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1 sed metastases in response to challenge with B16 melanoma cells.
2 lmonary metastases after i.v. injection with B16 melanoma cells.
3 non-malignant melan-a mouse melanocytes and B16 melanoma cells.
4 n mediating the biological activity of RA in B16 melanoma cells.
5 n expression in several cell types including B16 melanoma cells.
6 cted from subsequent challenge by unmodified B16 melanoma cells.
7 injected with CD48(+) and CD48(-) metastatic B16 melanoma cells.
8 eans of delivering gelonin to the cytosol of B16 melanoma cells.
9 einococcus radiodurans as well as from mouse B16 melanoma cells.
10 arious protein fractions of melanosomes from B16 melanoma cells.
11 ving high levels of luciferase expression in B16 melanoma cells.
12 o 17 microM in relatively insensitive murine B16 melanoma cells.
13 gene of an ecotropic retrovirus produced by B16 melanoma cells.
14 cells using Matrigel plugs supplemented with B16 melanoma cells.
15 other non-T non-B cells in the rejection of B16 melanoma cells after exogenous administration of IL-
18 erated IL-35-producing plasmacytoma J558 and B16 melanoma cells and observed that the expression of I
19 esions only in the brain parenchyma, whereas B16 melanoma cells and the somatic hybrid cells of B16 x
20 of common genes in the 48 h RA-treatment of B16 melanoma cells and untreated B16 vs. melan-a data se
23 h HLA-A2(neg) tumor (MC38 colon carcinoma or B16 melanoma) cells are not recognized by the CD8(+) T c
26 s into mice targeted HIV envelope-expressing B16 melanoma cells, but not normal tissue or envelope-ne
27 miR-21 regulates the metastatic behavior of B16 melanoma cells by promoting cell proliferation, surv
28 cient mutant mice, sialyl Lewis X-expressing B16 melanoma cells colonized the lung, and IELLQAR inhib
29 induced either with MCA or by inoculation of B16 melanoma cells, compared with mice with IFN-gamma-co
30 ailed to reject, arguing that the killing of B16 melanoma cells could occur either via the cytotoxic
32 by vaccination of recipients with irradiated B16 melanoma cells engineered to secrete granulocyte-mac
37 MDSCs from lal(-/-) mice directly stimulated B16 melanoma cell in vitro proliferation and in vivo gro
41 ty of pulmonary metastasis in mice receiving B16 melanoma cells is strongly influenced by the IL-4 re
45 cient mice displayed significantly decreased B16 melanoma cell metastasis to the lung, whereas treatm
48 eritoneal macrophages capable of suppressing B16 melanoma cell proliferation in vitro, an effect that
50 Lastly, vaccination with GM-CSF-secreting B16 melanoma cells stimulated high-titer antibodies to A
54 to reverse MDR was investigated using murine B16 melanoma cells that were transfected with the human
55 lysed tumors efficiently, and metastasis of B16 melanoma cells to draining lymph nodes was suppresse
56 d highly enriched apoptotic versus lysate of B16 melanoma cells to examine whether or not there are i
58 he lung, we observed decreased metastasis of B16 melanoma cells to the lung by treatment with a mAb b
59 ynebacterium parvum adjuvant, and irradiated B16 melanoma cells transduced with the gene for granuloc
62 -glycoprotein inhibits melanin production by B16 melanoma cells via post-transcriptional effects on t
64 1 in the invasive and metastatic capacity of B16 melanoma cells we analyzed local tumor growth and pu
66 o, empty vector- and antagomiR-21-transduced B16 melanoma cells were injected via tail vein into syng
68 organ-specific manner, we transduced murine B16 melanoma cells with CXCR4 (CXCR4-B16) and followed t
69 d for their ability to inhibit the growth of B16 melanoma cells with the most potent and selective HD
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