genome and RNA sequencing on human rhabdomyosarcoma and identified RAS mutations and oxidat
51 the protein level in primary EFT but not in rhabdomyosarcoma and neuroblastoma, and EFT cells exhibi
54 ng allows improved diagnosis of experimental rhabdomyosarcoma and therefore might influence clinical
56 pitulate gene-expression signatures of human rhabdomyosarcomas and identified a cluster of genes that
57 ctive target for therapeutic intervention in rhabdomyosarcomas and other tumors that amplify and/or o
58 occur in pediatric patients (Ewing sarcoma, rhabdomyosarcoma), and just as clearly, adjuvant chemoth
59 expression of HOTS inhibits Wilms, rhabdoid, rhabdomyosarcoma, and choriocarcinoma tumor cell growth,
61 ipoliovirus immunity (n = 17) on Vero, human rhabdomyosarcoma, and human epidermoid carcinoma 2 cells
63 icular germ-cell tumors, in 2 of 5 embryonal rhabdomyosarcomas, and in 1 of 266 epithelial ovarian an
66 age (alveolar rhabdomyosarcoma and embryonal rhabdomyosarcoma), are particularly sensitive to the ind
67 essful purification of RNA from the alveolar rhabdomyosarcoma (ARMS) cancer cell line, with 3.5-fold
68 ariant of rhabdomyosarcoma known as alveolar rhabdomyosarcoma (ARMS) have a 5-year survival of <30%.
75 The highly aggressive muscle cancer alveolar rhabdomyosarcoma (ARMS) is one of the most common soft t
76 e 2;13 chromosomal translocation in alveolar rhabdomyosarcoma (ARMS), a cancer associated with the sk
77 velopment and is a key component in alveolar rhabdomyosarcoma (ARMS), a childhood solid muscle tumor.
78 t the concept into use, we selected alveolar rhabdomyosarcoma (ARMS), a myogenic pediatric cancer who
79 transcription factor, which induces alveolar rhabdomyosarcoma (aRMS), an aggressive cancer of skeleta
80 dismal for patients with metastatic alveolar rhabdomyosarcoma (aRMS), where the chimeric transcriptio
85 protein is present in a majority of alveolar rhabdomyosarcomas associated with increased aggressivene
86 nd young adults (age range, 1-18 years) with rhabdomyosarcoma at two institutions (1999-2009) with re
88 nd mTOR-signaling pathways are implicated in rhabdomyosarcoma biology, and hence are promising therap
89 ferentiation and tumorigenesis, can classify rhabdomyosarcomas by clinical subtype, and can predict p
90 nic differentiation can be induced in the RD rhabdomyosarcomas by increasing the abundance of MyoD:E-
93 RI/II confirmed TNFRI-AlbudAb potency, human rhabdomyosarcoma cell line KYM-1D4 cytotoxicity, and hum
94 nd is stereospecific because exposure of the rhabdomyosarcoma cell line RD to the L-erythro and DL-th
95 , we developed two resistant models from the rhabdomyosarcoma cell line Rh41: Rh41-807R, with acquire
96 ditions, while in a patient-derived alveolar rhabdomyosarcoma cell line, harbouring the diagnostic t(
99 ression in ERMS cells was confirmed in human rhabdomyosarcoma cell lines and prompted further analysi
100 en in human ARMS tumor tissue, as both human rhabdomyosarcoma cell lines and tissue microarrays showe
101 pression and knockdown of GPC5 expression in rhabdomyosarcoma cell lines increased and decreased cell
105 gth E12 robustly restores differentiation in rhabdomyosarcoma cells and broadly suppresses multiple i
108 inhibition of PI3K-mTOR-AKT pathway in Rh30 rhabdomyosarcoma cells attenuated ICL-induced activation
109 oculated i.m. with the RH30-L cells had more rhabdomyosarcoma cells in the bone marrow and lung after
112 oma xenograft to radiotherapy and sensitized rhabdomyosarcoma cells to the DNA interstrand cross-link
113 Both HT1080 cells overexpressing hTDP1 and rhabdomyosarcoma cells with elevated levels of hTdp1 wer
114 e million alveolar (Rh30) and embryonal (RD) rhabdomyosarcoma cells with stably transfected mCherry a
118 is in both primary human muscle cells and RD rhabdomyosarcoma cells, we demonstrate that MyoD binds i
123 bryonal rhabdomyosarcoma (ERMS) and alveolar rhabdomyosarcoma constitute the two major subtypes and e
124 tion of miR-1 and miR-133a into an embryonal rhabdomyosarcoma-derived cell line is cytostatic, thereb
125 mosomal translocation that leads to alveolar rhabdomyosarcoma development generates a novel TAD that
127 des two histolopathologic subtypes: alveolar rhabdomyosarcoma, driven by the fusion protein PAX3-FOXO
128 Thus, MYOD1 p.Leu122Arg defines a subset of rhabdomyosarcomas eligible for high-risk protocols and t
129 ing of tumour-propagating cells in embryonal rhabdomyosarcoma, emergence of clonal dominance in T-cel
132 , or gross residual (orbital only) embryonal rhabdomyosarcoma (ERMS) had 5-year failure-free survival
137 tein PAX3-FOXO1 or PAX7-FOXO1, and embryonal rhabdomyosarcoma (ERMS), which is genetically heterogene
139 patients with subset-one low-risk embryonal rhabdomyosarcoma (ERMS; stage 1/2 group I/II ERMS or sta
141 ymphoma), solid malignancies (neuroblastoma, rhabdomyosarcoma, Ewing sarcoma, and osteosarcoma), and
142 tumors that affect children, particularly in rhabdomyosarcoma, Ewing sarcoma, and other round cell sa
143 of 61 (13%); osteosarcoma, two of 20 (10%); rhabdomyosarcoma, four of 26 (15%); and other sarcomas,
145 e signature we determined could discriminate rhabdomyosarcoma from muscle, revealing a subset of musc
149 therapeutic options for the pediatric cancer rhabdomyosarcoma have not improved significantly, especi
153 f origin for Sonic Hedgehog-driven embryonal rhabdomyosarcoma in an adipocyte-restricted conditional
159 tions and metastatic progression of alveolar rhabdomyosarcomas in humans, we found by immunoblotting
162 copy number and gene expression analyses of rhabdomyosarcomas indicated that GPC5 was the only gene
173 ock in the childhood muscle cancer embryonal rhabdomyosarcoma is often thought to hold promise as an
179 erapy, patients with a histologic variant of rhabdomyosarcoma known as alveolar rhabdomyosarcoma (ARM
180 omas, suppressed differentiation of myogenic rhabdomyosarcoma lines generated from Hip1+/- and Ptch1+
183 ipoma, leiomyoma, haemangioma) or malignant (rhabdomyosarcoma, melanotic neuroectodermal tumour of in
185 logic activities linked to PDGF signaling in rhabdomyosarcoma models and human sample collections.
188 shock of whole zebrafish embryos, including rhabdomyosarcoma, myeloproliferative disorder, intestina
189 ted satellite cells gave rise to pleomorphic rhabdomyosarcomas (MyoD-, Myogenin- and Desmin-positive)
190 ed in patients with medulloblastoma (n = 4), rhabdomyosarcoma (n = 1), neuroblastoma (n = 1), and ger
191 ant peripheral-nerve sheath tumor (n = 7), 0 rhabdomyosarcoma (n = 2), and three synovial sarcomas (n
192 number of additional malignancies, including rhabdomyosarcoma, neuroblastoma, anaplastic large cell l
193 onal study trials exist for the treatment of rhabdomyosarcoma, only very limited information is given
194 age 21 years with newly diagnosed metastatic rhabdomyosarcoma or undifferentiated sarcoma received wi
195 ne can lead to complete response in multiple rhabdomyosarcoma orthotopic patient-derived xenografts t
196 mphomas, astrocytomas, Ewing's sarcomas, and rhabdomyosarcomas (p<0.0001 in all cases), and osteosarc
198 cation that is the foundation of all present rhabdomyosarcoma protocols developed by the Children's O
200 greatly reduced the growth of two different rhabdomyosarcoma (RD embryonal P = 0.00008; Rh30 alveola
201 g passage of the prototype strain, Nancy, on rhabdomyosarcoma (RD) cells, which express DAF but very
206 ene expression profiles of 101 primary human rhabdomyosarcomas revealed elevated PDGF-C and -D expres
207 cated in drug-sensitive and -resistant human rhabdomyosarcoma Rh30 cells, suggesting that our finding
208 )-stimulated F-actin reorganization in human rhabdomyosarcoma (Rh30), Ewing sarcoma (Rh1), glioblasto
211 uding gastrointestinal stromal tumor (GIST), rhabdomyosarcoma (RMS) and leiomyosarcoma (LMS), feature
212 OR) pathway is often aberrantly activated in rhabdomyosarcoma (RMS) and represents a promising therap
214 nely lost in advanced, poorly differentiated rhabdomyosarcoma (RMS) but characteristically expressed
215 GFBP-6 was found to promote the migration of rhabdomyosarcoma (RMS) cells in an IGF-independent manne
216 ntial element for the growth and survival of rhabdomyosarcoma (RMS) cells using a bar-coded, tetracyc
219 r tumors from diagnostic biopsies of primary rhabdomyosarcoma (RMS) contain relevant prognostic infor
238 ntify novel signaling pathways necessary for rhabdomyosarcoma (RMS) survival, we performed a loss-of-
239 e outcome of patients with intermediate-risk rhabdomyosarcoma (RMS) treated with standard VAC (vincri
240 e poor prognosis of metastatic and recurrent rhabdomyosarcoma (RMS) under the current regimen of poly
245 n aggressive metastatic disease in pediatric rhabdomyosarcoma (RMS), irrespective of histological sub
246 atients with incompletely resected embryonal rhabdomyosarcoma (RMS), undifferentiated sarcoma, and so
247 g for new strategies to trigger apoptosis in rhabdomyosarcoma (RMS), we investigated the effect of tw
248 ession and underlying genetic aberrations in rhabdomyosarcoma (RMS), with special attention to clinic
257 from P2 MCMV-infected mice were pleomorphic rhabdomyosarcomas (RMS) harboring MCMV DNA, RNA, and pro
259 [a non-small-cell lung cancer (NSCLC) and a rhabdomyosarcoma] showed expression of highly phosphoryl
260 , 6.21 cases per 1 million person-years) and rhabdomyosarcoma (standardized incidence ratio, 2.62; 95
262 rom the Children's Oncology Group Intergroup Rhabdomyosarcoma Study (IRS) IV, D9502 and D9803, with 1
263 overall survival rates of 95% on Intergroup Rhabdomyosarcoma Study Group (IRSG) protocols III/IV.
266 oup, Children's Cancer Group, the Intergroup Rhabdomyosarcoma Study Group, and the National Wilms Tum
268 3/FOXO1 and PAX7/FOXO1 positive), Intergroup Rhabdomyosarcoma Study TNM stage, and age showed a signi
270 ediate-risk RMS enrolled onto the Intergroup Rhabdomyosarcoma Study-IV and the Children's Oncology Gr
272 eep miRNA profiling of the three major human rhabdomyosarcoma subtypes, along with cell lines and nor
273 ts of miR-1 and miR-133a are up-regulated in rhabdomyosarcomas, suggesting a causative role for these
274 ue in patients with relapsed Wilms tumor and rhabdomyosarcoma suggests that some patients may benefit
275 ue in patients with relapsed Wilms tumor and rhabdomyosarcoma suggests that some patients may benefit
276 is expressed in a subset of mouse and human rhabdomyosarcomas, suppressed differentiation of myogeni
278 specifically focus on embryonal and alveolar rhabdomyosarcoma, synovial sarcoma, and adult soft tissu
279 al rhabdomyosarcoma and a human cell line of rhabdomyosarcoma that harbored activated mutations in NR
281 region is reported in many tumors, including rhabdomyosarcomas that are primarily pediatric sarcomas
282 rexpression of the nuclear receptor NR4A1 in rhabdomyosarcomas that is sufficient to drive high expre
283 gested as potential targets for treatment of rhabdomyosarcoma, the most common soft tissue sarcoma in
284 se results point to the promise of enhancing rhabdomyosarcoma therapy using miRNAs as agents that med
287 ), a microtubule inhibitor currently used in rhabdomyosarcoma treatment regimens, resulted in a combi
288 showed a large variation in IGF-IR levels in rhabdomyosarcoma tumor specimens that were comparable wi
289 AX3-FKHR translocation to the development of rhabdomyosarcoma tumors has been further elucidated.
291 A KRAS(G12D)-induced zebrafish embryonal rhabdomyosarcoma was then used to assess the therapeutic
292 pping region of amplification at 13q31-32 in rhabdomyosarcomas was defined as containing two genes: G
293 rcoma Study (IRS) IV patients with group III rhabdomyosarcoma, we assessed whether reported response
294 o molecular subtypes of the pediatric cancer rhabdomyosarcoma, we show that an exhaustive iterative s
297 We established a unique model of metastatic rhabdomyosarcoma with a high frequency of tumor occurren
298 inical samples of the skeletal muscle cancer rhabdomyosarcoma, with the highest expression found in t
299 ficantly enhanced sensitivity of a pediatric rhabdomyosarcoma xenograft to radiotherapy and sensitize
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