ライフサイエンスコーパス: tumor gene

1 s, which are specific mutations in the Wilms tumor gene.

2 the product of the lethal(3)malignant brain tumor gene.

3 indicated that these sites may harbor Wilms tumor genes.

4 identify novel activities for existing anti-tumor genes.

5 ty, and immunogenicity of a polyvalent Wilms tumor gene 1 (WT1) peptide vaccine in patients with acut

6 WT2725 is a Wilms' tumor gene 1 (WT1)-derived-oligopeptide vaccine designed

7 presses the transcriptional regulator Wilm's Tumor Gene 1 (Wt1).

8 emonstrate increased expression of the Wilms tumor gene 1 product (WT1), making WT1 an attractive the

9 ty of administering TAA-Ts that target Wilms tumor gene 1, preferentially expressed antigen of melano

10 Wilms tumor, and its product enhances Wilms tumor gene 1-mediated transcription.

11 glomeruli showed reduced expression of Wilm tumor gene-1 (WT1), WT1-driven podocyte genes, and incre

12 Tumor gene analysis was used in 21 of 64 patients (33%),

13 e that PPP2R1A is not the 19q familial Wilms tumor gene and that mutation of PPP2R1A is not a common

14 wn to be overexpressed in AML such as Wilms' tumor gene, and multiparameter flow cytometry to detect

15 The OrCGDB is part of a larger WWW-based tumor gene database and represents a new approach to cat

16 structured digital publication software; the Tumor Gene Database, containing information about genes

17 to assess potential synergy of combined anti-tumor gene delivery and to identify novel activities for

18 One type of gene therapy of tumors, gene-directed enzyme-prodrug therapy (GDEPT), ho

19 iated with elevated expression of the Wilm's tumor gene encoded transcription factor (WT1).

20 Bulk tumor gene expression analysis and single-cell RNA seque

21 Comparative tumor gene expression analysis revealed that several hum

22 apeutic bacteria, tracked the progression of tumor gene expression and growth in a mouse model of bre

23 ramework to understand the vast diversity of tumor gene expression and mutations.

24 ermine the relationship between quantitative tumor gene expression and risk of cancer recurrence in p

25 rofiling data to understand how TFs regulate tumor gene expression are still limited.

26 ous risk of recurrence scores (CRS) based on tumor gene expression are vital prognostic tools for bre

27 We reported volumetric imaging of tumor gene expression at the cubic centimeter scale usin

28 changes) alter tumor biology as assessed by tumor gene expression changes, with a common mechanism p

29 approach based upon statistical analysis of tumor gene expression data combined with experimental va

30 Using patients' tumor gene expression data from 4 independent data sets,

31 ncer cell lines and applying these models to tumor gene expression data in the clinical data sets (e.

32 Deconvolution of primary tumor gene expression data revealed a strong association

33 Finally, we compared the murine lung tumor gene expression data to the expression of genes in

34 Integration of breast tumor gene expression data with the genes in the tumor s

35 e of absolute cell fraction predictions from tumor gene expression data, and provides a unique novel

36 lung cancer in a collection of 4,801 breast tumor gene expression data.

37 on of cancer and immune cell types from bulk tumor gene expression data.

38 This work demonstrates that tumor gene expression databases can be used to study the

39 Based on human tumor gene expression databases, HMGB1 was significantly

40 On a central nervous system embryonic tumor gene expression dataset of size 712,940, our algor

41 Analysis of breast tumor gene expression datasets revealed an inverse assoc

42 To reduce noise in the tumor gene expression datasets, FARDEEP utilizes an adap

43 rrying out a meta-analysis of primary breast tumor gene expression from 1,378 early-stage breast canc

44 Primary tumor gene expression is a good predictor of cancer drug

45 Our predicted TF impact on tumor gene expression is highly consistent with the know

46 Tumor gene expression is predictive of patient prognosis

47 In this study, tumor gene expression microarray profiles from pediatric

48 We compared the tumor gene expression of PCA3 and PRUNE2 to their corres

49 cing experiments than could be obtained from tumor gene expression or genomic data alone.

50 tability leading to mammary tumors that have tumor gene expression profiles closely resembling mature

51 be coexpressed with VEGFR-2 from a clinical tumor gene expression profiling database and between tum

52 Tumor gene expression profiling-targeted next-generation

53 However, this bias does not affect tumor gene expression profiling.

54 Accordingly, tumor gene expression signatures specific for myeloid ce

55 cluster of differentiation (CD)138-selected tumor gene expression to control for tumor burden, we id

56 ides an exciting new technology for relating tumor gene expression to patient outcome, but it also pr

57 possibility of pharmacologically modulating tumor gene expression to result in targeted radiotherapy

58 r predicts subtype and patient survival than tumor gene expression, and genes with coordinated expres

59 ial abundances, alone or in combination with tumor gene expression, can predict cancer prognosis and

60 l loci methylation inversely correlated with tumor gene expression, most notably KCNH2 (HERG, a potas

61 Entropy has been associated with tumor gene expression, tumor metabolism, tumor stage, pa

62 accounted for 1.2% of the total variation of tumor gene expression, while somatic copy-number alterat

63 and compared this to patient medulloblastoma tumor gene expression.

64 t attributes, cell expansion, cytokines, and tumor gene expression.

65 Among RET-CCDC6-driven tumors, gene expression in pediatric tumors was distingu

66 o integrated RNA-Seq data in various primary tumors, gene expression microarray data in over 1000 can

67 rgent BCR evolution also exhibited divergent tumor gene-expression and cell-surface protein profiles.

68 entiated tumors based upon unique immune and tumor gene-expression patterns.

69 n of PCPG and normal adrenal tissues, refine tumor gene-expression subtypes and make clinical and gen

70 find that trade-offs between tasks constrain tumor gene-expression to a continuum bounded by a polyhe

71 d constitutional epigenetic defects in Wilms tumor genes extend the understanding of Wilms tumor risk

72 cer-related, with 95 colon tumor and 67 lung tumor genes identified, respectively.

73 Finally, direct targeting of tumor genes in cancer cells with CRISPR/Cas9 may be achi

74 ighly similar between responding ILC and IDC tumors; genes involved in proliferation were downregulat

75 The ovarian tumor gene is required during both early and late stages

76 ered and one of the most prevalently mutated tumor genes is Ras.

77 With the decreasing cost of tumor gene mutation testing and the increasing number of

78 Wilms tumor gene on the X chromosome (WTX) is a putative tumor

79 The Drosophila ovarian tumor gene (otu) encodes cytoplasmic proteins that are r

80 the negative regulatory domain of the Wilms' tumor gene product (WT1) in a yeast two-hybrid screen an

81 In this study, we report that the Wilms' tumor gene product WT1, a zinc finger transcription fact

82 the adenovirus E1B-19K protein and the Wilms tumor gene product WT1.

83 Oncotype DX (ODX) is a tumor gene-profiling test that aids in adjuvant chemothe

84 and tumor cells and reduced expression of a tumor gene signature associated with worse patient survi

85 Additionally, we identified primary tumor gene signatures that were associated with increase

86 operties of siRNA-L2 facilitated significant tumor gene silencing for 7 d after two i.v. doses.

87 turbation transformations between normal and tumor gene states, enhancing biomarker identification.

88 krz(1) is a type 1 melanotic tumor gene; the fat body is the primary site of melanoti

89 ese findings have important implications for tumor gene therapy and for understanding the mechanism o

90 Clinical applications of tumor gene therapy require tumor-specific delivery or ex

91 , the vector being used in the ongoing brain tumor gene therapy trial.

92 nical applications in humans, especially for tumor gene therapy.

93 application for hematopoietic stem cell and tumor gene therapy.

94 tic interactions between cut and the ovarian tumor gene were identified as a result of the screen.

95 d genes, dominated the list of downregulated tumor genes, while genes that regulate cell-intrinsic ma

96 elopment requires the functions of the Wilms tumor gene WT1 and the WNT/beta-catenin signaling pathwa

97 The Wilms tumor gene WT1 encodes a zinc finger transcription facto

98 The tissue-specific Wilms' tumor gene WT1 is expressed in a range of acute leukemia

99 view recent findings showing that the Wilms' tumor gene (Wt1) is a key regulator of mesenchyme mainte

100 The Wilms' tumor gene (WT1) is an essential gene for kidney and gon

101 ostate cancer epithelial cells was the Wilms tumor gene (WT1).

102 The Wilms' tumor gene, WT1, encodes a zinc finger transcription fac

103 ed targets and regulators of the first Wilms tumor gene, WT1, has uncovered several candidate genes a

104 The product of the Wilms' tumor gene, WT1, is essential for male sex determination

105 One Wilms tumor gene, WT1, which encodes a zinc finger transcripti