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1                                  Analysis of premetastatic adenocarcinoma patient samples reveals enr
2 ed to obtain the transcriptional profiles of premetastatic and macrometastatic (non-premetastatic) lu
3 t that unraveling the molecular landscape of premetastatic BMICs allows for the identification of cli
4                    Importantly, we show that premetastatic BMICs exhibit increased expression of HLA-
5 e identified that lung, breast, and melanoma premetastatic BMICs share a common transcriptomic signat
6                                     To mimic premetastatic bone adaptation, immunocompromised mice we
7                                              Premetastatic cancer cells often spread from the primary
8 n and extracellular matrix remodeling in the premetastatic compartment.
9 our hypothesis that fibrocytes contribute to premetastatic conditioning by recruiting Ly-6C(+) monocy
10 ic signature that is distinct from their non-premetastatic counterparts.
11                        Elevation of CXCL1 in premetastatic liver tissue recruited CXCR2-positive myel
12                                 Importantly, premetastatic liver-infiltrating MDSCs induced tumor cel
13  MMP9 normalizes aberrant vasculature in the premetastatic lung and diminishes lung metastasis.
14 ion of Gr-1+CD11b+ cells could normalize the premetastatic lung environment, improve host immunosurve
15                      Characterization of the premetastatic lung in conjunction with pseudotime lineag
16 anism for Gr-1+CD11b+ cells that changes the premetastatic lung into an inflammatory and proliferativ
17     A decreased accumulation of MDSCs in the premetastatic lung produces longer periods of disease-fr
18 rrow-derived myeloid progenitor cells in the premetastatic lung secrete the proteoglycan versican, wh
19 ction with resident mesenchymal cells in the premetastatic lung.
20 es of premetastatic and macrometastatic (non-premetastatic) lung, breast, and melanoma BMICs.
21                                              Premetastatic lungs contained significantly upregulated
22                 RNA sequencing of MDSCs from premetastatic lungs in these models demonstrated the rol
23        We assessed ECM remodeling in vivo in premetastatic lungs of female mice growing orthotopic pr
24 id-derived suppressor cells recruited to the premetastatic lungs through complement C5a receptor 1 si
25                        AM accumulated in the premetastatic lungs through complement C5a receptor-medi
26                                       In the premetastatic lungs, these immature myeloid cells signif
27  we found upregulation of these genes in the premetastatic lungs.
28 11b(+)Gr1(+) myeloid progenitor cells in the premetastatic lungs.
29 creased when active NK cells were present in premetastatic lungs.
30 screte foci of vascular hyperpermeability in premetastatic lungs.
31 programs the biomechanical properties of the premetastatic lymph node niche to promote tumor invasion
32 l properties to favor tumor spreading in the premetastatic lymph node niche.
33   Factors secreted by melanoma cells promote premetastatic lymph node reprograming and tumor spreadin
34 DSCs are key factors in the formation of the premetastatic microenvironment after resection of primar
35 ose adjuvant epigenetic therapy disrupts the premetastatic microenvironment and inhibits both the for
36 vant epigenetic modifiers that disrupts this premetastatic microenvironment and inhibits metastases m
37 erventions that prevent the formation of the premetastatic microenvironment(6,7).
38 ne marrow contribute to the formation of the premetastatic microenvironment, which is required for di
39 chanical properties of distant lymph node in premetastatic mouse models.
40 st-derived murine CCL2, but not IL-6, in the premetastatic murine host significantly reduced the prom
41                                              Premetastatic niche (PMN) and macrometastatic niche (MMN
42 ating the activation of quiescent ECs at the premetastatic niche (PMN) remain elusive.
43 f cytotoxic natural killer (NK) cells in the premetastatic niche (PMN) to enhance metastasis, indepen
44 c melanoma cells within the LN by creating a premetastatic niche (PMN).
45 guishing it from a normal stem cell niche, a premetastatic niche and an ectopic niche.
46 icking, which stimulates the generation of a premetastatic niche and facilitates metastatic progressi
47 rostaglandin E2 (PGE2) in the formation of a premetastatic niche and LNM.
48  secretion and PTX3 protein cargo primes the premetastatic niche and suggests that inhibition of eith
49 cells, increases cell migration, and induces premetastatic niche at the distal organ of metastasis.
50             We characterize here the elusive premetastatic niche by examining the role of mesenchymal
51 , 5-azacytidine and entinostat, disrupts the premetastatic niche by inhibiting the trafficking of MDS
52 , our results suggest that the MDSC-mediated premetastatic niche created in the lymph node of TRL-pos
53     These results indicate that DCs induce a premetastatic niche during LNM via COX-2/EP3-dependent i
54 xis may be an effective strategy to suppress premetastatic niche formation and LNM.
55             Polarized M2 macrophages induced premetastatic niche formation and promoted GC metastasis
56  downstream effects, significantly inhibited premetastatic niche formation and the resulting metastat
57 ng the contributions of the primary tumor to premetastatic niche formation are not fully understood.
58 ow the tumor microenvironment contributes to premetastatic niche formation at distant sites, but they
59 w that hypoxia in the primary tumor promotes premetastatic niche formation in secondary organs.
60  nodes can be explained by the MDSC-mediated premetastatic niche formation in which proinflammatory f
61 tastatic cancer due to its role in promoting premetastatic niche formation.
62 teractions, cell migration and invasion, and premetastatic niche formation.
63 which primary tumor-derived exosomes promote premetastatic niche formation.
64 c genes, including important determinants of premetastatic niche formation.
65 expression of several cytokines that promote premetastatic niche formation.
66 y TIMP-1 as an essential promoter of hepatic premetastatic niche formation.
67 ous cells in premetastatic sites, leading to premetastatic niche formation.
68        The latter is further enhanced by the premetastatic niche generated by mobilization of myeloid
69                                          The premetastatic niche hypothesis proposes an active primin
70         Extracellular vesicles help form the premetastatic niche in lymph nodes and facilitate melano
71 vidence that angiogenesis contributes to the premetastatic niche in rapidly progressing cancers and t
72 phages, finally enabling the generation of a premetastatic niche in the inflammatory site.
73   Biomaterial implants acting as a synthetic premetastatic niche recruit metastatic cancer cells and
74  receptor 4 (TLR4) signaling, establishing a premetastatic niche that supports disease hyperprogressi
75 id-derived suppressor cells (MDSC) to form a premetastatic niche that ultimately promoted liver metas
76 c mice, Gal1 fostered the establishment of a premetastatic niche through polymorphonuclear myeloid-de
77 Ca cells educate the bone marrow to create a premetastatic niche through primary PCa exosome-mediated
78 nes and growth factors capable of creating a premetastatic niche through recruitment of CD11b+/Ly6Cme
79       Gal1 promoted MDSC accumulation in the premetastatic niche through the NF-kappaB signaling axis
80 hich recruits CXCR2-positive MDSCs to form a premetastatic niche to promote liver metastases.
81     We propose that these mediators create a premetastatic niche within the skin, thereby participati
82   Recent reports suggest the formation of a "premetastatic niche" before the metastatic cascade, wher
83 rior to arrival of tumor cells (i.e., in the premetastatic niche) in the models of breast carcinoma.
84 he lungs, CRP facilitates the formation of a premetastatic niche, allowing circulating tumor cells to
85 asion, angiogenesis, immune suppression, the premetastatic niche, intravasation and/or extravasation,
86 sens myeloid-derived suppressor cells in the premetastatic niche, synergized with the depletion of AM
87 tudy identifies AM as a new component of the premetastatic niche, which is harnessed by tumors to imp
88 s in the local microenvironment, termed the "premetastatic niche," which dictate the pattern of metas
89 the notion that the liver IRI can serve as a premetastatic niche.
90 celerate pulmonary metastasis by priming the premetastatic niche.
91 oteins involved in the ECM remodeling of the premetastatic niche.
92 crophages, and diminished the formation of a premetastatic niche.
93 nduced neutrophil migration, a marker of the premetastatic niche.
94 al role of neutrophils in the TIMP-1-induced premetastatic niche.
95  metastasis by triggering the formation of a premetastatic niche.
96 e tumor microenvironment and conceivably the premetastatic niche.
97 une cell lineages as key constituents of the premetastatic niche.
98  for noninvasive imaging of BMD cells in the premetastatic niche.
99 ruited to the lung during the formation of a premetastatic niche.
100 ticularly in the lungs, where S100A9 forms a premetastatic niche.
101  to enhanced collagen deposition in the lung premetastatic niche.
102 ation, and the primary tumor can condition a premetastatic niche.
103                                         Like premetastatic-niche monocytes, these recruited cells exp
104 mor progression through the establishment of premetastatic niches and inhibit antitumor immune respon
105 mour, MDSCs contribute to the development of premetastatic niches and settlement of residual tumour c
106 eatic cancer cells and their ability to form premetastatic niches for pancreatic cancer cells in mice
107 tential may exist for the reduction of liver premetastatic niches induced by liver IRI through the us
108 BMDCs are also credited with the creation of premetastatic niches to which metastatic cells adhere vi
109 sis, and metastasis, both at local sites and premetastatic niches where invasion occurs in distal org
110 metastatic microenvironments, referred to as premetastatic niches, in certain distant organs before a
111  control of cellular invasion, initiation of premetastatic niches, maintenance of inflammation, and e
112 astases by participating in the formation of premetastatic niches, promoting angiogenesis and tumor c
113 lation of tumor progression and formation of premetastatic niches.
114  or STAT3 in myeloid cells disrupts existing premetastatic niches.
115 s with the gene expression patterns of liver premetastatic niches.
116 ngs implicate NET formation in rendering the premetastatic omental niche conducive for implantation o
117  stages of the brain metastatic cascade-the "premetastatic" or early stage when they first colonize t
118 suppressed the anticancer immune response in premetastatic organs.
119 cancer and is essential for the formation of premetastatic osteolytic lesions.
120           Taken together, our data show that premetastatic priming of lungs by primary breast tumors
121 tes and/or metastasis, macrophages prime the premetastatic site and promote tumor cell extravasation,
122                Priming of the organ-specific premetastatic sites is thought to be an important yet in
123 hat activate S1PR1-STAT3 in various cells in premetastatic sites, leading to premetastatic niche form
124 melanoma cell lines generated from invasive, premetastatic stage tumors.
125 05 can be detected in the circulation at the premetastatic stage, and its levels in the blood and tum
126 and rewiring of lung fibroblasts occurred at premetastatic stages, suggesting systemic influence by t
127  In contrast, breast cancer development to a premetastatic state is associated with upregulation and
128 rous progression of prostate and breast to a premetastatic state.
129 il influx into the omentum is a prerequisite premetastatic step in orthotopic ovarian cancer models.

 
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