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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-
16                                              B16 melanoma cells and B16-enhanced green fluorescent pr
17                             DC1s loaded with B16 melanoma cells and injected into tumor-bearing mice
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
21 n of microtubules, their cytotoxicity toward B16 melanoma cells, and their solubility in water.
22                        In fluorescence mode, B16 melanoma cells appeared as dark objects in the brigh
23 h HLA-A2(neg) tumor (MC38 colon carcinoma or B16 melanoma) cells are not recognized by the CD8(+) T c
24               JAM-C expressed on both murine B16 melanoma cells as well as on endothelial cells promo
25 an lead to very high targeting efficiency to B16 melanoma cells, both in vitro and in vivo.
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
31                               cAMP in NC and B16 melanoma cells decreased CtBP2 protein levels, while
32 by vaccination of recipients with irradiated B16 melanoma cells engineered to secrete granulocyte-mac
33                  Vaccination with irradiated B16 melanoma cells expressing either GM-CSF (Gvax) or Fl
34                    The adhesion of HL-60 and B16 melanoma cells expressing sialyl Lewis X to E-select
35               Consistent with these results, B16 melanoma cells expressing WNT3A also exhibit decreas
36 rd, the cells were transfected with DNA from B16 melanoma cells (H-2b).
37 MDSCs from lal(-/-) mice directly stimulated B16 melanoma cell in vitro proliferation and in vivo gro
38 cantly influence the metastatic potential of B16 melanoma cells in a murine model.
39                                              B16 melanoma cells incubated with filipin (0.16-0.3 micr
40                                 Injection of B16 melanoma cells into the left cardiac ventricle resul
41 ty of pulmonary metastasis in mice receiving B16 melanoma cells is strongly influenced by the IL-4 re
42                                     COS7 and B16 melanoma cells lack myosin IIA and IIB, respectively
43             Cells derived from the cutaneous B16 melanoma cell line (B16LS9) were transplanted either
44                           In the spontaneous B16 melanoma cell lines, expression of p16Ink4a and p19A
45 cient mice displayed significantly decreased B16 melanoma cell metastasis to the lung, whereas treatm
46                               Binding to the B16 melanoma cells occurred at a lipid composition that
47                    We previously showed that B16 melanoma cells produce ecotropic melanoma-associated
48 eritoneal macrophages capable of suppressing B16 melanoma cell proliferation in vitro, an effect that
49 sis factor-alpha from MDSCs are required for B16 melanoma cell proliferation in vitro.
50    Lastly, vaccination with GM-CSF-secreting B16 melanoma cells stimulated high-titer antibodies to A
51                     In vitro modification of B16 melanoma cell surface uPA activity has been shown to
52 ly properties and cytotoxic activity against B16 melanoma cells than paclitaxel.
53 ies, Stat3beta, induced cell death in murine B16 melanoma cells that harbored activated Stat3.
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
57                         Here, we used murine B16 melanoma cells to observe functional aspects of how
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
60       In the ex vivo tumor vaccine approach, B16 melanoma cells, transduced in vitro by adenovirus co
61                          Deletion of p205 in B16 melanoma cells using CRISPR/Cas9 showed a similar lo
62 -glycoprotein inhibits melanin production by B16 melanoma cells via post-transcriptional effects on t
63 bcutaneous challenge injection of unmodified B16 melanoma cells was performed 15 d later.
64 1 in the invasive and metastatic capacity of B16 melanoma cells we analyzed local tumor growth and pu
65                Melanotic PC1A and amelanotic B16 melanoma cells were incubated with increasing concen
66 o, empty vector- and antagomiR-21-transduced B16 melanoma cells were injected via tail vein into syng
67                                       Murine B16 melanoma cells, which overproduce TGFbeta, were lyse
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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