ライフサイエンスコーパス: premetastatic

1 our hypothesis that fibrocytes contribute to premetastatic conditioning by recruiting Ly-6C(+) monocy

2 Elevation of CXCL1 in premetastatic liver tissue recruited CXCR2-positive myel

3 Importantly, premetastatic liver-infiltrating MDSCs induced tumor cel

4 MMP9 normalizes aberrant vasculature in the premetastatic lung and diminishes lung metastasis.

5 ion of Gr-1+CD11b+ cells could normalize the premetastatic lung environment, improve host immunosurve

6 anism for Gr-1+CD11b+ cells that changes the premetastatic lung into an inflammatory and proliferativ

7 rrow-derived myeloid progenitor cells in the premetastatic lung secrete the proteoglycan versican, wh

8 AM accumulated in the premetastatic lungs through complement C5a receptor-medi

9 In the premetastatic lungs, these immature myeloid cells signif

10 11b(+)Gr1(+) myeloid progenitor cells in the premetastatic lungs.

11 creased when active NK cells were present in premetastatic lungs.

12 screte foci of vascular hyperpermeability in premetastatic lungs.

13 st-derived murine CCL2, but not IL-6, in the premetastatic murine host significantly reduced the prom

14 guishing it from a normal stem cell niche, a premetastatic niche and an ectopic niche.

15 rostaglandin E2 (PGE2) in the formation of a premetastatic niche and LNM.

16 cells, increases cell migration, and induces premetastatic niche at the distal organ of metastasis.

17 We characterize here the elusive premetastatic niche by examining the role of mesenchymal

18 These results indicate that DCs induce a premetastatic niche during LNM via COX-2/EP3-dependent i

19 xis may be an effective strategy to suppress premetastatic niche formation and LNM.

20 downstream effects, significantly inhibited premetastatic niche formation and the resulting metastat

21 ng the contributions of the primary tumor to premetastatic niche formation are not fully understood.

22 ow the tumor microenvironment contributes to premetastatic niche formation at distant sites, but they

23 w that hypoxia in the primary tumor promotes premetastatic niche formation in secondary organs.

24 c genes, including important determinants of premetastatic niche formation.

25 y TIMP-1 as an essential promoter of hepatic premetastatic niche formation.

26 ous cells in premetastatic sites, leading to premetastatic niche formation.

27 expression of several cytokines that promote premetastatic niche formation.

28 The latter is further enhanced by the premetastatic niche generated by mobilization of myeloid

29 id-derived suppressor cells (MDSC) to form a premetastatic niche that ultimately promoted liver metas

30 nes and growth factors capable of creating a premetastatic niche through recruitment of CD11b+/Ly6Cme

31 hich recruits CXCR2-positive MDSCs to form a premetastatic niche to promote liver metastases.

32 We propose that these mediators create a premetastatic niche within the skin, thereby participati

33 Recent reports suggest the formation of a "premetastatic niche" before the metastatic cascade, wher

34 asion, angiogenesis, immune suppression, the premetastatic niche, intravasation and/or extravasation,

35 sens myeloid-derived suppressor cells in the premetastatic niche, synergized with the depletion of AM

36 tudy identifies AM as a new component of the premetastatic niche, which is harnessed by tumors to imp

37 s in the local microenvironment, termed the "premetastatic niche," which dictate the pattern of metas

38 nduced neutrophil migration, a marker of the premetastatic niche.

39 al role of neutrophils in the TIMP-1-induced premetastatic niche.

40 metastasis by triggering the formation of a premetastatic niche.

41 e tumor microenvironment and conceivably the premetastatic niche.

42 une cell lineages as key constituents of the premetastatic niche.

43 for noninvasive imaging of BMD cells in the premetastatic niche.

44 ruited to the lung during the formation of a premetastatic niche.

45 Like premetastatic-niche monocytes, these recruited cells exp

46 mor progression through the establishment of premetastatic niches and inhibit antitumor immune respon

47 BMDCs are also credited with the creation of premetastatic niches to which metastatic cells adhere vi

48 sis, and metastasis, both at local sites and premetastatic niches where invasion occurs in distal org

49 metastatic microenvironments, referred to as premetastatic niches, in certain distant organs before a

50 control of cellular invasion, initiation of premetastatic niches, maintenance of inflammation, and e

51 astases by participating in the formation of premetastatic niches, promoting angiogenesis and tumor c

52 or STAT3 in myeloid cells disrupts existing premetastatic niches.

53 suppressed the anticancer immune response in premetastatic organs.

54 cancer and is essential for the formation of premetastatic osteolytic lesions.

55 tes and/or metastasis, macrophages prime the premetastatic site and promote tumor cell extravasation,

56 Priming of the organ-specific premetastatic sites is thought to be an important yet in

57 hat activate S1PR1-STAT3 in various cells in premetastatic sites, leading to premetastatic niche form

58 melanoma cell lines generated from invasive, premetastatic stage tumors.

59 05 can be detected in the circulation at the premetastatic stage, and its levels in the blood and tum

60 In contrast, breast cancer development to a premetastatic state is associated with upregulation and

61 rous progression of prostate and breast to a premetastatic state.