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

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

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

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

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

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

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

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

8 Carcinoma-associated fibroblasts (CAF) have recently bee

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

10 Carcinoma-associated fibroblasts (CAF) mediate the onset

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

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

13 Carcinoma-associated fibroblasts (CAF) support and promo

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

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

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

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

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

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

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

21 Carcinoma-associated fibroblasts (CAFs), frequently pres

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

23 Thus, carcinoma-associated fibroblasts can direct tumor progre

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

25 Human prostatic carcinoma-associated fibroblasts grown with initiated hu

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

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

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

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

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

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

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

33 Carcinoma-associated fibroblasts stimulated T47D cell pr

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

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

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