ライフサイエンスコーパス: tumor antigen

1 t recovery of cells expressing low levels of tumor antigen.

2 accharide that was proposed to be a prostate tumor antigen.

3 of T cells that cross-react with the native tumor antigen.

4 response against a naturally occurring mouse tumor antigen.

5 T cells that have increased avidity for the tumor antigen.

6 t do not crossreact or have low affinity for tumor antigen.

7 react with or that have low affinity for the tumor antigen.

8 xpressing ovalbumin (E.G7-OVA) as a specific tumor antigen.

9 f endogenous T cells specific for the native tumor antigen.

10 dies affinity-matured in a healthy host to a tumor antigen.

11 ostatic acid phosphatase (PAP) is a prostate tumor antigen.

12 anzyme-B and interferon-gamma in response to tumor antigens.

13 e responses is the induction of tolerance to tumor antigens.

14 sion, loss of which inhibits presentation of tumor antigens.

15 Treg) that contribute to immune tolerance of tumor antigens.

16 e context of therapeutic vaccination against tumor antigens.

17 end), typically found in Globo H and related tumor antigens.

18 itory pathways in tolerance to both self and tumor antigens.

19 cells and does not require identification of tumor antigens.

20 s by targeting immune cells, irrespective of tumor antigens.

21 ad-based therapeutic targeting of tolerizing tumor antigens.

22 PD-1:T-bet ratio increased upon exposure to tumor antigens.

23 ed to redirect the specificity of T cells to tumor antigens.

24 lopment of long-term CD8(+) T-cell memory to tumor antigens.

25 activate Tms without extensive knowledge of tumor antigens.

26 differential intrinsic immune reactivity to tumor antigens.

27 pulations, as well as other liquid and solid tumor antigens.

28 th CAR T cells that are redirected to single tumor antigens.

29 ls of human solid tumors expressing relevant tumor antigens.

30 ccine strategies targeting tissue-restricted tumor antigens.

31 s to weakly immunogenic and poorly expressed tumor antigens.

32 CD8+ T cells by preventing MHC I display of tumor antigens.

33 ature associated with T cell priming against tumor antigens.

34 sed on our ability to direct T cells against tumor antigens.

35 osuppression and enhance T-cell responses to tumor antigens.

36 These events can result in formation of tumor antigens.

37 Although metastasis tumor antigen 1 (MTA1) contributes to the responsiveness

38 static chromatin modifier protein metastasis tumor antigen 1 (MTA1) in human cancer contributes to tu

39 Metastasis tumor antigen 1 (MTA1), a component of the Mi-2.nucleoso

40 Although both metastatic tumor antigen 1 (MTA1), a master chromatin modifier, and

41 iR-661 inhibits the expression of metastatic tumor antigen 1 (MTA1), a widely up-regulated gene produ

42 Recently, vaccines against the Wilms Tumor antigen 1 (WT1) have been tested in cancer patient

43 s as well as cytoplasmic level of metastatic tumor antigen 1 short form (MTA1s) are elevated in human

44 The MTA1 coregulator (metastatic tumor antigen 1), a component of the nucleosome remodeli

45 und for the first time that MTA1 (metastatic tumor antigen 1), a master chromatin modifier, regulates

46 melanoma model targeting naturally occurring tumor antigens.2,3

47 rs of chemoresponsiveness, we identified the tumor antigen acrosin binding protein (ACRBP)/OY-TES-1 a

48 Lymphocytic immune responses to tumor antigens also trended to higher level in the tumor

49 ng lymphocytes (TILs) that recognize a model tumor antigen and have features of both activation and f

50 success depends on both the presence of the tumor antigen and its accessibility by the antibody.

51 f cancerous cells expressing lower levels of tumor antigen and should have general application in enh

52 The two major components, tumor antigens and adjuvant, are presented concurrently

53 struction through loss or down-regulation of tumor antigens and antigen-presenting major histocompati

54 These findings could apply to other tumor antigens and are relevant for vaccination strategi

55 esponse, we elucidated the dynamic nature of tumor antigens and autoantibody interactions.

56 (i.e., Flagrp170) is capable of transporting tumor antigens and concurrently inducing functional acti

57 herapeutic strategy to overcome tolerance to tumor antigens and elicit a strong immunity against MCL

58 lf-peptides as pathophysiologically relevant tumor antigens and encourages their implementation for c

59 of invading peripheral tissue can recognize tumor antigens and exert cytotoxic functions there.

60 for cross-presentation of ablation-released tumor antigens and for the induction of long-term antitu

61 oss-present clinically relevant, full-length tumor antigens and how vaccine formulation impacts CTL r

62 Dual-antigen targeting increases targetable tumor antigens and reduces the risk of antigen-negative

63 cines enhance the response of T cells toward tumor antigens and represent a strategy to augment antig

64 enhances the processing and presentation of tumor antigens and thereby stimulates anti-tumor immunit

65 ospinal fluid (CSF) that are specific to the tumor antigen, and treatment with the immunosuppressant

66 restore responses of HCC-derived T cells to tumor antigens, and combinations of the antibodies have

67 to accumulate in tumors, become activated by tumor antigens, and to express the cytolytic factor gran

68 We find that a combination of an anti-tumor antigen antibody and an untargeted IL-2 fusion pro

69 However, many commonly targeted tumor antigens are also expressed by healthy tissues, an

70 immunogenic antigens is more challenging, as tumor antigens are generally weak, and high avidity T ce

71 T cells directed to endogenous tumor antigens are powerful mediators of tumor regressio

72 Tumor antigens are proteins selectively expressed by tum

73 r vaccines is primarily due to the fact that tumor antigens are variations of self proteins and would

74 ECENT FINDINGS: Strategies including bladder tumor antigen assay, NMP22, ImmunoCyt, and UroVysion hol

75 injections of pDCs activated and loaded with tumor antigen-associated peptides ex vivo.

76 ubstantial enthusiasm for the development of tumor antigen-based vaccines for the treatment of cancer

77 ces in numbers of mutations or expression of tumor antigens between the immune-specific class and oth

78 ells with the mimotope, followed by a native tumor-antigen boost, improves tumor immunity compared wi

79 s demonstrated remarkable efficacy targeting tumor antigens, but immunogenicity and endogenous biotin

80 ial site for the development of tolerance to tumor antigens, but there remains incomplete knowledge a

81 tricted epitopes within the same full-length tumor antigen by human DCs.

82 ection by impairing indirect presentation of tumor antigen by infiltrating macrophages.

83 cer cells requires efficient presentation of tumor antigens by human leukocyte antigen class I (HLA-I

84 tients with metastatic cancer expressing the tumor antigen carcinoembryonic antigen (CEA) and that it

85 fibronectin domains) targeting two different tumor antigens (carcinoembryonic antigen and EGF recepto

86 tigen receptors (CAR) specific to the B cell tumor antigen CD19 can successfully eradicate systemic h

87 ncer (EOC) and is among the most immunogenic tumor antigens defined to date.

88 Subsequent tumor antigen delivery to the draining LN resulted in CD

89 of effector and costimulatory molecules in a tumor antigen-dependent manner.

90 IRX-2-matured DC carried a higher density of tumor antigen-derived peptides, and CTL primed with thes

91 T cells targeting viral tumor antigens did not display preferential in vivo expa

92 lanoma cell lysate was used to load DCs with tumor antigens during exosome production together with p

93 Mimotopes, or peptide mimics of tumor antigens, elicit increased numbers of T cells that

94 ents also developed responses to nontargeted tumor antigens (epitope spreading).

95 ue to their ability to selectively recognize tumor antigens, expand and persist to provide long-term

96 MUC1 is a shared tumor antigen expressed on >80% of human cancers.

97 at selectively recruit gammadelta T cells to tumor antigens expressed by cancer cells illustrate the

98 igen receptors (CARs) targeting a variety of tumor antigens expressed in cancer patients.

99 In this study, autoantibody response and tumor antigen expression are associated.

100 Many of the most promising tumor antigens for T-cell-based cancer immunotherapies a

101 Here we investigated the MART-1(27-35) tumor antigen, for which anchor modification (replacemen

102 Dendritic cells (DC) loaded with tumor antigens from apoptotic/necrotic tumor cells are c

103 cells, whereas CAR-T cells specific for the tumor antigen GD2 (GD2.CAR-T cells) were not damaged.

104 ral genomes have a tumor-specific pattern of tumor antigen gene mutation that incapacitates viral DNA

105 ancies requires CD4(+) T-cell help, but weak tumor antigens generally fail to induce adequate T-cell

106 and sustained transcription of the oncogenic tumor antigen genes, we cultured primary raccoon tumor c

107 mor vasculature and T-cells specific for the tumor antigens gp100 (PMEL), TRP-1 (TYRP1), or TRP-2 (DC

108 V infection, but the immune response to this tumor antigen has been significantly altered in nasophar

109 ion of mutated and aberrantly expressed self-tumor antigens has historically been time consuming and

110 Immuno-PET imaging of the tumor antigen HER2/neu allows for the noninvasive detect

111 ed with TCRs of incremental affinity for the tumor antigen HLA-A2/NY-ESO-1, we investigated the molec

112 increase in effector T cells recognizing the tumor antigens IGFBP2 and FRalpha, indicating that MV-NI

113 One of these proteins, L23, a novel tumor antigen in SCCHN, was validated as an oncogene.

114 Whereas fetuin-A is an established tumor antigen in several types of cancer, including brea

115 e vaccine formulation would deliver multiple tumor antigens in a fashion that potently stimulates end

116 ector function longitudinally in response to tumor antigens in living mice.

117 8(+) T-cell responses to multiple endogenous tumor antigens in poorly immunogenic mouse carcinomas.

118 Identification of novel tumor antigens in SCCHN will facilitate the identificati

119 antitumor immunity against in situ released tumor antigens in the absence or presence of the Toll-li

120 ming of CD8(+) T-cells that recognize shared tumor antigens in the context of host MHC class I molecu

121 requires the release of a broad spectrum of tumor antigens in the context of potent immune activatio

122 f functional T cells that recognize multiple tumor antigens, including HPV16 E7, and these T cells pr

123 lating rare CTCs from blood samples by using tumor antigen-independent microfluidic CTC-iChip technol

124 The molecular identification of tumor antigens initially catalyzed substantial enthusias

125 urface, thereby facilitating the transfer of tumor antigens into dendritic cells.

126 these infiltrating T cells are specific for tumor antigens is not known.

127 ome functionally exhausted owing to the high tumor-antigen load and accompanying inhibitory mechanism

128 noma DC-based immunotherapy is enhanced when tumor antigen-loaded DCs used for vaccination express cP

129 Simian virus 40 (SV40) large tumor antigen (LT) triggers oncogenic transformation by

130 frequently results in mutations in the large tumor antigen (LT), leading to expression of a truncated

131 T(H)17 (IL-17(+)) response to the important tumor antigen MAGE-A3, which occurred concurrently with

132 s capable of delivering autologously derived tumor antigen material together with a highly immunostim

133 lar mechanisms have been attributed to MCPyV tumor antigen-mediated cellular transformation or replic

134 ith peptides derived from the major melanoma tumor antigens, MelA/MART-1, gp100/pmel17, tyrosinase, a

135 transduced with CARs specific for the human tumor antigen mesothelin showed greatly enhanced cytokin

136 ) T cell response to the recently identified tumor antigen Midkine (MDK).

137 The CD4 T cell response to the tumor antigen Midkine was unknown.

138 ck against large tumors carrying a surrogate tumor antigen (mimicking a "passenger" mutation) by T(E)

139 Using a defined tumor antigen model, UV-8101-RE, we found that concomita

140 ides and glycopeptides from the common human tumor antigen MUC1, a mucin that is coated with O-linked

141 Here, we used the human tumor antigen NY-ESO-1 (ESO) and the human leukocyte ant

142 nses directed against the well-characterized tumor antigen NY-ESO-1.

143 set that directly recognizes the cytoplasmic tumor antigen, NY-ESO-1, presented by MHC class II on ca

144 ne such mimotope of the dominant MHC class I tumor antigen of a mouse colon carcinoma cell line stimu

145 investigated whether the HCC-associated self/tumor antigen of alpha-fetoprotein (AFP) could be engine

146 r a foreign (ova) antigen or fully syngeneic tumor antigens (on Panc02 tumor cells), provided that Tr

147 ted in vitro using the viral helicase (large tumor antigen, or Tag) and purified human proteins.

148 Vaccines that incorporate peptide mimics of tumor antigens, or mimotope vaccines, are commonly used

149 lished brain tumors expressing the surrogate tumor antigen ovalbumin and labeled antigen-specific ant

150 aive T cells specific for exogenous and self/tumor antigens persist in the host and contribute to per

151 bundance of CD4(+) T cells specific for self-tumor antigen positively correlated with antitumor effic

152 The role of the HLA system in tumor antigen presentation could be involved in suscepti

153 The nature and site of tumor-antigen presentation to immune T cells by bone-mar

154 Intracellular tumor antigens presented on the cell surface in the cont

155 facilitated interactions between T cells and tumor-antigen-presenting dendritic cells (DCs).

156 e were vaccinated with magnetically labeled, tumor antigen-primed dendritic cells (DCs).

157 ing first generation DC vaccines pulsed with tumor antigens provided a proof-of-principle that therap

158 Using the prostate tumor antigens PSMA and PSCA, we show that co-transduced

159 owever, peptide vaccines that include native tumor antigens rarely prevent tumor growth.

160 who respond to vaccination directed against tumor antigens recognized by T cells.

161 y for enhancing adaptive immune responses to tumor antigens released by radiotherapy.

162 ment of T-cell vaccines against pathogen and tumor antigens remains challenged by inefficient identif

163 monoclonal antibody (mAb) therapy targeting tumor antigens represents a gold standard for assessing

164 -2 (TRP-2, Dct) harbor T cells that maintain tumor antigen responsiveness but lack the ability to con

165 cells de novo primed for only 7 days against tumor antigens resulted in the durable rejection of othe

166 s of T cells that crossreact with the native tumor antigen, resulting in potent antitumor responses.

167 eutic monoclonal antibodies (mAbs) targeting tumor antigens results primarily from their ability to e

168 AML following allogeneic HCT and suggests a tumor antigen role.

169 mor cells were phagocytosed, delivering both tumor antigen(s) and the immunostimulatory CpG molecule

170 eptides, induces a T-cell population that is tumor antigen specific.

171 to overcome this suppression and/or enhance tumor-antigen specific T cell responses has shown promis

172 y molecules to license effector functions of tumor-antigen specific T cells.

173 , we determined that TIGIT is upregulated on tumor antigen-specific (TA-specific) CD8(+) T cells and

174 -alpha expression delineates a population of tumor antigen-specific (TA-specific) cytotoxic T lymphoc

175 feasible to modify T cells to secrete solid tumor antigen-specific BITEs, enabling T cells to redire

176 CTLA4-CD28 chimera gene modification of both tumor antigen-specific CD4 and CD8 T cells would be an i

177 Tumor antigen-specific CD4(+) T cells generally orchestr

178 hey suggest a differentiation model in which tumor antigen-specific CD4(+) T cells that are primed un

179 eficiency blunted the induction of anergy in tumor antigen-specific CD4+ T cells, enhancing antitumor

180 Immunotherapy based on adoptive transfer of tumor antigen-specific CD8(+) T cell (TC) is generally l

181 n, TLR7/RT therapy leads to the expansion of tumor antigen-specific CD8(+) T cells and improved survi

182 d led to a synergistic increase in total and tumor antigen-specific CD8(+) T cells expressing both IF

183 Yet a fundamental feature of most tumor antigen-specific CD8(+) T cells is that this avidi

184 treatment combined with adoptive transfer of tumor antigen-specific CD8(+) T cells led to elimination

185 T-cell responses detected ex vivo, however, tumor antigen-specific CD8(+) T cells produced more IFN-

186 se (RTK) inhibitor, and adoptive transfer of tumor antigen-specific CD8(+) T cells to eliminate HCC.

187 Although melanoma vaccines stimulate tumor antigen-specific CD8(+) T cells, objective clinica

188 ound to evolve in the presence of autologous tumor antigen-specific CD8(+) T cells.

189 Both vaccines stimulated rapid tumor antigen-specific CD8(+) T-cell responses detected

190 ectly through the STAT3 pathway and prevents tumor antigen-specific CD8(+) T-cell tolerance, thus def

191 s LAG-3 and 4-1BB can identify dysfunctional tumor antigen-specific CD8(+) TIL.

192 of ex vivo-activated adoptively transferred tumor antigen-specific CD8+ T cell killing of cognate an

193 The phenotype and proliferative ability of tumor antigen-specific CD8+ T cells was assessed in the

194 Treg subset was enriched in the fraction of tumor antigen-specific cells in the dLN, where they disp

195 ation suggested that CD4(+) T cells included tumor antigen-specific cells, which may be generated by

196 focused, functional heterogeneity in active tumor antigen-specific CTLs, with the major functional p

197 of a dozen effector molecules secreted from tumor antigen-specific cytotoxic T lymphocytes (CTLs) th

198 with increased proliferation and function of tumor antigen-specific effector CD8(+) T cells, inhibiti

199 d a population of Th1 cytokine producing and tumor antigen-specific effector cells.

200 ity is strongly influenced by the balance of tumor antigen-specific effector T cells (Teff) and regul

201 ased bifunctional switches that consist of a tumor antigen-specific Fab molecule engrafted with a pep

202 Recently, tumor antigen-specific IgEs were reported to restrict ca

203 Unlike IgG1, an engineered tumor antigen-specific IgG4 was ineffective in triggerin

204 The paradoxical coexistence of spontaneous tumor antigen-specific immune responses with progressive

205 njections of CpG-Stat3 siRNA generate potent tumor antigen-specific immune responses, increase the ra

206 pression with concurrent approaches to favor tumor antigen-specific immune responses, such as vaccine

207 well as improving the antitumor activity of tumor antigen-specific lymphocytes.

208 outcomes were associated with induction of a tumor antigen-specific memory immune response.

209 mined using an ex-vivo model system in which tumor antigen-specific primary CD8(+) T cell responses w

210 spondingly, cps treatment markedly increased tumor antigen-specific responses by CD8(+) T cells.

211 de of TGF-beta signaling in T cells enhanced tumor antigen-specific T cell responses and inhibited tu

212 -specific T-cell activation ex vivo and that tumor antigen-specific T cells could only be isolated fr

213 ed and distal tumors, enhanced activation of tumor antigen-specific T cells in draining lymph nodes,

214 ells and silencing of STAT3, which activated tumor antigen-specific T cells in murine models.

215 or persistence of the adoptively transferred tumor antigen-specific T cells in the tumor microenviron

216 was associated with enhanced accumulation of tumor antigen-specific T cells in the tumor microenviron

217 Both viral and nonviral tumor antigen-specific T cells resided predominantly in

218 ovel CTLA4 mutant that could be expressed in tumor antigen-specific T cells to enhance antitumor effe

219 t to be dispensable for the proliferation of tumor antigen-specific T cells within neoplastic lesions

220 maturation, T-cell activation, generation of tumor antigen-specific T cells, and long-lasting antitum

221 Immune checkpoint therapies target tumor antigen-specific T cells, but less is known about

222 ion of effector CD8(+) T cells that included tumor antigen-specific T cells.

223 nced tumor cell lysis and expansion of human tumor antigen-specific T cells.

224 at can predict the conversion of short-lived tumor antigen-specific T effector cells into long-lived

225 is being investigated, but the existence of tumor antigen-specific T(H)17 cells has yet to be ascert

226 Notably, these reagents rescued tumor antigen-specific T-cell activation, which was othe

227 robust proliferation, resulting in increased tumor antigen-specific T-cell activity and tumor growth

228 Although adoptive transfer of autologous tumor antigen-specific T-cell immunotherapy can produce

229 Retroviral transduction of tumor antigen-specific T-cell receptor (TCR) genes into

230 Tumor antigen-specific T-cell responses were confirmed i

231 indings indicate that chemoradiation induces tumor antigen-specific T-cell responses, and HMGB1 produ

232 levels of Tregs while specifically enhancing tumor antigen-specific T-cell responses.

233 T-cell activation rather than the priming of tumor antigen-specific T-cell responses.

234 iable human lung tumor slices and autologous tumor antigen-specific T-lymphocyte clones to provide ev

235 -L1 was associated with increased numbers of tumor antigen-specific tetramer-positive CD8 T cells, in

236 dritic cell (DC) vaccine failed to develop a tumor-antigen-specific CD4 and CD8 T-cell immune respons

237 Adoptive transfer of tumor-antigen-specific T(H)9 cells into both WT and Rag1

238 CC, respectively, which contributed to local tumor-antigen-specific tolerance.

239 Notably, the tumor-antigen specificities and TCR repertoires of the c

240 Therapeutic activity required tumor antigen specificity and perforin expression by the

241 We demonstrate that the MCPyV small tumor antigen (ST) promotes the destabilization of the h

242 ion of tumor-promoting simian virus 40 small tumor antigen (ST), a reported PP2A inhibitor, promotes

243 the expression of the MCPyV small and large tumor antigens (ST and LT, respectively).

244 ieve simultaneous cross-linking of CD3 and a tumor antigen such as epithelial cell adhesion molecule

245 odels in which polyclonal antibodies against tumor antigens, such as Neu5Gc, can alter tumor progress

246 Of particular interest are mutated tumor antigen T-cell epitopes, because neoepitope-specif

247 The large tumor antigen (T antigen) encoded by simian virus 40 is

248 Tumor antigen (TA) -targeted monoclonal antibodies (mAb)

249 t that programmed death-1(high) (PD-1(high)) tumor antigen (TA)-specific CD8(+) T cells present at pe

250 We hypothesized that IRX-2 enhanced tumor antigen-(TA)-specific immunity by up-regulating fu

251 pecific antigen simian virus 40 (SV40) large tumor antigen (Tag) following experimental pulmonary met

252 onstitutively express splice variants of the tumor antigen (TAg) gene.

253 ral oncoprotein simian virus 40 (SV40) large tumor antigen (Tag) has previously been described by our

254 ause of the weak activity toward subdominant tumor antigens (TAg) and to tumors expressing suboptimal

255 However, the tumor antigens targeted in successful treatments remain

256 titumor efficacy required four components: a tumor-antigen-targeting antibody, a recombinant interleu

257 ve overcome these limitations by introducing tumor-antigen-targeting receptors into human T lymphocyt

258 tive transfer of T cells specific for native tumor antigens (TAs) is an increasingly popular cancer t

259 ody reactivity against up to 7 out of the 33 tumor antigens tested.

260 tumor protein, WT-1, is a widely recognized tumor antigen that is aberrantly expressed in myeloid an

261 mor protein (WT-1) is widely recognized as a tumor antigen that is expressed differentially by severa

262 Mesothelin is a tumor antigen that is highly expressed in many human can

263 IL-13Ralpha2 is a novel tumor antigen that is overexpressed in a variety of soli

264 d for natural killer cells and T cells and a tumor antigen that is widely expressed among human solid

265 cines are mostly based on native shared-self/tumor antigens that are only able to induce weak immune

266 e is fundamentally no limit to the number of tumor antigens that immune cells can recognize.

267 oss-presentation of systemically circulating tumor antigens that may influence immunotherapy of cance

268 and induce immune responses against broader tumor antigens that may protect against tumor recurrence

269 endow patient's T cells with reactivity for tumor antigens through the stable or regulated introduct

270 rred antigen-specific T cells that recognize tumor antigens through their native receptors have many

271 ns and enables the facile indentification of tumor antigens through unbiased screening.

272 olysaccharide (ZPS) PS A1 and the well-known tumor antigen Tn has been designed, synthesized, and stu

273 a critical role for these DC in trafficking tumor antigen to lymph nodes (LN), resulting in both dir

274 macrophages process and present the secreted tumor antigen to Th1 cells, resulting in induction of ma

275 ndritic cells (DCs) to cross-present protein tumor antigens to cytotoxic T lymphocytes (CTLs) underpi

276 ed subset of conventional DCs that transport tumor antigens to draining lymph nodes and cross-present

277 tumor-derived proteins and present processed tumor antigens to reactive T cells.

278 due to MHC-restricted cross-presentation of tumor antigens to T cells, may be essential.

279 ritic cells to stimulate the presentation of tumor antigens to T cells.

280 id and polymeric nanoparticles for targeting tumor antigens to the dendritic cells.

281 fic T cells by elevating the presentation of tumor antigens to the immune system.

282 y and that it improves cross-presentation of tumor antigens to the immune system.

283 nstruction of DNA vaccines encoding selected tumor antigens together with molecules to direct and amp

284 nes in the tumor, enhanced antibody-mediated tumor antigen uptake and promoted antigen spreading.

285 rm A (36%) developed immune responses to the tumor antigen vaccine by tetramer assays, but this cohor

286 and after transplantation and a multipeptide tumor antigen vaccine derived from the human telomerase

287 Adoptive transfer of tumor antigen vaccine-primed and costimulated T cells le

288 es (ADC) are designed to selectively bind to tumor antigens via the antibody and release their cytoto

289 n with recombinant VACV (rVACV) expressing a tumor antigen was protective against tumor challenge onl

290 Phage-displayed tumor antigens were enriched by biopanning with normal a

291 e cells, specific to multiple viral and self-tumor antigens, were found within a CD45RO(-), CCR7(+),

292 dendritic cells (DCs) are thought to take up tumor antigens, which are processed into peptides and lo

293 Antibody-based therapies targeting tumor antigens will benefit from a better understanding

294 Efforts to identify novel prostate specific tumor antigens will facilitate the development of effect

295 further enhanced by targeting an additional tumor antigen with the VSV-antigen + ACT combination str

296 tro demonstrating the natural association of tumor antigens with alpha(2)M.

297 Combining tumor antigens with an immunostimulant can induce the im

298 rs expressed by T cells mediate tolerance to tumor antigens, with coexpression of these receptors exa

299 ce of infiltrating CD8+ T cells specific for tumor antigens within the tumor microenvironment.

300 oosting the mimotope vaccine with the native tumor antigen would focus the T-cell response elicited b