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1 endogenous hyperinsulinemia promotes mammary tumor metastases.
2 a broad range of primary melanoma tumors and tumor metastases.
3 l cancer cells was associated with increased tumor metastases.
4 l lines and fresh tissue obtained from human tumor metastases.
5 t angiogenesis or apoptosis, within advanced tumor metastases.
6 to retarget adenovirus vectors to epithelial tumor metastases.
7 otential role for TXAS-regulated pathways in tumor metastases.
8 LT1 and inflammatory responses within breast 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 ccordingly, suppression of DNA-PKcs inhibits tumor metastases.
14 s and macrophages at tumor sites may promote tumor metastases.
15 ance viral DNA replication and spread within tumor metastases.
16 malignancies and may play a critical role in tumor metastases.
17 t tumors in nude mice and the development of tumor metastases.
18  gastrinomas occur before the development 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 g various roles of MDSCs in the formation of tumor metastases.
25  not reduce primary tumor size but decreases tumor metastases.
26                                              Tumor metastases account for nearly 90% of cancer-relate
27 creatic nerves, neurogenic inflammation, and tumor metastases along extrapancreatic nerves are key fe
28                  As a principal site of both tumor metastases and immature NK cells, the liver repres
29 ar factor-kappaB (NF-kappaB), which promotes tumor metastases and invasion.
30  suppression of spontaneous and experimental tumor metastases and methylcholanthrene (MCA)-induced sa
31    Aberrant expression of ROCK is related to tumor metastases and poor clinical outcome.
32 e significant potential in the prevention of tumor metastases and recurrence.
33 ent mice have diminished capacity to control tumor metastases and support the role for NKLAM in NK fu
34 response capable of eradicating disseminated tumor metastases and the establishment of a persistent t
35  representing cancers with dismal prognoses, tumor metastases, and multidrug resistant cells.
36 abundance to 36 human thyroid cancer primary tumors, metastases, and patient-match normal tissue.
37 compare the mutation spectrum in the primary tumors, metastases, and the corresponding CTCs from two
38                  A large proportion of solid tumor metastases are bone metastases, known to usurp HSC
39 l-mesenchymal transition and FOXC2-dependent tumor metastases but did not confer resistance to androg
40 n, for lipid metabolism, and as conduits for tumor metastases, but they have been difficult to visual
41 el strategy achieved the eradication of lung tumor metastases by joint suppression of angiogenesis in
42  are directly implicated in the promotion of tumor metastases by participating in the formation of pr
43 lso inhibit the growth of preexisting breast tumor metastases by repetitive immunizations initiated e
44 r immunotherapies to specific organs bearing tumor metastases by taking advantage of differential tro
45 ture was significantly higher in luminal/ER+ tumor metastases compared with their primaries.
46         The clinical presence and absence of tumor metastases correlated significantly with vWf-cleav
47 lay between elements of the TME and advanced tumor metastases directs end-stage metastatic progressio
48                                          All tumor metastases exhibited a higher initial uptake when
49  for the whole body, red marrow, organs, and tumor metastases for the therapeutic (177)Lu-cG250, simu
50 and solid tumors, but not acute infection or tumor metastases, highlighting fundamental differences w
51 astic mathematical model of the evolution of tumor metastases in an expanding cancer cell population.
52  ability to inhibit tumor growth and abolish tumor metastases in animal models.
53 7-induced sorafenib resistance and prevented tumor metastases in HCC.
54 nt of overlap and degree of diversity across tumor metastases in individual patients has not been ful
55 T116 stable transfectants strongly decreased tumor metastases in nude mice, indicating the requiremen
56 le for decorin in reduction or prevention of tumor metastases in this breast cancer model and could e
57  augment antitumor immunity and rejection of tumor metastases in this setting.
58 tated control of subcutaneous tumors but not tumor metastases in two independent tumor models.
59 cells was crucial for their ability to limit tumor metastases in vivo in both liver and lungs using p
60 e to the liver and to enter liver tissue and tumor metastases in vivo.
61 ring inhibitor of angiogenesis and growth of tumor metastases, is generated by cancer-mediated proteo
62 astases-associated gene MTA1 correlates with tumor metastases, its role in regulating type IV collage
63 ary tumor nodules and eradicated established tumor metastases more efficiently than T cells generated
64                                              Tumor metastases suppressor protein KAI1/CD82 is capable
65 ns (SPK), showing a much higher incidence of tumor metastases than the Kras(G12D), p53(fl/fl) (PK) mi
66  these clones were isolated from progressing tumor metastases, the accumulation of these specific cyt
67 e effects including those due to the primary tumor, metastases, the effects and toxicity of cancer th
68 T disruption sensitizes experimental mammary tumor metastases to chemotherapy, thus providing insight
69                                 In contrast, tumor metastases to lung often exhibited reduced WWOX le
70 shown to play an important role in promoting tumor metastases to lymph nodes.
71                    Bioluminescent imaging of tumor metastases to the liver, lungs, and spleen reveale
72 A vaccine also showed efficacy in inhibiting tumor metastases using a PSCA-expressing B16-F10 model.
73  Since M-CSF(-/-) mice are protected against tumor metastases, we hypothesized that M-CSF induced mon
74    ESFT cells, primary tumor xenografts, and tumor metastases were all highly sensitive to PARP1 inhi
75 s of pAkt and pErk1/2 in IL4Ralpha knockdown tumor metastases were associated with limited outgrowth,
76 e perfusion estimates for normal tissues and tumor metastases were made in 18 paired baseline and tre
77                             Regression of >1 tumor metastases were observed in seven of these patient
78 src cells was associated with a reduction in tumor metastases while the shRNA-induced knockdown of Tr
79 ene set-phenotype association that predicted tumor metastases within tumor subtypes.
80 protein KAI1/CD82 is capable of blocking the tumor metastases without affecting the primary tumor for