ライフサイエンスコーパス: cancer-associated fibroblast

1 patocarcinoma HepG2 cancer cells, and breast cancer-associated fibroblasts.

2 on of matrix proteins secreted by dermal and cancer-associated fibroblasts.

3 h vimentin and phospho-S6 in Cav-1-deficient cancer-associated fibroblasts.

4 expression is down-regulated in human breast cancer-associated fibroblasts.

5 ) MSFs share many characteristics with human cancer-associated fibroblasts.

6 etween RhoA knockout fibroblasts and classic cancer-associated fibroblasts.

7 nuclear cells caused by Cxcl-1 released from cancer-associated fibroblasts.

8 nding stromal cells that acquire features of cancer-associated fibroblasts.

9 l-regulated kinase 1/2 activation in ovarian cancer-associated fibroblasts.

10 uld be counteracted by cytokines secreted by cancer-associated fibroblasts.

11 llate cells (PSC) are a subset of pancreatic cancer-associated fibroblasts.

12 ures of prostate cancer epithelial cells and cancer-associated fibroblasts, active CFL promoted invas

13 unlikely, but the opportunities for studying cancer-associated fibroblast activity in tumor models an

14 esmoplastic microenvironment, which includes cancer-associated fibroblasts [also known as pancreatic

15 This results in activation of cancer-associated fibroblasts and expression of CXCL16,

16 stic phenotype, which have been described as cancer-associated fibroblasts and have been shown to ind

17 we identified four proteins overexpressed in cancer-associated fibroblasts and linked to Rho GTPase s

18 t implications for understanding the role of cancer-associated fibroblasts and RB inactivation in pro

19 st time, that Angpts promote accumulation of cancer-associated fibroblasts and tumor angiogenesis in

20 Finally, we show that cancer-associated fibroblasts are significantly outnumbe

21 senchymal transition, including signals from cancer-associated fibroblasts, are able to increase the

22 Mesenchymal cells in tumors, called cancer-associated fibroblasts, arise via activation of r

23 nscriptome significantly overlaps with human cancer-associated fibroblasts; both show a nearly identi

24 t recruitment to tumours and activation to a cancer-associated fibroblast (CAF) phenotype has been im

25 Functional studies identified cancer-associated fibroblast (CAF)-derived EVs (from pat

26 at compared with normal fibroblasts, primary cancer-associated fibroblasts (CAF) and fibroblasts acti

27 n in tumor burden by affecting cancer cells, cancer-associated fibroblasts (CAF) and myeloid cells.

28 ymal stem cells (MSC) can differentiate into cancer-associated fibroblasts (CAF) and promote tumor pr

29 his study, Ang-(1-7) inhibited the growth of cancer-associated fibroblasts (CAF) and reduced fibrosis

30 Cancer-associated fibroblasts (CAF) are abundant in the

31 Cancer-associated fibroblasts (CAF) are among the abunda

32 Cancer-associated fibroblasts (CAF) comprise the majorit

33 deletion mouse model, on primary cultures of cancer-associated fibroblasts (CAF) derived from these t

34 Recent results suggest that cancer-associated fibroblasts (CAF) drive progression of

35 Cancer-associated fibroblasts (CAF) engage in tumor prog

36 Cancer-associated fibroblasts (CAF) have been reported t

37 Cancer-associated fibroblasts (CAF) have been shown to s

38 Cancer-associated fibroblasts (CAF) have been suggested

39 erminant for the tumor-promoting activity of cancer-associated fibroblasts (CAF) in both wild-type (W

40 Metastasis is facilitated by cancer-associated fibroblasts (CAF) in the tumor microen

41 Here, we demonstrate that cancer-associated fibroblasts (CAF) increase the stiffne

42 Notably, cancer-associated fibroblasts (CAF) isolated from patien

43 Signals originating from cancer-associated fibroblasts (CAF) may positively regul

44 DNA damage found in prostate cancer-associated fibroblasts (CAF) promotes tumor progr

45 Cancer-associated fibroblasts (CAF) regulate tumor progr

46 Cancer-associated fibroblasts (CAF) stimulate tumor grow

47 Cancer-associated fibroblasts (CAF) support tumorigenesi

48 rogression by modulating the contribution of cancer-associated fibroblasts (CAF) that are present in

49 rogenic signaling in breast cancer cells and cancer-associated fibroblasts (CAF) that contribute to c

50 demonstrating how microvesicles derived from cancer-associated fibroblasts (CAF) transfer miR-221 to

51 rthermore, co-cultures of KYSE-410 cells and cancer-associated fibroblasts (CAF) were investigated.

52 cells (MSC) contribute to stroma in part as cancer-associated fibroblasts (CAF), but a complete unde

53 row-derived mesenchymal stem cells to obtain cancer-associated fibroblasts (CAF)-like features via in

54 cancer cells and other cell types, including cancer-associated fibroblasts (CAF).

55 racterized by desmoplastic stroma containing cancer-associated fibroblasts (CAF).

56 i in breast epithelial cells cocultured with cancer-associated fibroblasts (CAF).

57 files of breast cancer cells in contact with cancer-associated fibroblasts (CAF).

58 ion, as it is required for the activation of cancer-associated fibroblasts (CAF).

59 aining an abundance of myofibroblasts termed cancer-associated fibroblasts (CAF).

60 gnaling is a major functional determinant of cancer-associated fibroblasts (CAF).

61 s (TEC) can become irreversibly activated as cancer-associated-fibroblasts (CAF) that stimulate oncog

62 downstream target SMAD2 (pSMAD2) (n=319) in cancer-associated fibroblasts (CAFs) and assessed links

63 ponse to the tumor, suggesting a key role of cancer-associated fibroblasts (CAFs) and fibrosis in its

64 he ANXA6/LRP1/TSP1 complex was restricted to cancer-associated fibroblasts (CAFs) and required physio

65 Desmoplasia, a fibrotic mass including cancer-associated fibroblasts (CAFs) and self-sustaining

66 peritoneal fibroblasts to express markers of cancer-associated fibroblasts (CAFs) and to stimulate gr

67 Cancer-associated fibroblasts (CAFs) are a major cancer-

68 Cancer-associated fibroblasts (CAFs) are a major cellula

69 Cancer-associated fibroblasts (CAFs) are important for t

70 Cancer-associated fibroblasts (CAFs) are major component

71 Cancer-associated fibroblasts (CAFs) are one of the most

72 Cancer-associated fibroblasts (CAFs) are pivotal in tumo

73 Cancer-associated fibroblasts (CAFs) are the most abunda

74 The role of cancer-associated fibroblasts (CAFs) as regulators of tu

75 We identified cancer-associated fibroblasts (CAFs) as the main source

76 wnregulated in 15 out of 16 samples (94%) of cancer-associated fibroblasts (CAFs) compared with match

77 Cancer-associated fibroblasts (CAFs) comprise one of the

78 Cancer-associated fibroblasts (CAFs) comprise the majori

79 The molecular mechanism by which cancer-associated fibroblasts (CAFs) confer chemoresista

80 Cancer-associated fibroblasts (CAFs) contribute to the p

81 Cancer-associated fibroblasts (CAFs) have been implicate

82 itate the interplay between cancer cells and cancer-associated fibroblasts (CAFs) in head and neck ca

83 Specialized cancer-associated fibroblasts (CAFs) in the ECM influenc

84 Interactions between tumor cells and cancer-associated fibroblasts (CAFs) in the tumor microe

85 Cancer-associated fibroblasts (CAFs) in triple-negative

86 s highly expressed by dermal fibroblasts and cancer-associated fibroblasts (CAFs) isolated from mutan

87 Such cancer-associated fibroblasts (CAFs) modulate the tumor

88 Cancer-associated fibroblasts (CAFs) regulate diverse in

89 oles in prostate development and cancer, and cancer-associated fibroblasts (CAFs) stimulate tumourige

90 tic stellate cells (PSCs) differentiate into cancer-associated fibroblasts (CAFs) that produce desmop

91 ct3/4(+)/Nanog(+) lung CSCs fed with CD90(+) cancer-associated fibroblasts (CAFs) to further advance

92 This effect was also confirmed in cancer-associated fibroblasts (CAFs) when co-cultured wi

93 esponded by upregulating S100A4, a marker of cancer-associated fibroblasts (CAFs), and this effect wa

94 Cancer-associated fibroblasts (CAFs), one of the princip

95 Emerging evidence suggests that cancer-associated fibroblasts (CAFs), the most abundant

96 talk between normal stromal cells, including cancer-associated fibroblasts (CAFs), vascular endotheli

97 k factor 1 (HSF1) is frequently activated in cancer-associated fibroblasts (CAFs), where it is a pote

98 ith known carcinogenic potential, can affect cancer-associated fibroblasts (CAFs), which are a key co

99 wed that Hic-5 is primarily expressed in the cancer-associated fibroblasts (CAFs).

100 re the secretome of human mammary normal and cancer-associated fibroblasts (CAFs).

101 RCA, we identified two distinct subtypes of cancer-associated fibroblasts (CAFs).

102 rget cells, which resembles the phenotype of cancer-associated fibroblasts (CAFs).

103 moting the reprogramming of these cells into cancer-associated fibroblasts (CAFs).

104 ut CIC chemoresistance was also increased by cancer-associated fibroblasts (CAFs).

105 ow that the MRTF-SRF pathway is activated in cancer-associated fibroblasts (CAFs).

106 In microarray expression analysis, cancer-associated fibroblasts clustered tightly into one

107 RDEB cancer-associated fibroblasts conferred increased adhesi

108 The conditioned media from the cancer-associated fibroblast cultures enhanced prolifera

109 that of cancer-associated fibroblasts, RDEB cancer-associated fibroblasts exhibited a distinct and d

110 ely 170 of 22,000 genes were up-regulated in cancer-associated fibroblasts (fold change > 2, P < 0.05

111 sively produced and used by cancer cells and cancer-associated fibroblasts for degrading stromal coll

112 Cancer-associated fibroblasts have a variety of activiti

113 he distinct molecular expression profiles of cancer-associated fibroblasts in colon cancer metastasis

114 o, we confirmed COX2 and TGFB2 expression in cancer-associated fibroblasts in metastatic colon cancer

115 ma protein (Rb), through phosphorylation, in cancer-associated fibroblasts in oro-pharyngeal cancer s

116 nfiltration of inflammatory/immune cells and cancer-associated fibroblasts in the tumor microenvironm

117 Cancer-associated fibroblasts induce malignant behavior

118 Fibroblasts in the tumour stroma (cancer-associated fibroblasts) influence tumour progress

119 atrix, either produced by cancer cells or by cancer-associated fibroblasts, influences angiogenesis,

120 bset of the NSCLC cells induced an activated cancer-associated fibroblast-like fibroblast phenotype d

121 ed differential expression of one or several cancer-associated fibroblast markers such as vimentin, f

122 Cancer-associated fibroblasts/myofibroblasts and inflamm

123 that interleukin 6 (IL6) derived mainly from cancer-associated fibroblasts played the most important

124 ate into myofibroblasts (also referred to as cancer-associated fibroblasts) primarily, but not exclus

125 EB normal skin fibroblasts resembled that of cancer-associated fibroblasts, RDEB cancer-associated fi

126 licited from group I (normal) and group III (cancer-associated) fibroblasts, respectively, approximat

127 Loss of Cav-1 expression in cancer-associated fibroblasts results in an activated tu

128 Cancer-associated fibroblasts secrete growth factors and

129 Recently, we reported that human breast cancer-associated fibroblasts show functional inactivati

130 , and E-cadherin expression, with pancreatic cancer-associated fibroblasts showing the opposite expre

131 inducing microenvironment changes, including cancer-associated fibroblasts, T regulatory cells, and i

132 ling pathways exist between cancer cells and cancer-associated fibroblasts that contribute to hypoxic

133 healing, which induces their conversion into cancer-associated fibroblasts that facilitate metastasis

134 expression and activity in cancer cells and cancer-associated fibroblasts that strongly contribute t

135 promote disease pathogenesis, including via cancer-associated fibroblasts, the hematopoietic stem ce

136 CXCL12 expressed by cancer-associated fibroblasts then binds to CXCR4 on tum

137 or xenografts, but they were not produced by cancer-associated fibroblasts, thereby comprising a spec

138 Similarly, when LIMK activity is blocked in cancer-associated fibroblasts, they are unable to lead t

139 o studies indicated that exposure of primary cancer-associated fibroblasts to MEDI-575 can directly a

140 and the metabolic/catabolic reprogramming of cancer-associated fibroblast, to fuel the growth of adja

141 We generated expression profiles of cancer-associated fibroblasts using oligochip arrays and

142 rounded by a dense stroma that contains many cancer-associated fibroblasts, which promotes their prog

143 he conversion of mesenchymal stem cells into cancer-associated fibroblasts, which secrete stromal-der