ライフサイエンスコーパス: B16 melanoma

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

2 nt improvement in antitumor activity against B16 melanoma.

3 able therapeutic effects against established B16 melanoma.

4 fer in treatment of established subcutaneous B16 melanoma.

5 ells better mediated destruction of advanced B16 melanoma.

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

7 RALBP1 causes regression of syngeneic mouse B16 melanoma.

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

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

10 ased protection from a lethal challenge with B16 melanoma.

11 >85% tumor rejection in mice challenged with B16 melanoma.

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

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

14 r antitumor activity in the immunotherapy of B16 melanoma.

15 estigated in mice bearing poorly immunogenic B16 melanoma.

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

17 vival of mice against the poorly immunogenic B16 melanoma.

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

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

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

21 mors established from the poorly immunogenic B16 melanoma.

22 L261 glioma and subcutaneous implants of the B16 melanoma.

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

24 Fats(-/-) macrophages protects mice against B16 melanoma.

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

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

27 ufficient to delay the growth of established B16 melanoma.

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

29 rge pre-established lymphomas and aggressive B16 melanomas.

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

31 ulation to control the growth of established B16 melanomas.

32 ed to surgical excision of large established B16 melanomas.

33 yeloid-derived suppressor cell ratios within B16 melanomas.

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

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

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

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

38 tion of Rasal1 expression in T-cells shrinks B16 melanoma and EL-4 lymphoma tumors, concurrent with a

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

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

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

42 Fats(-/-) mice show reduced subcutaneous B16 melanoma and H7 pancreatic tumor growth compared wit

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

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

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

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

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

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

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

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

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

52 e significantly reduced metastatic burden in B16 melanoma and MPC-11 myeloma models, showing tumor gr

53 NKp46 recognition of ecto-CRT controls mouse B16 melanoma and RAS-driven lung cancers and enhances tu

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

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

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

57 cer, including mice harbouring GL261 glioma, B16 melanoma, and in a spontaneous model of diffuse intr

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

59 y shown that BLS has a therapeutic effect in B16 melanoma-bearing mice only when administered at earl

60 gation and puncture surgery was performed on B16 melanoma-bearing mice to show that sepsis has detrim

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

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

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

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

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

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

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

68 l vein endothelial cells, incubated with the B16 melanoma cell medium for 2 hours, expressed decrease

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

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

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

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

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

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

75 B16 melanoma cells and B16-enhanced green fluorescent pr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 Similar experiments performed with B16 melanoma cells showed higher tumor growth rates in a

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

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

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

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

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

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

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

105 estigated this further by engineering murine B16 melanoma cells to overexpress various IFN-I subtypes

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

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

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

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

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

111 1 in the invasive and metastatic capacity of B16 melanoma cells we analyzed local tumor growth and pu

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

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

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

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

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

117 In B16 melanoma cells, ArhGAP12 suppresses basal Rac and Cd

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

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

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

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

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

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

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

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

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

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

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

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

130 arious protein fractions of melanosomes from B16 melanoma cells.

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

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

133 cted from subsequent challenge by unmodified B16 melanoma cells.

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

135 chemotherapeutic drug oxaliplatin in murine B16 melanoma cells.

136 cells using Matrigel plugs supplemented with B16 melanoma cells.

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

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

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

140 2 antigens induced only partial rejection of B16 melanoma challenge.

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

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

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

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

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

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

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

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

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

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

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

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

153 0.3-10 mg/kg dose ranges) activities against B16 melanoma growth in C57BL/6 mice and P388D1 leukemia

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

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

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

157 surgery renders mice permissive to increased B16 melanoma growth weeks/months after sepsis induction.

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

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

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

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

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

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

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

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

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

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

168 This was used to transfect B16 melanoma in vitro for use in an orthotopic preclinic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

191 matopoietic CD19(+)-A20 lymphoma and CD19(+)-B16 melanoma, mice receiving vancomycin in combination w

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

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

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

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

196 human M14 melanoma xenograft and a syngeneic B16 melanoma model provided significant therapeutic bene

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

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

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

200 As a proof-of-concept, we used the B16 melanoma model to test the system's predictive capab

201 In B16 melanoma model, intratumor VBL injection induced apo

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

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

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

205 ulations of OT-II and OT-I T cells, and in a B16 melanoma model.

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

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

208 )Ac in a human CD20 and ovalbumin expressing B16-melanoma model.

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

210 Using the mouse E0771 breast cancer and B16 melanoma models, we found that both NK and NKT cells

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

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

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

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

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

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

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

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

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

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

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

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

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

224 on in syngeneic mouse tumor models including B16 melanoma, Renca kidney cancer, and Hepa1-6 hepatocel

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

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

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

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

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

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

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

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

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

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

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

236 anscript to enhance ICB efficacy and inhibit B16 melanoma tumor growth.

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

238 or, resulting in a significant inhibition of B16 melanoma tumor growth.

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

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

241 D-L1 significantly impedes DC migration in a B16 melanoma tumor model.

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

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

244 significantly inhibit the development of the B16 melanoma tumor.

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

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

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

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

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

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

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

252 trigger the regression of large, established B16 melanoma tumors in mice.

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

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

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

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

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

258 -1 -/- mice are susceptible to metastasis of B16 melanoma tumors, although their in vitro NK cell act

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

260 f regressing established, poorly immunogenic B16 melanoma tumors.

261 djuvant controlled the growth of established B16 melanoma tumors.

262 -infiltrating and nonspecific CD8 T cells in B16 melanoma tumors.

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

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

265 B16 melanoma vaccines genetically engineered to express

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

267 CMV delayed the growth of poorly immunogenic B16 melanomas via an undefined mechanism.

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

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

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

271 rol of tumor vessels in C57BL/6 mice bearing B16 melanoma was performed using volume expansion (salin

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

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

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

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

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

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

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

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

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

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

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