ライフサイエンスコーパス: B16 melanoma

1 able therapeutic effects against established B16 melanoma.

2 fer in treatment of established subcutaneous B16 melanoma.

3 ells better mediated destruction of advanced B16 melanoma.

4 Fv was shown also with the TC1 carcinoma and B16 melanoma.

5 RALBP1 causes regression of syngeneic mouse B16 melanoma.

6 mel-1) to treat large, well-established s.c. B16 melanoma.

7 ased protection from a lethal challenge with B16 melanoma.

8 >85% tumor rejection in mice challenged with B16 melanoma.

9 matically reduced tumor burden in a model of B16 melanoma.

10 hough the same regimen was not effective for B16 melanoma.

11 r antitumor activity in the immunotherapy of B16 melanoma.

12 estigated in mice bearing poorly immunogenic B16 melanoma.

13 mune response in a syngeneic murine model of B16 melanoma.

14 ot all tumor rejection models, including the B16 melanoma.

15 vival of mice against the poorly immunogenic B16 melanoma.

16 d epitope unable to bind D(b) did not reject B16 melanoma.

17 ect the expression or function of the RAR in B16 melanoma.

18 l as greater resistance to metastases of the B16 melanoma.

19 mors established from the poorly immunogenic B16 melanoma.

20 L261 glioma and subcutaneous implants of the B16 melanoma.

21 , but not in TME with scarce TILeus, such as B16 melanoma.

22 V-10 led to tumor regression in mice bearing B16 melanoma.

23 rapy in a hormone-independent cancer, murine B16 melanoma.

24 ufficient to delay the growth of established B16 melanoma.

25 one marrow-derived dendritic cells (DCs) and B16 melanoma.

26 PC3M prostate cancer cells, but not those of B16 melanoma.

27 nt improvement in antitumor activity against B16 melanoma.

28 rge pre-established lymphomas and aggressive B16 melanomas.

29 n, with apparent cures of large, established B16 melanomas.

30 ulation to control the growth of established B16 melanomas.

31 ed to surgical excision of large established B16 melanomas.

32 yeloid-derived suppressor cell ratios within B16 melanomas.

33 or and its ability to delay the outgrowth of B16 melanoma after adoptive transfer.

34 activity were observed in the liver and s.c. B16 melanoma after poly-ICLC injection or in the lungs a

35 ritical for inhibiting antitumor immunity in B16 melanoma and a genetically engineered melanoma.

36 high levels in poorly metastatic variants of B16 melanoma and at much reduced levels in highly metast

37 unity generated against live variants of the B16 melanoma and EL4 thymic lymphoma tumors were highly

38 T-cell response that eradicates established B16 melanoma and find that the recognized epitope is gen

39 MO-MDSCs isolated from B16 melanoma and from skin tumor-bearing ret transgenic

40 sal post electroporation for both homogenous B16 melanoma and heterogeneous human serum-derived popul

41 ide inhibited the lung colonization of mouse B16 melanoma and human lung tumor cells expressing sialy

42 nduces a superior antitumor response against B16 melanoma and its distant lung metastasis compared wi

43 MHC expression in the widely studied murine B16 melanoma and its variants B16F1, B16F10, BL6-2, BL6-

44 tumor growth and tumor angiogenesis in both B16 melanoma and Lewis Lung Cancer mouse models.

45 ine CT26 colon carcinoma tumors (BALB/c) and B16 melanoma and Lewis lung cell carcinoma (C57Bl/6) wer

46 We show that growth of B16 melanoma and MB49 bladder carcinoma is reduced in IL

47 muris and within the tumor microenvironment (B16 melanoma and MC38 colorectal adenocarcinoma), where

48 id DNA significantly inhibited the growth of B16 melanoma and MCA205 fibrosarcoma in a dose-dependent

49 he poorly immunogenic, spontaneously arising B16 melanoma and the immunogenic, chemically induced LiH

50 have been reported using the gp75-expressing B16 melanoma and the protective anti-gp75 mAb TA99.

51 umor resection, to confer protection against B16 melanoma, and against JBRH, an independently derived

52 ad little or no effect on the growth of s.c. B16 melanomas, and only Ad-Ii-TRP-2 was able to induce a

53 elated protein-1 (TRP-1), respectively, into B16-melanoma-bearing mice.

54 n CD8alpha KO mice that were challenged with B16 melanoma both s.c. and in the brain.

55 We have previously shown that small B16 melanomas can be successfully treated using a combin

56 e potent control of tumor development in the B16 melanoma cancer model in mice.

57 MDSCs from lal(-/-) mice directly stimulated B16 melanoma cell in vitro proliferation and in vivo gro

58 Cells derived from the cutaneous B16 melanoma cell line (B16LS9) were transplanted either

59 In the spontaneous B16 melanoma cell lines, expression of p16Ink4a and p19A

60 cient mice displayed significantly decreased B16 melanoma cell metastasis to the lung, whereas treatm

61 eritoneal macrophages capable of suppressing B16 melanoma cell proliferation in vitro, an effect that

62 sis factor-alpha from MDSCs are required for B16 melanoma cell proliferation in vitro.

63 In vitro modification of B16 melanoma cell surface uPA activity has been shown to

64 rd, the cells were transfected with DNA from B16 melanoma cells (H-2b).

65 other non-T non-B cells in the rejection of B16 melanoma cells after exogenous administration of IL-

66 B16 melanoma cells and B16-enhanced green fluorescent pr

67 DC1s loaded with B16 melanoma cells and injected into tumor-bearing mice

68 erated IL-35-producing plasmacytoma J558 and B16 melanoma cells and observed that the expression of I

69 esions only in the brain parenchyma, whereas B16 melanoma cells and the somatic hybrid cells of B16 x

70 of common genes in the 48 h RA-treatment of B16 melanoma cells and untreated B16 vs. melan-a data se

71 In fluorescence mode, B16 melanoma cells appeared as dark objects in the brigh

72 JAM-C expressed on both murine B16 melanoma cells as well as on endothelial cells promo

73 miR-21 regulates the metastatic behavior of B16 melanoma cells by promoting cell proliferation, surv

74 cient mutant mice, sialyl Lewis X-expressing B16 melanoma cells colonized the lung, and IELLQAR inhib

75 ailed to reject, arguing that the killing of B16 melanoma cells could occur either via the cytotoxic

76 cAMP in NC and B16 melanoma cells decreased CtBP2 protein levels, while

77 by vaccination of recipients with irradiated B16 melanoma cells engineered to secrete granulocyte-mac

78 Vaccination with irradiated B16 melanoma cells expressing either GM-CSF (Gvax) or Fl

79 The adhesion of HL-60 and B16 melanoma cells expressing sialyl Lewis X to E-select

80 Consistent with these results, B16 melanoma cells expressing WNT3A also exhibit decreas

81 cantly influence the metastatic potential of B16 melanoma cells in a murine model.

82 B16 melanoma cells incubated with filipin (0.16-0.3 micr

83 Injection of B16 melanoma cells into the left cardiac ventricle resul

84 ty of pulmonary metastasis in mice receiving B16 melanoma cells is strongly influenced by the IL-4 re

85 COS7 and B16 melanoma cells lack myosin IIA and IIB, respectively

86 Binding to the B16 melanoma cells occurred at a lipid composition that

87 We previously showed that B16 melanoma cells produce ecotropic melanoma-associated

88 Lastly, vaccination with GM-CSF-secreting B16 melanoma cells stimulated high-titer antibodies to A

89 ly properties and cytotoxic activity against B16 melanoma cells than paclitaxel.

90 ies, Stat3beta, induced cell death in murine B16 melanoma cells that harbored activated Stat3.

91 to reverse MDR was investigated using murine B16 melanoma cells that were transfected with the human

92 lysed tumors efficiently, and metastasis of B16 melanoma cells to draining lymph nodes was suppresse

93 d highly enriched apoptotic versus lysate of B16 melanoma cells to examine whether or not there are i

94 Here, we used murine B16 melanoma cells to observe functional aspects of how

95 he lung, we observed decreased metastasis of B16 melanoma cells to the lung by treatment with a mAb b

96 ynebacterium parvum adjuvant, and irradiated B16 melanoma cells transduced with the gene for granuloc

97 Deletion of p205 in B16 melanoma cells using CRISPR/Cas9 showed a similar lo

98 -glycoprotein inhibits melanin production by B16 melanoma cells via post-transcriptional effects on t

99 bcutaneous challenge injection of unmodified B16 melanoma cells was performed 15 d later.

100 1 in the invasive and metastatic capacity of B16 melanoma cells we analyzed local tumor growth and pu

101 Melanotic PC1A and amelanotic B16 melanoma cells were incubated with increasing concen

102 o, empty vector- and antagomiR-21-transduced B16 melanoma cells were injected via tail vein into syng

103 organ-specific manner, we transduced murine B16 melanoma cells with CXCR4 (CXCR4-B16) and followed t

104 d for their ability to inhibit the growth of B16 melanoma cells with the most potent and selective HD

105 n of microtubules, their cytotoxicity toward B16 melanoma cells, and their solubility in water.

106 an lead to very high targeting efficiency to B16 melanoma cells, both in vitro and in vivo.

107 s into mice targeted HIV envelope-expressing B16 melanoma cells, but not normal tissue or envelope-ne

108 induced either with MCA or by inoculation of B16 melanoma cells, compared with mice with IFN-gamma-co

109 In the ex vivo tumor vaccine approach, B16 melanoma cells, transduced in vitro by adenovirus co

110 Murine B16 melanoma cells, which overproduce TGFbeta, were lyse

111 sed metastases in response to challenge with B16 melanoma cells.

112 non-malignant melan-a mouse melanocytes and B16 melanoma cells.

113 n mediating the biological activity of RA in B16 melanoma cells.

114 n expression in several cell types including B16 melanoma cells.

115 cted from subsequent challenge by unmodified B16 melanoma cells.

116 injected with CD48(+) and CD48(-) metastatic B16 melanoma cells.

117 eans of delivering gelonin to the cytosol of B16 melanoma cells.

118 einococcus radiodurans as well as from mouse B16 melanoma cells.

119 arious protein fractions of melanosomes from B16 melanoma cells.

120 ving high levels of luciferase expression in B16 melanoma cells.

121 o 17 microM in relatively insensitive murine B16 melanoma cells.

122 gene of an ecotropic retrovirus produced by B16 melanoma cells.

123 cells using Matrigel plugs supplemented with B16 melanoma cells.

124 lmonary metastases after i.v. injection with B16 melanoma cells.

125 h HLA-A2(neg) tumor (MC38 colon carcinoma or B16 melanoma) cells are not recognized by the CD8(+) T c

126 rotein-2 to protect mice against intravenous B16 melanoma challenge.

127 2 antigens induced only partial rejection of B16 melanoma challenge.

128 ulfur pair was evaluated in vivo against the B16 melanoma, colon carcinoma 26, and M5076 sarcoma muri

129 nogenic in generating antitumor responses to B16 melanoma, compared with DCs from wild-type mice.

130 lymphoid tissue chemokine (SLC) into growing B16 melanoma could result in a substantial, sustained in

131 Immunity elicited by B16 melanoma cross-reacted with a distinct syngeneic mel

132 ted gene therapy for treatment of metastatic B16 melanomas, established in syngeneic C57BL/6 mice, wa

133 nergize when used in combination in treating B16 melanoma even in the context of CD25+ regulatory T-c

134 ficient (C1qa(-/-)) mice bearing a syngeneic B16 melanoma exhibit a slower tumour growth and prolonge

135 the endothelium in MCA/129 fibrosarcomas and B16 melanomas exhibits a wild-type apoptotic phenotype i

136 B16 melanomas expressing Tyrp1-WM induced minimal T-cell

137 oral administration of ISF35 in subcutaneous B16 melanomas generates tumor-specific, CD8(+) T cells t

138 Lewis lung carcinoma (LLC) or B16 melanoma grafted in KOR knockout mice showed increas

139 ided evidence that MCA/129 fibrosarcomas and B16 melanomas grow 2- to 4-fold faster in acid sphingomy

140 0.3-10 mg/kg dose ranges) activities against B16 melanoma growth in C57BL/6 mice and P388D1 leukemia

141 expression of full-length ADAMTS5 suppressed B16 melanoma growth in mice.

142 growth factor-induced neovascularization and B16 melanoma growth in syngeneic mice are also substanti

143 ective at controlling Listeria infection and B16 melanoma growth in vivo, and they could provide help

144 rs of gp100-specific T cells that suppressed B16 melanoma growth.

145 ssed subcutaneous MB49-bladder carcinoma and B16-melanoma growth and prolonged survival.

146 wth of CT26 (colon adenocarcinoma; H-2d) and B16 (melanoma; H-2b) murine s.c. tumors is significantly

147 Treated mice were also protected against B16 melanoma hepatic metastases.

148 injection into subcutaneous solid tumors of B16 melanoma in a mouse model showed that pH-sensitive l

149 CD8+ T cells and able to enhance control of B16 melanoma in a therapeutic autologous vaccination mod

150 ll kill = 2.3 and 2.0, respectively) against B16 melanoma in B6D2F1 mice via intravenous administrati

151 tive against L1210 leukemia and subcutaneous B16 melanoma in mice.

152 f DC-HIL delays the growth of transplantable B16 melanoma in syngeneic mice, which is accompanied by

153 report that growth of the poorly immunogenic B16 melanoma in the absence of regulatory T cells (T(reg

154 s either alone in promoting the rejection of B16 melanomas in conjunction with Fvax.

155 S-deficient, mice exhibited slower growth of B16 melanomas in response to a PD-L1 antibody treatment.

156 we show that lymphatic drainage from murine B16 melanomas in syngeneic, immune-competent C57Bl/6 mic

157 an survival of mice with EGFRvIII-expressing B16 melanomas in the brain; however, treatment with a si

158 s from Ceacam1-deficient mice implanted with B16 melanoma, increasing the infiltration of Gr1(+)CD11b

159 These mice rejected a lethal challenge of B16 melanoma, indicating the immune response against TRP

160 on proliferation of cancer cells, including B16 melanoma, Lewis lung carcinoma and transgenic mouse

161 in mice bearing established OVA-transfected B16 melanoma lung metastases.

162 ng Zeb2 in NK cells were more susceptible to B16 melanoma lung metastases.

163 f the injected lesion as well as the distant B16 melanoma lung metastases.

164 revent development or mediate eradication of B16 melanoma lung pseudometastases.

165 is hypothesis using sialyl Lewis X-dependent B16 melanoma lung targeting and its inhibition with sele

166 ors, including the P388 and L1210 leukemias, B16 melanoma, M109 lung carcinoma, and M5076 reticulum c

167 delayed tumor recurrence in mouse models of B16 melanoma, MB49 bladder cancer, and CT26 colon cancer

168 supernatants (SN) of murine tumor cell lines B16 (melanoma), MCA207, and MCA102 (fibrosarcoma) increa

169 Successful immunotherapy of established B16 melanoma metastases in C57BL/6 mice can be achieved

170 Resistance to experimental B16 melanoma metastases was not affected by treatment wi

171 n-2 peptide results in enhanced reduction of B16 melanoma metastases; the effect is most pronounced i

172 xamine the immunoregulatory role of MDSCs in B16 melanoma metastasis and Nippostrongylus brasiliensis

173 and CD8(+) T and B lymphocytes, and reduced B16 melanoma metastasis in the lung.

174 ells to paclitaxel and significantly reduced B16 melanoma metastasis in vivo.

175 As a result, B16 melanoma metastasis to the liver was almost complete

176 subcutaneous syngeneic grafts, specifically, B16 melanoma, MO5076 sarcoma, and COLON26 carcinoma.

177 e an underlying immune mechanism, the murine B16 melanoma model and the MT-901 breast cancer model we

178 differences between the EG7 and the previous B16 melanoma model are discussed.

179 (+) T cells in the immunotherapy-susceptible B16 melanoma model in response to checkpoint blockade.

180 , sensitive, and reproducible bioluminescent B16 melanoma model that allows for serial, real-time ana

181 We then used the murine B16 melanoma model to investigate the potential antitumo

182 We have used the preclinical transplantable B16 melanoma model to profile chemokines in tumor lesion

183 In B16 melanoma model, intratumor VBL injection induced apo

184 Using the mouse B16 melanoma model, we found that post-HSCT DNA immuniza

185 Using the B16 melanoma model, we found that vaccination elicited p

186 in both RelB-/- and NIK-/- mice by using the B16 melanoma model.

187 ribute to the antitumor effect of CpG in the B16 melanoma model.

188 Using an OVA-transfected B16-melanoma model, we show that tumor-reactive Tc2 effe

189 m survivors were noted in L1210 leukemia and B16 melanoma models, and both complete and partial tumor

190 t advanced tumors in OT-I/B16-OVA and Pmel-1/B16 melanoma models.

191 knockout mice producing anti-Gal and bearing B16 melanoma or B16/OVA producing OVA as a surrogate tum

192 etion of P2X7R in the mouse on the growth of B16 melanoma or CT26 colon carcinoma cells.

193 ed in DC-flk1-immunized mice challenged with B16 melanoma or Lewis lung carcinoma cells.

194 a, and HT-29 colon carcinoma, but not murine B16 melanoma or P388 leukemia.

195 C57BL/6 (B6) mice were fused with syngeneic B16 melanoma or RMA-S lymphoma cells by polyethylene gly

196 Similarly, STING failed to promote growth of B16 melanoma or to induce IDO activity in TDLN in this s

197 PD-L1-blocking antibodies in the control of B16 melanoma, or EL4 lymphoma, in primary tumor and meta

198 was effective at delaying the growth of s.c. B16 melanomas, orthotopic 4T1 mammary carcinomas, and re

199 nce inhibition of established, vascularized, B16 melanoma (P = 0.009) and improve survival (P = 0.003

200 reased the life span of mice inoculated with B16 melanoma, P388 leukemia, and Adriamycin-resistant P3

201 icantly suppresses outgrowth of experimental B16 melanoma pulmonary metastases as well as growth of s

202 GITR-stimulated hosts that were primed with B16 melanoma rejected B16, but not the unrelated JBRH me

203 extent, Lewis lung carcinoma cells, whereas B16 melanomas showed little to no BM contribution.

204 ich encodes anti-CD137 scFv into established B16 melanomas, significantly prolonged the survival of t

205 umor models, CT26 (colon adenocarcinoma) and B16 (melanoma), that the number and activation state of

206 i.v. in mice bearing CT26 colon carcinoma or B16 melanoma, the 4PD nanoparticles predominantly accumu

207 In vivo, using a model of established B16 melanoma, the combination of an IDO-inhibitor drug p

208 essing a recombinant HLA-A*0201 molecule and B16 melanoma transfected to express this molecule.

209 Systemic treatment with i.p. Y10 of s.c. B16 melanomas transfected to express stably the murine E

210 on are not inhibited by the presence of live B16 melanoma tumor cells, and tumor-loaded DC1s induce d

211 e CTL and induce protective immunity against B16 melanoma tumor cells.

212 antibody, we demonstrate a striking delay in B16 melanoma tumor growth and increased overall survival

213 owed that dual costimulation therapy reduced B16 melanoma tumor growth while increasing IL-36R gene e

214 R(hi) T cells initially delayed subcutaneous B16 melanoma tumor growth.

215 Using a murine B16 melanoma tumor model, we show that a variant of FUS

216 -linking antibody using a poorly immunogenic B16 melanoma tumor model.

217 adult mice using CD20 mAb prior to syngeneic B16 melanoma tumor transfers.

218 wing TBI-induced lymphopenia was measured in B16 melanoma tumor-bearing mice.

219 significantly inhibit the development of the B16 melanoma tumor.

220 When challenged with B16 melanoma, tumor growth was delayed in TEM8(-/-) mice

221 ted into both endometriosis lesions and into B16 melanoma tumors and enhanced their growth at 8 days

222 primary murine Lewis lung, 4T1 mammary, and B16 melanoma tumors and growth of Lewis lung metastases.

223 Mice bearing B16 melanoma tumors expressing the gp100 tumor antigen w

224 (DCT) synergistically eradicated established B16 melanoma tumors in mice and dramatically increased t

225 approximately 83%, p < 0.002) the growth of B16 melanoma tumors in mice at a tolerated oral dose in

226 rmulated interfering RNA for NPRA attenuated B16 melanoma tumors in mice.

227 Finally, mice with pre-established B16 melanoma tumors responded to FIST15 treatment more s

228 urthermore, neither MCA/129 fibrosarcoma nor B16 melanoma tumors showed differences in growth or radi

229 bitor bortezomib could sensitize established B16 melanoma tumors to dendritic cell (DC)-activated imm

230 onses, mice bearing established subcutaneous B16 melanoma tumors were administered TLR9-activated pDC

231 cts, leading to eradication of large (>1 cm) B16 melanoma tumors within 72 h.

232 -1 -/- mice are susceptible to metastasis of B16 melanoma tumors, although their in vitro NK cell act

233 nt efficacy in mice bearing GM-CSF-secreting B16 melanoma tumors.

234 f regressing established, poorly immunogenic B16 melanoma tumors.

235 djuvant controlled the growth of established B16 melanoma tumors.

236 with mgp100 in vitro and treated established B16 melanoma upon adoptive transfer.

237 studied immune responses against the murine B16 melanoma using a tyrosinase-related protein 2 (TRP-2

238 B16 melanoma vaccines genetically engineered to express

239 olecules on a liver-metastasizing subline of B16 melanoma versus the parental B16-F0 revealed unique

240 recognized by MM2-9B6 monoclonal antibody in B16 melanoma was closely associated with C-type ecotropi

241 ells on experimental pulmonary metastasis of B16 melanoma was investigated in a murine model implante

242 arance was never achieved, growth kinetic of B16 melanoma was markedly reduced in C57BL/6 mice by int

243 Using the D5 subline of B16 melanoma, we demonstrate that DCs pulsed with both K

244 In CD47-deficient syngeneic hosts, engrafted B16 melanomas were 50% more sensitive to irradiation, es

245 with a suicide gene therapy and subcutaneous B16 melanomas were directly injected with (i) IL-2/recom

246 minigene construct of hgp100(25-33) rejected B16 melanoma, whereas mice immunized with the mgp100(25-

247 d protein 2 (TRP-2), expressed by the murine B16 melanoma which was found by screening a cDNA library

248 urine tumor lines (4T1 mammary carcinoma and B16 melanoma), which constitutively expressed GFP, in do

249 DCs to generate protective immunity against B16 melanoma, which expresses murine MART-1, was also ab

250 into lymphopenic mice leads to rejection of B16 melanoma, which generated an opportunity to study ho

251 equent challenge with human gp100-transduced B16 melanoma, which involves both CD4(+) and CD8(+) T-ce

252 sp110-gp100 vaccine in mice established with B16 melanoma, which was accompanied by enhanced activati

253 I]IPBS was studied in C57 black mice bearing B16 melanoma xenograft.