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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 cal features and molecular profiles of human rhabdoid tumors.
4 ly undefined genomic rearrangements in human rhabdoid tumors.
5 plex, is inactivated in nearly all pediatric rhabdoid tumors.
6 1 hepatocellular carcinoma, and 2 malignant rhabdoid tumors.
7 uppressor in familial and sporadic malignant rhabdoid tumors.
8 of childhood solid tumors, including lethal rhabdoid tumors.
9 WHO grade III), and seven atypical teratoid rhabdoid tumors.
10 rhabdoid tumors (MRTs) or atypical teratoid rhabdoid tumors.
11 nt a therapeutic target in atypical teratoid/rhabdoid tumors.
12 ly effective as novel therapeutic agents for rhabdoid tumors.
13 yclin D1 is a key mediator in the genesis of rhabdoid tumors.
14 osely resemble those of human Snf5-deficient rhabdoid tumors.
15 ed sarcoma (US), osteosarcoma, and malignant rhabdoid tumors.
16 toid tumor of the brain and three with renal rhabdoid tumors.
17 d in both rhabdoid cell lines and in primary rhabdoid tumors.
18 ir absence contributes to the progression of rhabdoid tumors.
19 per-enhancers, such as SOX2 in brain-derived rhabdoid tumors.
20 itive neuroectodermal tumor, ependymoma, and rhabdoid tumors, 5-year EFS rates were 32% +/- 5%, 17% +
21 g mutations of the SMARCB1 gene in malignant rhabdoid tumors, a highly aggressive childhood cancer.
22 driving roles first identified in malignant rhabdoid tumor, an aggressive pediatric cancer character
23 selected rare tumors (ie, atypical teratoid/rhabdoid tumor and CNS primitive neuroectodermal tumor).
26 n about the biology and clinical behavior of rhabdoid tumors and to begin to develop treatment strate
27 umor suppressor gene hSNF5/INI1 in malignant rhabdoid tumor, and the association of c-kit mutations w
28 epatoblastomas, 7 of 8 Wilms' tumors, 3 of 3 rhabdoid tumors, and 12 of 27 adenocarcinomas also teste
39 lecular intertumor heterogeneity in teratoid/rhabdoid tumors (ATRTs) and extra-cranial MRTs (ecMRTs)
40 ecular inter-tumor heterogeneity in teratoid/rhabdoid tumors (ATRTs) and extra-cranial MRTs (ecMRTs)
41 We recently reported that atypical teratoid rhabdoid tumors (ATRTs) comprise at least two transcript
45 distinguishable mutational landscapes, human rhabdoid tumors exhibit distinct enhancer H3K27ac signat
46 genetically engineered models for malignant rhabdoid tumors exist, none of them recapitulate AT/RT,
47 rs of the brain and 7 renal and 4 extrarenal rhabdoid tumors for mutations in the candidate rhabdoid
49 the requirement of Cyclin D1 for genesis of rhabdoid tumors in vivo, we developed Ini1 heterozygous
50 gh a mechanism that is distinct from that of rhabdoid tumors in which SMARCB1 protein is completely a
51 identified in children with brain and renal rhabdoid tumors, indicating that INI1 is a tumor suppres
54 tumor (WT) share a similar genetic link with rhabdoid tumors, it was hypothesized that they may also
55 clear chromatin-remodeling factor SMARCB1 in rhabdoid tumors led to increased phosphorylation of eIF2
57 F5 function is usually observed in malignant rhabdoid tumor (MRT), a highly aggressive pediatric neop
62 mutations that result primarily in malignant rhabdoid tumors (MRTs) in humans and MRTs as well as oth
63 s extremely prevalent in pediatric malignant rhabdoid tumors (MRTs) or atypical teratoid rhabdoid tum
65 astoma multiforme (n = 2), atypical teratoid/rhabdoid tumor (n = 1), malignant glioma (n = 1), and ch
66 n = 5), germinoma (n = 3), atypical teratoid rhabdoid tumor (n = 2), choroid plexus carcinoma (n = 2)
68 study is to determine prognostic factors in rhabdoid tumor of the kidney (RTK), including both demog
71 ygously or homozygously deleted in pediatric rhabdoid tumors of the brain, kidney and soft tissues.
72 INI1 is a tumor suppressor gene involved in rhabdoid tumors of the brain, kidney, and other extraren
73 A workshop on childhood atypical teratoid/rhabdoid tumors of the central nervous system, sponsored
74 predispose to two distinct tumor syndromes: rhabdoid tumor predisposition syndrome, with malignant p
76 inoma, medulloblastoma and atypical teratoid rhabdoid tumor) respond to JQ1 even when harboring genet
81 ially involved in the formation of malignant rhabdoid tumors, such as atypical teratoid/rhabdoid tumo
84 e retained super-enhancers are essential for rhabdoid tumor survival, including some that are shared
85 ich SMARCB1 germline mutations predispose to rhabdoid tumors versus schwannomas are still unknown.
86 dels and show that early Smarcb1 loss causes rhabdoid tumors whereas loss at later stages combined wi
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