ライフサイエンスコーパス: rhabdoid

1 wn tumor suppressor gene (TSG) for malignant rhabdoid and childhood central nervous system tumors.

2 ted in decreased colony-forming potential in rhabdoid and NSCLC tumor cells, thereby demonstrating fu

3 Rhabdoid brain tumours, also called atypical teratoid rh

4 f the complex has been found mutated in both rhabdoid cell lines and in primary rhabdoid tumors.

5 lines, the BAF47 protein was missing in all rhabdoid cell lines and one RMS cell line.

6 Using rhabdoid cell lines overexpressing WT1, we show that WT1

7 yclin D1, induced G1 arrest and apoptosis in rhabdoid cell lines.

8 chorage-dependent and -independent growth of rhabdoid cells and caused synergistic induction of cell

9 at INI1 represses Cyclin D1 transcription in rhabdoid cells by directly recruiting histone deacetylas

10 found that RNA interference of cyclin D1 in rhabdoid cells was sufficient to induce G1 arrest and ap

11 e tumors developed in these Ini1+/- mice are rhabdoid, defective for Ini1 protein, and like the human

12 and PBRM1 in a few RCCs was associated with rhabdoid features (q = 0.0007).

13 h poorly differentiated tumors with variable rhabdoid features.

14 euroectodermal tumors, and atypical teratoid/rhabdoid-like tumors from postnatal mouse neural stem/pr

15 ucleus, the rostromedial tegmental area, the rhabdoid nucleus, the mesencephalic raphe nuclei, and th

16 Overexpression of HOTS inhibits Wilms, rhabdoid, rhabdomyosarcoma, and choriocarcinoma tumor ce

17 Atypical teratoid/rhabdoid tumor (AT/RT) of the CNS is an extremely rare a

18 mors (sPNET) correspond to atypical teratoid/rhabdoid tumor (AT/RT), a rare childhood tumor.

19 t rhabdoid tumors, such as atypical teratoid/rhabdoid tumor (AT/RT).

20 Atypical teratoid/rhabdoid tumor (ATRT) is one of the most common brain tu

21 Atypical teratoid rhabdoid tumor (ATRT) of the CNS is a highly malignant n

22 Malignant rhabdoid tumor (MRT) is an aggressive, highly lethal can

23 F5 function is usually observed in malignant rhabdoid tumor (MRT), a highly aggressive pediatric neop

24 astoma multiforme (n = 2), atypical teratoid/rhabdoid tumor (n = 1), malignant glioma (n = 1), and ch

25 n = 5), germinoma (n = 3), atypical teratoid rhabdoid tumor (n = 2), choroid plexus carcinoma (n = 2)

26 selected rare tumors (ie, atypical teratoid/rhabdoid tumor and CNS primitive neuroectodermal tumor).

27 blastoma, glioblastoma and atypical teratoid rhabdoid tumor cell lines.

28 mediate PGBD5-induced DNA rearrangements in rhabdoid tumor cells.

29 study is to determine prognostic factors in rhabdoid tumor of the kidney (RTK), including both demog

30 The G401 cell line derived from a rhabdoid tumor of the kidney secretes the heparin-bindin

31 predispose to two distinct tumor syndromes: rhabdoid tumor predisposition syndrome, with malignant p

32 abdoid tumors for mutations in the candidate rhabdoid tumor suppressor gene, INI1.

33 on in 22q11, was identified as the candidate rhabdoid tumor suppressor gene.

34 e retained super-enhancers are essential for rhabdoid tumor survival, including some that are shared

35 inoma, medulloblastoma and atypical teratoid rhabdoid tumor) respond to JQ1 even when harboring genet

36 driving roles first identified in malignant rhabdoid tumor, an aggressive pediatric cancer character

37 umor suppressor gene hSNF5/INI1 in malignant rhabdoid tumor, and the association of c-kit mutations w

38 e Beckwith-Wiedemann syndrome patients and a rhabdoid tumor.

39 e derepression of this gene is essential for rhabdoid tumorigenesis.

40 these tumors are known as atypical teratoid/rhabdoid tumors (AT/RT).

41 ve pediatric atypical teratoid and malignant rhabdoid tumors (AT/RT).

42 lecular intertumor heterogeneity in teratoid/rhabdoid tumors (ATRTs) and extra-cranial MRTs (ecMRTs)

43 ecular inter-tumor heterogeneity in teratoid/rhabdoid tumors (ATRTs) and extra-cranial MRTs (ecMRTs)

44 We recently reported that atypical teratoid rhabdoid tumors (ATRTs) comprise at least two transcript

45 Malignant rhabdoid tumors (MRT) are rare aggressive cancers that o

46 emodeling complex, is lost in most malignant rhabdoid tumors (MRT).

47 and a tumor suppressor mutated in malignant rhabdoid tumors (MRT).

48 Malignant rhabdoid tumors (MRTs) are rare lethal tumors of childho

49 mutations that result primarily in malignant rhabdoid tumors (MRTs) in humans and MRTs as well as oth

50 s extremely prevalent in pediatric malignant rhabdoid tumors (MRTs) or atypical teratoid rhabdoid tum

51 F5), which is inactivated in human malignant rhabdoid tumors (MRTs), interacts with GLI1.

52 y and minimum tumor ADC in atypical teratoid rhabdoid tumors (rho = -0.786, P < .05).

53 Rhabdoid tumors (RT) are aggressive pediatric malignanci

54 Rhabdoid tumors (RTs) are aggressive and currently incur

55 Rhabdoid tumors (RTs) are rare, highly aggressive pediat

56 SMARCB1 mutations predispose to rhabdoid tumors and schwannomas but the mechanisms under

57 an SWI/SNF complexes occur in most malignant rhabdoid tumors and some other malignancies.

58 n about the biology and clinical behavior of rhabdoid tumors and to begin to develop treatment strate

59 Rhabdoid tumors are aggressive pediatric malignancies fo

60 Rhabdoid tumors arise because of the loss of the tumor s

61 Malignant rhabdoid tumors arise in several anatomic locations and

62 sociated with the poor prognosis seen in all rhabdoid tumors but only some RMS.

63 distinguishable mutational landscapes, human rhabdoid tumors exhibit distinct enhancer H3K27ac signat

64 genetically engineered models for malignant rhabdoid tumors exist, none of them recapitulate AT/RT,

65 rs of the brain and 7 renal and 4 extrarenal rhabdoid tumors for mutations in the candidate rhabdoid

66 the requirement of Cyclin D1 for genesis of rhabdoid tumors in vivo, we developed Ini1 heterozygous

67 gh a mechanism that is distinct from that of rhabdoid tumors in which SMARCB1 protein is completely a

68 y INI1 and Cyclin D1 overexpression in human rhabdoid tumors is a common phenomenon.

69 ogeneity observed in patients with malignant rhabdoid tumors is unknown.

70 clear chromatin-remodeling factor SMARCB1 in rhabdoid tumors led to increased phosphorylation of eIF2

71 We examined 18 atypical teratoid and rhabdoid tumors of the brain and 7 renal and 4 extrarena

72 ygously or homozygously deleted in pediatric rhabdoid tumors of the brain, kidney and soft tissues.

73 INI1 is a tumor suppressor gene involved in rhabdoid tumors of the brain, kidney, and other extraren

74 A workshop on childhood atypical teratoid/rhabdoid tumors of the central nervous system, sponsored

75 enografts of WiT49 cells resembled malignant rhabdoid tumors rather than Wilms tumors.

76 ich SMARCB1 germline mutations predispose to rhabdoid tumors versus schwannomas are still unknown.

77 dels and show that early Smarcb1 loss causes rhabdoid tumors whereas loss at later stages combined wi

78 or stem cell transplant in the treatment of rhabdoid tumors will be published separately.

79 A series of primary rhabdoid tumors with chromosome 22q11 deletions were scr

80 (e.g., lung, synovial sarcoma, leukemia, and rhabdoid tumors).

81 itive neuroectodermal tumor, ependymoma, and rhabdoid tumors, 5-year EFS rates were 32% +/- 5%, 17% +

82 g mutations of the SMARCB1 gene in malignant rhabdoid tumors, a highly aggressive childhood cancer.

83 epatoblastomas, 7 of 8 Wilms' tumors, 3 of 3 rhabdoid tumors, and 12 of 27 adenocarcinomas also teste

84 Here we sequenced the exomes of 35 rhabdoid tumors, highly aggressive cancers of early chil

85 identified in children with brain and renal rhabdoid tumors, indicating that INI1 is a tumor suppres

86 tumor (WT) share a similar genetic link with rhabdoid tumors, it was hypothesized that they may also

87 In atypical teratoid rhabdoid tumors, no correlation was found between cellul

88 ially involved in the formation of malignant rhabdoid tumors, such as atypical teratoid/rhabdoid tumo

89 cal features and molecular profiles of human rhabdoid tumors.

90 d in both rhabdoid cell lines and in primary rhabdoid tumors.

91 ir absence contributes to the progression of rhabdoid tumors.

92 ly undefined genomic rearrangements in human rhabdoid tumors.

93 plex, is inactivated in nearly all pediatric rhabdoid tumors.

94 1 hepatocellular carcinoma, and 2 malignant rhabdoid tumors.

95 of childhood solid tumors, including lethal rhabdoid tumors.

96 uppressor in familial and sporadic malignant rhabdoid tumors.

97 WHO grade III), and seven atypical teratoid rhabdoid tumors.

98 rhabdoid tumors (MRTs) or atypical teratoid rhabdoid tumors.

99 nt a therapeutic target in atypical teratoid/rhabdoid tumors.

100 ly effective as novel therapeutic agents for rhabdoid tumors.

101 yclin D1 is a key mediator in the genesis of rhabdoid tumors.

102 osely resemble those of human Snf5-deficient rhabdoid tumors.

103 ed sarcoma (US), osteosarcoma, and malignant rhabdoid tumors.

104 per-enhancers, such as SOX2 in brain-derived rhabdoid tumors.

105 toid tumor of the brain and three with renal rhabdoid tumors.

106 al analyses identified two atypical teratoid rhabdoid tumour subgroups with differential enrichment o

107 sarcoma, (congenital) mesoblastic nephroma, rhabdoid tumour, and renal medullary carcinoma form a he

108 sarcoma, (congenital) mesoblastic nephroma, rhabdoid tumour, and renal medullary carcinoma.

109 ed chromosomal translocation in an embryonal rhabdoid tumour.

110 ctodermal tumours (PNETs), atypical teratoid/rhabdoid tumours (AT/RTs) and malignant gliomas.

111 Extracranial rhabdoid tumours are rare, and often occur in infants.

112 We obtained 259 rhabdoid tumours from 37 international institutions and

113 Despite multimodal therapy, outcome in rhabdoid tumours remains poor with only 31% of patients

114 a cohort of patients with atypical teratoid rhabdoid tumours to find out the molecular basis for cli

115 brain tumours, also called atypical teratoid rhabdoid tumours, are lethal childhood cancers with char

116 ification of patients with atypical teratoid rhabdoid tumours.

117 ver molecular subgroups of atypical teratoid rhabdoid tumours.