ライフサイエンスコーパス: pulmonary metastasis

1 ration, and all these contributed to inhibit pulmonary metastasis.

2 ressive malignancy with a tendency for early pulmonary metastasis.

3 cal tumor development, stromal invasion, and pulmonary metastasis.

4 f carcinoma and to a significant increase in pulmonary metastasis.

5 ry breast tumor growth but strongly inhibits pulmonary metastasis.

6 onment in the metastatic niche to facilitate pulmonary metastasis.

7 on, and enabled highly penetrant spontaneous pulmonary metastasis.

8 e response to control Chi3l1 elaboration and pulmonary metastasis.

9 ificantly reduced HCC progression as well as pulmonary metastasis.

10 rimary breast cancer cells and inhibition of pulmonary metastasis.

11 a HIF-1-dependent manner in murine models of pulmonary metastasis.

12 Sema7a, there was a significant reduction in pulmonary metastasis.

13 of systemic metastasis and a mouse model of pulmonary metastasis.

14 hibited invasion, anoikis, angiogenesis, and pulmonary metastasis.

15 ctivation in myeloid cell recruitment during pulmonary metastasis.

16 stic of coagulation abnormalities as well as pulmonary metastasis.

17 ant spontaneous mouse model of breast cancer pulmonary metastasis.

18 mor activity in a mouse model of established pulmonary metastasis.

19 ent carcinoma, and staging scans disclosed a pulmonary metastasis.

20 e is known about its activity in established pulmonary metastasis.

21 es, is associated with the aggressiveness of pulmonary metastasis.

22 atic human breast cancers, was important for pulmonary metastasis.

23 One patient developed pulmonary metastasis.

24 t phosphorylation, primary tumor growth, and pulmonary metastasis.

25 terization of the genetics and mechanisms of pulmonary metastasis.

26 ed E2F1 target genes with an unknown role in pulmonary metastasis.

27 ooxygenase 2 gene expression associated with pulmonary metastasis.

28 ased tumor latency and increased the rate of pulmonary metastasis.

29 breast cancer cells and depict its effect on pulmonary metastasis.

30 the mammary epithelium resulted in decreased pulmonary metastasis.

31 illaries by circulating tumour cells to seed pulmonary metastasis.

32 ocal mammary tumors with a high incidence of pulmonary metastasis.

33 nd a structural basis for cell arrest during pulmonary metastasis.

34 4 blocked DPPIV/poly-FN adhesion and impeded pulmonary metastasis.

35 s done for hepatic recurrence (28 patients), pulmonary metastasis (20 patients), local recurrence (24

36 TRAP-treated B16F10 tumor cells enhance pulmonary metastasis 41- to 48-fold (n = 17).

37 ely in the lung and observed a wide range of pulmonary metastasis among inbred mouse strains.

38 tes biomarker, and thrombin, a biomarker for pulmonary metastasis and cardiovascular disease, were co

39 inant CXCL1 protein induced intrahepatic and pulmonary metastasis and CXCR2 knockout (KO) in HepG2 ce

40 cancer, HB22.7 inhibited the development of pulmonary metastasis and extended overall survival.

41 de of SHP2 in the adjuvant setting decreased pulmonary metastasis and extended the survival of system

42 This patient underwent resection of a pulmonary metastasis and is alive, 63.6 months from OLT.

43 at there is also a gender difference between pulmonary metastasis and lymph node metastasis showing t

44 In vivo experimental B16-F10 pulmonary metastasis and primary tumor growth assays fou

45 ntibodies represents a promising therapy for pulmonary metastasis and progression.

46 rvations to evaluate the function of CCR5 in pulmonary metastasis and the mechanism underlying the di

47 Ms infiltrating mouse breast tumors prevents pulmonary metastasis and tumor lymphangiogenesis.

48 iod of minimal residual disease, spontaneous pulmonary metastasis, and cell line variants that differ

49 pletely suppressing tumor growth, inhibiting pulmonary metastasis, and preventing recurrence under pr

50 rvival < 30%, except for those with isolated pulmonary metastasis (approximately 50%).

51 d from an experimental murine tumor model of pulmonary metastasis are quantified using a digital imag

52 ancer resected for cure (isolated hepatic or pulmonary metastasis) are candidates for endoscopic surv

53 Here, we describe an ex vivo pulmonary metastasis assay (PuMA) in which the metastati

54 tified melanotic lesions in both primary and pulmonary metastasis B16F10 tumor models.

55 ed with control vaccine had no effect in the pulmonary metastasis burden.

56 anced tumor cell sEV secretion to accelerate pulmonary metastasis by priming the premetastatic niche.

57 demonstrated marked increases (>10-fold) in pulmonary metastasis compared with vector (pLNCX2)-B16 a

58 These data demonstrate an asymptomatic pulmonary metastasis detection rate of 0.099% (95% confi

59 he overall median survival from diagnosis of pulmonary metastasis for all patients was 15 months.

60 cutaneous tumor growth and strongly impaired pulmonary metastasis formation by generating anti-xCT an

61 f EDG2 expression augmented the incidence of pulmonary metastasis from 51.9% to 90.4% (P = 2.4 x 10(-

62 antly prolonged lung retention and inhibited pulmonary metastasis from melanoma and breast cancer wit

63 presenting a potential therapeutic target in pulmonary metastasis from melanoma.

64 27, and suppressed HCC motility in vitro and pulmonary metastasis in a nude mouse model.

65 ration or viability, and maraviroc decreased pulmonary metastasis in a preclinical mouse model of bre

66 The level of a pulmonary metastasis in BF1 mice increased to the level

67 The level of pulmonary metastasis in BF10 mice or in BF1 mice inocula

68 One possible mechanism of resistance to pulmonary metastasis in BTBRT+tf/J mice may require T-ce

69 These results support a model for pulmonary metastasis in mice in which 1) tumor cells can

70 These results suggest that the severity of pulmonary metastasis in mice receiving B16 melanoma cell

71 cal tumor invasion as well as lymph node and pulmonary metastasis in mouse cancer models.

72 e tumor antigen (Tag) following experimental pulmonary metastasis in naive mice.

73 ion inhibits prostate cancer progression and pulmonary metastasis in TRAMP mice by reducing cell prol

74 icantly inhibits prostate carcinogenesis and pulmonary metastasis in TRAMP mice without causing any s

75 oma cells we analyzed local tumor growth and pulmonary metastasis in transgenic mice engineered to ov

76 kout mice, whereas KAI1 completely abrogated pulmonary metastasis in wild-type and heterozygous litte

77 ately 50% and 63% decrease, respectively, in pulmonary metastasis incidence and multiplicity compared

78 Pulmonary metastasis is a frequent cause of poor outcome

79 The formation of pulmonary metastasis is greatly facilitated by recruitme

80 The development of pulmonary metastasis is the major cause of death in oste

81 In mouse models of breast cancer pulmonary metastasis, MAMs uniquely express FLT1.

82 of CXCR4 in B16 cells dramatically enhanced pulmonary metastasis, metastasis to the lymph nodes, liv

83 antigen (Tag) within an experimental murine pulmonary metastasis model of SV40 Tag-expressing tumors

84 abrogates MSC homing to tumors in an in vivo pulmonary metastasis model, confirming the in vitro two-

85 We then found, using a pulmonary metastasis model, systemically delivered MSCs

86 wild-type BALB/c mice using an experimental pulmonary metastasis model, we attempted to address whet

87 d in a statistically significant decrease in pulmonary metastasis multiplicity compared with controls

88 poorly differentiated prostate carcinoma and pulmonary metastasis multiplicity in transgenic adenocar

89 e key hemostatic factors on the hematogenous pulmonary metastasis of 2 established murine tumors, Lew

90 ines produced by these cells on experimental pulmonary metastasis of B16 melanoma was investigated in

91 ion of beta3 integrin rescues the growth and pulmonary metastasis of beta1 integrin-deficient 4T1 tum

92 ver an unprecedented role for GALNT14 in the pulmonary metastasis of breast cancer and elucidate the

93 Pulmonary metastasis of breast cancer cells is promoted

94 Pulmonary metastasis of breast cancer requires recruitme

95 the physiologic level of MTA1 in supporting pulmonary metastasis of breast cancer.

96 We confirmed roles for Sema7a and Chi3l1 in pulmonary metastasis of EMT6 breast cancer cells.

97 trated that overexpression of Ang-3 inhibits pulmonary metastasis of Lewis lung carcinoma and TA3 mam

98 ntly decreased the growth, angiogenesis, and pulmonary metastasis of mammary tumors produced in mice.

99 tegrin alpha v beta 5 to promote spontaneous pulmonary metastasis of multiple tumor cell types in bot

100 receptors were both required for spontaneous pulmonary metastasis of multiple tumor types even though

101 le by exogenous RANKL, which also stimulated pulmonary metastasis of RANK(+) human breast cancer cell

102 ted that overexpression of ADAMTS-1 promotes pulmonary metastasis of TA3 mammary carcinoma and Lewis

103 The dependence of pulmonary metastasis on T cells was replaceable by exoge

104 Surface polyFn is critical for pulmonary metastasis, presumably by facilitating lung va

105 osed nascent tumor growth in mouse models of pulmonary metastasis, reflecting systemic lineage-specif

106 Pulmonary metastasis remains the leading ca use of death

107 A 50-year-old man developed progressive pulmonary metastasis resistant to interferon alfa-2b tre

108 und that tumor cell lines derived from focal pulmonary metastasis secreted relatively greater quantit

109 umor immunity in an established experimental pulmonary metastasis setting.

110 Moreover, in a murine model of HCC pulmonary metastasis, stable knockdown of HMGB1 suppress

111 Patterns of distant pulmonary metastasis tended to follow the same patterns

112 rocess, we aimed to develop a mouse model of pulmonary metastasis that can be assayed in multiple inb

113 in mouse models of spontaneous breast cancer pulmonary metastasis that fibrotic changes and rewiring

114 tumor-derived MIF promotes tumor growth and pulmonary metastasis through control of inflammatory cel

115 expression on CD8(+) T cells and limited B16 pulmonary metastasis to the same degree as PD-1 gene def

116 Confirmation of pulmonary metastasis usually requires serial imaging bec

117 n of MEK-dependent pathways by E(2) leads to pulmonary metastasis via enhanced survival of detached t

118 lete tumor immunity within a murine model of pulmonary metastasis was achieved upon two i.m. injectio

119 Pulmonary metastasis was associated with advanced pathol

120 In mice in protocol B, the incidence of pulmonary metastasis was decreased 1.9-fold (P = 0.069)

121 Pulmonary metastasis was either eliminated or significan

122 fect of treatment on mouse renal cancer cell pulmonary metastasis was investigated.

123 er, a dramatic reduction of tumor growth and pulmonary metastasis was observed after s.c. implantatio

124 The largest reduction in pulmonary metastasis was observed in sphingosine-1-phosp

125 melanoma cell line B16 as a murine model of pulmonary metastasis, we examined whether the pro- versu

126 To define genetic determinants of pulmonary metastasis, we have applied cDNA microarrays t

127 Here, using mouse models of pulmonary metastasis, we identify bone marrow (BM)-deriv

128 mouse melanoma B16F10 model of experimental pulmonary metastasis, we show that infiltrating macropha

129 57%, 36%, 27%, and 27%; rates for colorectal pulmonary metastasis were 87%, 78%, 57%, 57%, and 57%.

130 AdsGRP94 injections, local tumor growth and pulmonary metastasis were markedly inhibited.

131 ieved increased protection from experimental pulmonary metastasis when NK cells were further activate

132 dy significantly suppressed tumor growth and pulmonary metastasis, which was associated with reduced

133 the expression of receptor IL-13Ralpha2 and pulmonary metastasis while restoring NK cell accumulatio

134 n the mammary epithelium displayed increased pulmonary metastasis, with no differences in tumor onset

135 their sensitivity to apoptosis; and reduces pulmonary metastasis, with no effect on primary tumor gr

136 th an enhanced SPANXB1:SH3GL2 ratio achieved pulmonary metastasis within 5 weeks, whereas controls ce