ライフサイエンスコーパス: kidney tumor

1 WT) is a genetically heterogeneous childhood kidney tumor.

2 ely on the expression profile in the primary kidney tumor.

3 for metastatic pancreatic neuroendocrine and kidney tumors.

4 ssic indications of hereditary and bilateral kidney tumors.

5 grams dictate major phenotypic attributes of kidney tumors.

6 egulators in a large cohort of primary human kidney tumors.

7 mediates POX/PRODH down-regulation in human kidney tumors.

8 served in both TFEB- and TFE3-mediated human kidney tumors.

9 ll WT samples analyzed, in contrast to other kidney tumors.

10 ls may be a useful adjunct to RF ablation of kidney tumors.

11 istochemical analysis on 40 cases of primary kidney tumors.

12 with betaE2 developed target organ specific kidney tumors.

13 s observed in two murine models of pediatric kidney tumors.

14 sion is altered in several breast, lung, and kidney tumors.

15 rimary breast tumors, pancreatic tumors, and kidney tumors.

16 tomatous disease marked by mitochondria-rich kidney tumors.

17 nth decade of life; she has no pancreatic or kidney tumors.

18 Kidney tumors account for about 3% of tumors in adults.

19 an essential surgical approach to the small kidney tumor and provides equivalent local tumor control

20 prone to lung adenocarcinoma, lymphoma, and kidney tumor and that PCBP4-deficient mouse embryo fibro

21 oncogene ABL1 is upregulated in FH-deficient kidney tumors and drives a metabolic and survival signal

22 s characterized by hair follicle hamartomas, kidney tumors and spontaneous pneumothorax.

23 d clinically for treating advanced liver and kidney tumors, and also has shown efficacy against other

24 ent ELT3 cells, mutant Tsc2-associated mouse kidney tumors, and human lung lymphangioleiomyomatosis n

25 Subcellular fractionation of the liver, kidneys, tumor, and pancreas showed that the majority of

26 rm oncologic outcomes after cryoablation for kidney tumors are satisfactory.

27 e laparoscopic approach in the management of kidney tumors are unequivocal and the role of laparoscop

28 emely reduced or undetectable in DES-induced kidney tumors as compared to its age-matched control kid

29 ic alteration that was common in DES-induced kidney tumors as well as in its surrounding non-tumor ti

30 eptibility disease characterized by skin and kidney tumors, as well as cystic lung disease, which res

31 n differentiating benign and malignant solid kidney tumors based on the initial stage of the study.

32 for the del3 allele have a markedly reduced kidney tumor burden in comparison with conventional Tsc2

33 been postulated to mediate the induction of kidney tumors by estradiol in male Syrian hamsters.

34 ne that becomes biallelically inactivated in kidney tumors by second-hit mutations.

35 on of wild-type Rpb1 stimulated formation of kidney tumors by VHL(+) cells, and this effect was aboli

36 of five groups: (a) subcutaneous tumors, (b) kidney tumors, (c) lung tumors with blood flow, and (d)

37 m both baby hamster kidney cells and a human kidney tumor cell line, suggesting that Tax enters the s

38 Introducing wild-type pVHL into human kidney tumor cell lines carrying endogenous mutant non-f

39 It is particularly effective against kidney tumor cell lines, with >250-fold higher anti-tumo

40 strate that iPSCs derived from Dox-withdrawn kidney tumor cells give rise to nonneoplastic kidney cel

41 ognize HLA-A*0201-positive HERV-E-expressing kidney tumor cells.

42 restingly, total AKT protein was elevated in kidney tumors compared to normal kidney tissue, but with

43 ecause the surgical management of hereditary kidney tumors depends on the genetic and histologic subt

44 tumors, three different histologic types of kidney tumors developed in BHD(d/+) mice including oncoc

45 The mechanisms leading to kidney tumor development remain uncharacterized and effe

46 rt a role for PI3K-AKT pathway activation in kidney tumor formation caused by loss of BHD and suggest

47 led to both mTORC1 and mTORC2 activation in kidney tumors from BHD(d/+) mice and human BHD patients.

48 TSC1-TSC2 complex in cell culture models and kidney tumors from both Tsc2(+/-) mice (adenoma) and TSC

49 y prove to be an effective way of inhibiting kidney tumor growth.

50 from Streptomyces achromogenes to induce new kidney tumors in BALB/c mice.

51 activated in both human BHD renal tumors and kidney tumors in BHD(d/+) mice.

52 l pediatric cancers and more than 95% of all kidney tumors in children.

53 Hyperphosphorylation of S6 is also seen in kidney tumors in the heterozygote mice, suggesting that

54 mallest coagulation diameter was observed in kidney tumors in the presence of blood flow (7.3 mm +/-

55 or multiple doses of streptozotocin induced kidney tumors in up to 25% of mice by 50-90 weeks of age

56 Elimination of blood flow in kidney tumors increased coagulation diameter to 10.3 mm

57 xposed non-tumor kidney tissue, and in frank kidney tumors indicate that these genetic aberrations ar

58 omas at high frequency, but the incidence of kidney tumors is somewhat lower than in Tsc2 heterozygot

59 The etiology of Wilms tumor, an embryonic kidney tumor, is genetically heterogeneous.

60 isposition to Wilms' tumor (WT), a childhood kidney tumor, is inherited as an autosomal dominant trai

61 methodological and standardized analysis of kidney tumor location.

62 posed that allow for objective assessment of kidney tumor location.

63 emia, Hodgkin disease, non-Hodgkin lymphoma, kidney tumor, neuroblastoma, soft-tissue sarcoma, or mal

64 We analysed the expression profiles of 70 kidney tumors of different histological subtypes to dete

65 in humans leads to Wilms' tumor, a pediatric kidney tumor, or other kidney diseases, such as Denys-Dr

66 d detrimental to the long-term health of the kidney tumor patient.

67 cally, early detection of small asymptomatic kidney tumors presages better patient outcome.

68 d growth rates of other transplantable mouse kidney tumors), propensity for lung metastases, and hype

69 physicochemical properties, solubility, and kidney:tumor ratio while maintaining potency (6; IC(50)

70 urine specimens obtained in 50 patients with kidney tumors, representing all major histological types

71 med a neuroblastoma resection, 170 (55.2%) a kidney tumor resection, and 123 (39.9%) an operation to

72 , or 51% reduction in the volume of SN12-PM6 kidney tumors, respectively.

73 elanomas (SIR = 2.93, 95% CI: 2.23-3.78) and kidney tumors (SIR = 1.91, 95% CI: 1.27-2.76), primarily

74 ved in several glioma, breast, prostate, and kidney tumor specimens or cell lines.

75 1 family was highest in WT relative to other kidney tumor subtypes.

76 identified a reduced expression of BCCIP in kidney tumor, suggesting a role of BCCIP in cancer etiol

77 diagnosis, ranging from 4.0 years (6.0%) for kidney tumor survivors to more than 17.8 years (> or =28

78 Partial nephrectomy for larger kidney tumors (T1b) has gained widespread acceptance in

79 cer syndromes can lead to multiple bilateral kidney tumors that occur at a younger age than do nonher

80 As observed in human BHD kidney tumors, three different histologic types of kidne

81 When samples of human kidney tumor tissue were compared with samples of normal

82 n that found for heparan sulfate from either kidney, tumor tissue, or growth plate aggrecan.

83 With the exception of the kidneys, tumor-to-tissue and tumor-to-blood ratios were

84 Moreover, except for a subset of kidney tumors, tuberin was expressed in both human and m

85 Focusing on breast and clear-cell kidney tumors, we report the existence of key metabolic