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1 (e.g., lung, synovial sarcoma, leukemia, and rhabdoid tumors).
2 e Beckwith-Wiedemann syndrome patients and a rhabdoid tumor.
3 image-guided metabolic radiosensitization of rhabdoid tumors.
4 luding medulloblastoma and atypical teratoid/rhabdoid tumors.
5  of childhood solid tumors, including lethal rhabdoid tumors.
6 per-enhancers, such as SOX2 in brain-derived rhabdoid tumors.
7 cal features and molecular profiles of human rhabdoid tumors.
8 ly undefined genomic rearrangements in human rhabdoid tumors.
9 plex, is inactivated in nearly all pediatric rhabdoid tumors.
10  1 hepatocellular carcinoma, and 2 malignant rhabdoid tumors.
11 uppressor in familial and sporadic malignant rhabdoid tumors.
12  WHO grade III), and seven atypical teratoid rhabdoid tumors.
13  rhabdoid tumors (MRTs) or atypical teratoid rhabdoid tumors.
14 nt a therapeutic target in atypical teratoid/rhabdoid tumors.
15 ly effective as novel therapeutic agents for rhabdoid tumors.
16 yclin D1 is a key mediator in the genesis of rhabdoid tumors.
17 osely resemble those of human Snf5-deficient rhabdoid tumors.
18 ed sarcoma (US), osteosarcoma, and malignant rhabdoid tumors.
19 toid tumor of the brain and three with renal rhabdoid tumors.
20 d in both rhabdoid cell lines and in primary rhabdoid tumors.
21 ir absence contributes to the progression of rhabdoid tumors.
22 ma (AAIR 0.14 cases/1 million) and malignant rhabdoid tumors (0.06 cases/1 million) were most common.
23 raniopharyngioma (16), and atypical teratoid rhabdoid tumor (12).
24 itive neuroectodermal tumor, ependymoma, and rhabdoid tumors, 5-year EFS rates were 32% +/- 5%, 17% +
25 g mutations of the SMARCB1 gene in malignant rhabdoid tumors, a highly aggressive childhood cancer.
26  driving roles first identified in malignant rhabdoid tumor, an aggressive pediatric cancer character
27  selected rare tumors (ie, atypical teratoid/rhabdoid tumor and CNS primitive neuroectodermal tumor).
28 ency (D(max)) > 90% against BRD9 in the G401 rhabdoid tumor and HS-SY-II synovial sarcoma cell lines
29              SMARCB1 mutations predispose to rhabdoid tumors and schwannomas but the mechanisms under
30 an SWI/SNF complexes occur in most malignant rhabdoid tumors and some other malignancies.
31 n about the biology and clinical behavior of rhabdoid tumors and to begin to develop treatment strate
32 ation for the treatment of synovial sarcoma, rhabdoid tumor, and other BRD9-dependent human diseases.
33 umor suppressor gene hSNF5/INI1 in malignant rhabdoid tumor, and the association of c-kit mutations w
34 epatoblastomas, 7 of 8 Wilms' tumors, 3 of 3 rhabdoid tumors, and 12 of 27 adenocarcinomas also teste
35                                              Rhabdoid tumors are aggressive pediatric malignancies fo
36                                              Rhabdoid tumors arise because of the loss of the tumor s
37                                    Malignant rhabdoid tumors arise in several anatomic locations and
38                            Atypical Teratoid Rhabdoid Tumor (AT/RT) is a rare pediatric central nervo
39                            Atypical teratoid/rhabdoid tumor (AT/RT) is an aggressive, early-childhood
40                            Atypical teratoid/rhabdoid tumor (AT/RT) of the CNS is an extremely rare a
41 mors (sPNET) correspond to atypical teratoid/rhabdoid tumor (AT/RT), a rare childhood tumor.
42 t rhabdoid tumors, such as atypical teratoid/rhabdoid tumor (AT/RT).
43  these tumors are known as atypical teratoid/rhabdoid tumors (AT/RT).
44 ve pediatric atypical teratoid and malignant rhabdoid tumors (AT/RT).
45 mutations can give rise to atypical teratoid/rhabdoid tumors (AT/RTs) in the pediatric central nervou
46                            Atypical teratoid rhabdoid tumor (ATRT) is an aggressive embryonal brain t
47                            Atypical teratoid/rhabdoid tumor (ATRT) is one of the most common brain tu
48                            Atypical teratoid rhabdoid tumor (ATRT) of the CNS is a highly malignant n
49                            Atypical teratoid rhabdoid tumors (ATRT) are incurable high-grade pediatri
50 mark genetic aberration of atypical teratoid rhabdoid tumors (ATRT).
51 lecular intertumor heterogeneity in teratoid/rhabdoid tumors (ATRTs) and extra-cranial MRTs (ecMRTs)
52 ecular inter-tumor heterogeneity in teratoid/rhabdoid tumors (ATRTs) and extra-cranial MRTs (ecMRTs)
53                            Atypical teratoid rhabdoid tumors (ATRTs) are challenging pediatric brain
54  We recently reported that atypical teratoid rhabdoid tumors (ATRTs) comprise at least two transcript
55                            Atypical teratoid/rhabdoid tumors (ATRTs) typically arise in the central n
56 enic dependency on EZH2 in atypical teratoid rhabdoid tumors (ATRTs), but the underlying mechanism ha
57  complexes in synovial sarcoma and malignant rhabdoid tumors, both of which possess aberrations in ca
58 sociated with the poor prognosis seen in all rhabdoid tumors but only some RMS.
59 blastoma, glioblastoma and atypical teratoid rhabdoid tumor cell lines.
60 he tumor suppressor gene CDKN2A in malignant rhabdoid tumor cells reactivates the gene and induces se
61 e performed CRISPR screens in SMARCB1-mutant rhabdoid tumor cells to identify genetic contributors to
62 first revealed by cell viability assays that rhabdoid tumor cells' sensitivity to homoharringtonine w
63 ed SMARCB1 potential roles in translation in rhabdoid tumor cells.
64  mediate PGBD5-induced DNA rearrangements in rhabdoid tumor cells.
65                                              Rhabdoid tumors, characterized and driven by the loss of
66 distinguishable mutational landscapes, human rhabdoid tumors exhibit distinct enhancer H3K27ac signat
67  genetically engineered models for malignant rhabdoid tumors exist, none of them recapitulate AT/RT,
68 rs of the brain and 7 renal and 4 extrarenal rhabdoid tumors for mutations in the candidate rhabdoid
69 is study reveals that the loss of SMARCB1 in rhabdoid tumors has specific consequences on mRNAs trans
70           Here we sequenced the exomes of 35 rhabdoid tumors, highly aggressive cancers of early chil
71  the requirement of Cyclin D1 for genesis of rhabdoid tumors in vivo, we developed Ini1 heterozygous
72 gh a mechanism that is distinct from that of rhabdoid tumors in which SMARCB1 protein is completely a
73  identified in children with brain and renal rhabdoid tumors, indicating that INI1 is a tumor suppres
74 y INI1 and Cyclin D1 overexpression in human rhabdoid tumors is a common phenomenon.
75 ogeneity observed in patients with malignant rhabdoid tumors is unknown.
76 tumor (WT) share a similar genetic link with rhabdoid tumors, it was hypothesized that they may also
77 clear chromatin-remodeling factor SMARCB1 in rhabdoid tumors led to increased phosphorylation of eIF2
78  lineage, while group 2a/b atypical teratoid/rhabdoid tumors may originate outside the neuroectoderm.
79                                    Malignant rhabdoid tumor (MRT) is an aggressive, highly lethal can
80 F5 function is usually observed in malignant rhabdoid tumor (MRT), a highly aggressive pediatric neop
81     We find that Ewing sarcoma and malignant rhabdoid tumor (MRT), two pediatric cancers that are sen
82                                    Malignant rhabdoid tumors (MRT) are highly aggressive pediatric ca
83                                    Malignant rhabdoid tumors (MRT) are rare aggressive cancers that o
84                                    Malignant rhabdoid tumors (MRT) are rare but deadly pediatric tumo
85 emodeling complex, is lost in most malignant rhabdoid tumors (MRT).
86  and a tumor suppressor mutated in malignant rhabdoid tumors (MRT).
87                                    Malignant rhabdoid tumors (MRTs) are rare lethal tumors of childho
88 mutations that result primarily in malignant rhabdoid tumors (MRTs) in humans and MRTs as well as oth
89 s extremely prevalent in pediatric malignant rhabdoid tumors (MRTs) or atypical teratoid rhabdoid tum
90 d embryonic mosaic mouse models of malignant rhabdoid tumors (MRTs) that faithfully recapitulate the
91 F5), which is inactivated in human malignant rhabdoid tumors (MRTs), interacts with GLI1.
92 se clinical outcomes for pediatric malignant rhabdoid tumors (MRTs).
93 astoma multiforme (n = 2), atypical teratoid/rhabdoid tumor (n = 1), malignant glioma (n = 1), and ch
94 n = 5), germinoma (n = 3), atypical teratoid rhabdoid tumor (n = 2), choroid plexus carcinoma (n = 2)
95 ts of medulloblastomas (n = 2325), malignant rhabdoid tumors (n = 229) and pediatric high-grade gliom
96                         In atypical teratoid rhabdoid tumors, no correlation was found between cellul
97  study is to determine prognostic factors in rhabdoid tumor of the kidney (RTK), including both demog
98            The G401 cell line derived from a rhabdoid tumor of the kidney secretes the heparin-bindin
99         We examined 18 atypical teratoid and rhabdoid tumors of the brain and 7 renal and 4 extrarena
100 ygously or homozygously deleted in pediatric rhabdoid tumors of the brain, kidney and soft tissues.
101  INI1 is a tumor suppressor gene involved in rhabdoid tumors of the brain, kidney, and other extraren
102    A workshop on childhood atypical teratoid/rhabdoid tumors of the central nervous system, sponsored
103  predispose to two distinct tumor syndromes: rhabdoid tumor predisposition syndrome, with malignant p
104 enografts of WiT49 cells resembled malignant rhabdoid tumors rather than Wilms tumors.
105 inoma, medulloblastoma and atypical teratoid rhabdoid tumor) respond to JQ1 even when harboring genet
106 y and minimum tumor ADC in atypical teratoid rhabdoid tumors (rho = -0.786, P < .05).
107 F mutations drive cancer, we contributed ten rhabdoid tumor (RT) cell lines mutant for SWI/SNF subuni
108                                              Rhabdoid tumors (RT) are aggressive pediatric malignanci
109                                              Rhabdoid tumors (RTs) are aggressive and currently incur
110                                              Rhabdoid tumors (RTs) are rare, highly aggressive pediat
111 pecific vulnerability in pediatric malignant rhabdoid tumors (RTs), which are driven by inactivation
112 ially involved in the formation of malignant rhabdoid tumors, such as atypical teratoid/rhabdoid tumo
113 abdoid tumors for mutations in the candidate rhabdoid tumor suppressor gene, INI1.
114 on in 22q11, was identified as the candidate rhabdoid tumor suppressor gene.
115 e retained super-enhancers are essential for rhabdoid tumor survival, including some that are shared
116 ich SMARCB1 germline mutations predispose to rhabdoid tumors versus schwannomas are still unknown.
117 dels and show that early Smarcb1 loss causes rhabdoid tumors whereas loss at later stages combined wi
118  or stem cell transplant in the treatment of rhabdoid tumors will be published separately.
119                          A series of primary rhabdoid tumors with chromosome 22q11 deletions were scr

 
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