ライフサイエンスコーパス: tumor metastases

1 endogenous hyperinsulinemia promotes mammary tumor metastases.

2 l cancer cells was associated with increased tumor metastases.

3 l lines and fresh tissue obtained from human tumor metastases.

4 t angiogenesis or apoptosis, within advanced tumor metastases.

5 LT1 and inflammatory responses within breast tumor metastases.

6 to retarget adenovirus vectors to epithelial tumor metastases.

7 otential role for TXAS-regulated pathways in tumor metastases.

8 ccordingly, suppression of DNA-PKcs inhibits tumor metastases.

9 mode of gene delivery on established murine tumor metastases.

10 dies also observed significant inhibition of tumor metastases.

11 argeting of (225)Ac to sites of disseminated tumor metastases.

12 py may vary depending on the location of the tumor metastases.

13 s and macrophages at tumor sites may promote tumor metastases.

14 ance viral DNA replication and spread within tumor metastases.

15 malignancies and may play a critical role in tumor metastases.

16 t tumors in nude mice and the development of tumor metastases.

17 gastrinomas occur before the development of tumor metastases.

18 g various roles of MDSCs in the formation of tumor metastases.

19 matrix remodeling in disease states such as tumor metastases.

20 ay a part in modulating some early events in tumor metastases.

21 therapy markedly reduced the number of lung tumor metastases.

22 icantly (p<0.02) enhanced the development of tumor metastases.

23 igher for metastatic melanoma than for other tumor metastases.

24 a broad range of primary melanoma tumors and tumor metastases.

25 creatic nerves, neurogenic inflammation, and tumor metastases along extrapancreatic nerves are key fe

26 As a principal site of both tumor metastases and immature NK cells, the liver repres

27 ar factor-kappaB (NF-kappaB), which promotes tumor metastases and invasion.

28 suppression of spontaneous and experimental tumor metastases and methylcholanthrene (MCA)-induced sa

29 Aberrant expression of ROCK is related to tumor metastases and poor clinical outcome.

30 ent mice have diminished capacity to control tumor metastases and support the role for NKLAM in NK fu

31 response capable of eradicating disseminated tumor metastases and the establishment of a persistent t

32 representing cancers with dismal prognoses, tumor metastases, and multidrug resistant cells.

33 compare the mutation spectrum in the primary tumors, metastases, and the corresponding CTCs from two

34 A large proportion of solid tumor metastases are bone metastases, known to usurp HSC

35 l-mesenchymal transition and FOXC2-dependent tumor metastases but did not confer resistance to androg

36 n, for lipid metabolism, and as conduits for tumor metastases, but they have been difficult to visual

37 el strategy achieved the eradication of lung tumor metastases by joint suppression of angiogenesis in

38 are directly implicated in the promotion of tumor metastases by participating in the formation of pr

39 lso inhibit the growth of preexisting breast tumor metastases by repetitive immunizations initiated e

40 r immunotherapies to specific organs bearing tumor metastases by taking advantage of differential tro

41 The clinical presence and absence of tumor metastases correlated significantly with vWf-cleav

42 lay between elements of the TME and advanced tumor metastases directs end-stage metastatic progressio

43 for the whole body, red marrow, organs, and tumor metastases for the therapeutic (177)Lu-cG250, simu

44 astic mathematical model of the evolution of tumor metastases in an expanding cancer cell population.

45 ability to inhibit tumor growth and abolish tumor metastases in animal models.

46 7-induced sorafenib resistance and prevented tumor metastases in HCC.

47 T116 stable transfectants strongly decreased tumor metastases in nude mice, indicating the requiremen

48 le for decorin in reduction or prevention of tumor metastases in this breast cancer model and could e

49 augment antitumor immunity and rejection of tumor metastases in this setting.

50 cells was crucial for their ability to limit tumor metastases in vivo in both liver and lungs using p

51 e to the liver and to enter liver tissue and tumor metastases in vivo.

52 ring inhibitor of angiogenesis and growth of tumor metastases, is generated by cancer-mediated proteo

53 astases-associated gene MTA1 correlates with tumor metastases, its role in regulating type IV collage

54 ary tumor nodules and eradicated established tumor metastases more efficiently than T cells generated

55 Tumor metastases suppressor protein KAI1/CD82 is capable

56 these clones were isolated from progressing tumor metastases, the accumulation of these specific cyt

57 e effects including those due to the primary tumor, metastases, the effects and toxicity of cancer th

58 In contrast, tumor metastases to lung often exhibited reduced WWOX le

59 shown to play an important role in promoting tumor metastases to lymph nodes.

60 Bioluminescent imaging of tumor metastases to the liver, lungs, and spleen reveale

61 A vaccine also showed efficacy in inhibiting tumor metastases using a PSCA-expressing B16-F10 model.

62 Since M-CSF(-/-) mice are protected against tumor metastases, we hypothesized that M-CSF induced mon

63 ESFT cells, primary tumor xenografts, and tumor metastases were all highly sensitive to PARP1 inhi

64 s of pAkt and pErk1/2 in IL4Ralpha knockdown tumor metastases were associated with limited outgrowth,

65 e perfusion estimates for normal tissues and tumor metastases were made in 18 paired baseline and tre

66 Regression of >1 tumor metastases were observed in seven of these patient

67 src cells was associated with a reduction in tumor metastases while the shRNA-induced knockdown of Tr

68 ene set-phenotype association that predicted tumor metastases within tumor subtypes.

69 protein KAI1/CD82 is capable of blocking the tumor metastases without affecting the primary tumor for