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

1 etic stem cells (HSCs) are a novel source of carcinoma-associated fibroblasts.

2 persistent STAT-1 and NF-kappaB activity in carcinoma-associated fibroblasts.

3 e emergence of a heterogeneous population of carcinoma-associated fibroblasts.

4 blasts with the molecular characteristics of carcinoma-associated fibroblasts.

5 fness can transform stromal fibroblasts into carcinoma-associated fibroblasts.

6 s a unique mechanism for the accumulation of carcinoma-associated fibroblasts and suggest that antian

7 Carcinoma-associated fibroblasts (CAF) are a potential t

8 We demonstrated that carcinoma-associated fibroblasts (CAF) are major sources

9 Heterogeneous prostatic carcinoma-associated fibroblasts (CAF) contribute to tum

10 Heterogeneity of carcinoma-associated fibroblasts (CAF) has long been rec

11 Carcinoma-associated fibroblasts (CAF) have recently bee

12 ores the mechanisms by which human prostatic carcinoma-associated fibroblasts (CAF) induce tumorigene

13 Carcinoma-associated fibroblasts (CAF) mediate the onset

14 Carcinoma-associated fibroblasts (CAF) play a critical r

15 Tumor-associated fibroblasts or carcinoma-associated fibroblasts (CAF) play an important

16 Carcinoma-associated fibroblasts (CAF) support and promo

17 tumors lacked the pronounced infiltration of carcinoma-associated fibroblasts (CAF) that characterize

18 th was assessed separately for cancer cells, carcinoma-associated fibroblasts (CAF), infiltrative lym

19 -cyclin D1) cells) similar to that seen with carcinoma-associated fibroblasts (CAF).

20 Interaction between carcinoma-associated fibroblasts (CAFs) and tumor cells

21 ment where hepatic stellate cells (HSCs) and carcinoma-associated fibroblasts (CAFs) are critical com

22 n tumor xenograft model, we demonstrate that carcinoma-associated fibroblasts (CAFs) extracted from h

23 Here, we report that carcinoma-associated fibroblasts (CAFs) induce B5 integr

24 either by recombination with human prostatic carcinoma-associated fibroblasts (CAFs) or by exposure t

25 A growth was achieved, however, by depleting carcinoma-associated fibroblasts (CAFs) that express fib

26 f fibroblast-like cells, collectively termed carcinoma-associated fibroblasts (CAFs), are key players

27 Carcinoma-associated fibroblasts (CAFs), frequently pres

28 increase the invasion-promoting potential of carcinoma-associated fibroblasts (CAFs).

29 Thus, carcinoma-associated fibroblasts can direct tumor progre

30 In contrast, carcinoma-associated fibroblasts did not affect growth o

31 Human prostatic carcinoma-associated fibroblasts grown with initiated hu

32 d that tRNAi(Met) expression is increased in carcinoma-associated fibroblasts, implicating deregulate

33 nderscores the need for caution in targeting carcinoma-associated fibroblasts in PDAC.

34 ivation protein (FAP) is highly expressed on carcinoma-associated fibroblasts in the stroma of pancre

35 blast activation protein (FAP), expressed by carcinoma-associated fibroblasts in various cancer types

36 oma and other carcinomas in patients contain carcinoma-associated fibroblasts, in contrast to primary

37 losartan inhibited collagen I production by carcinoma-associated fibroblasts isolated from breast ca

38 s, as the adoptively transferred MSC develop carcinoma-associated fibroblast-like characteristics.

39 lating recruitment and homing of HSC-derived carcinoma-associated fibroblasts or their precursors to

40 de that in this human prostate cancer model, carcinoma-associated fibroblasts stimulate progression o

41 Carcinoma-associated fibroblasts stimulated T47D cell pr

42 we demonstrate that partial depletion of the carcinoma-associated fibroblasts, which spontaneously sp

43 rmore, we show that therapeutic depletion of carcinoma-associated fibroblasts with an inhibitor of th