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 are confirmed for mesothelin as alternative tumor antigen.

10 hallenge is identifying a safe and effective tumor antigen.

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

12 lies on T lymphocyte-mediated recognition of tumor antigens.

13 ls of human solid tumors expressing relevant tumor antigens.

14 vel groups of potentially highly immunogenic tumor antigens.

15 ccine strategies targeting tissue-restricted tumor antigens.

16 erties and allows the sensitive detection of tumor antigens.

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

18 ature associated with T cell priming against tumor antigens.

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

20 These events can result in formation of tumor antigens.

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

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

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

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

25 e context of therapeutic vaccination against tumor antigens.

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

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

28 he absence of T cells specific for displayed tumor antigens.

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

30 ad-based therapeutic targeting of tolerizing tumor antigens.

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

32 n order to activate the immune system toward tumor antigens.

33 s to weakly immunogenic and poorly expressed tumor antigens.

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

35 cells and does not require identification of tumor antigens.

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

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

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

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

40 Overexpression of metastatic tumor antigen 1 (MTA1) was correlated with poor prognosi

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

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

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

44 We therefore isolated a high-affinity Wilms' Tumor Antigen 1-specific TCR (TCR(C4)) from HLA-A2(+) no

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

46 focused on CD4(+) T-cell responses against a tumor antigen, 5T4 oncofetal trophoblast glycoprotein (5

47 ression of underglycosylated mucin 1 (uMUC1) tumor antigen, a biomarker for ovarian cancer progressio

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 pression of PD-L1 in cancer was regulated by tumor antigen and sterile inflammatory cues.

53 Liposomal codelivery of tumor antigen and Toll-like receptor ligand to CD169(+)

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

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

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

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

58 Because tumor antigens and DNA released by dying cancer cells ha

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

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

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

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

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

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

65 ecific for EGFRvIII, a glioblastoma-specific tumor antigen, and a bispecific T-cell engager (BiTE) ag

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

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

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

69 und increased infiltration of both surrogate tumor antigen- and oHSV antigen-specific CD8+ T cells wi

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

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

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

73 While tumor antigens are needed for effective immunotherapy, a

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

75 Tumor antigens are proteins selectively expressed by tum

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

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

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

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

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

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

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

85 used to a single chain antibody specific for tumor antigen CD20.

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

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

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

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

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

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

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

93 ith antifluorescein CAR T cells can overcome tumor antigen escape mechanisms that lead to disease rec

94 , without the need for a priori knowledge of tumor antigen, ex vivo cellular manipulation, or cellula

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

96 Adoptive transfer of tumor antigen-experienced T cells eliminated Pik3ca-null

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

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

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

100 umor models, vaccination with tumor cells or tumor antigen-expressing cells, that lack CD47 or were p

101 ollowing goals: debulk large tumors, release tumor antigen for cross-presentation and cross-priming,

102 mise for the discovery of previously unknown tumor antigens for cancer immunotherapy.

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

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

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

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

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

108 that concentrates DCs to present endogenous tumor antigens generated in situ may broadly serve as a

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

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

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

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

113 therapeutic strategy is seriously limited by tumor antigen heterogeneity since antibodies can only re

114 rong potential to overcome the limitation of tumor antigen heterogeneity, broadening the applications

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

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

117 expression of Merkel cell polyomavirus-large tumor antigen in human lung fibroblasts resulted in upre

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

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

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

121 8(+) T-cell responses to multiple endogenous tumor antigens in poorly immunogenic mouse carcinomas.

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

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

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

125 . demonstrate that transport and transfer of tumor antigens in vesicles is a dominant pathway to load

126 cruited dendritic cells (DCs) to capture the tumor antigens in vivo.

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

128 enic epitopes of both melanoma gp100 and WT1 tumor antigen induced a CD8+ T-cell-mediated response in

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

130 Regarding shared (self) tumor antigens, it is unclear whether the human CD4+ T c

131 enous genes, and thereby the presentation of tumor antigens, leading to dramatic antitumor immune res

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

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

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

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

136 re lacking, providing the immune system with tumor antigen material for processing and presentation i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

151 or cells, we demonstrate in vivo that fusing tumor-antigen peptide to AnxA5 significantly enhances it

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

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

154 dentified IFN-independent effect of RIG-I on tumor antigen presentation and T cell recognition propos

155 anic framework, W-TBP, is used to facilitate tumor antigen presentation by enabling immunogenic photo

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

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

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

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

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

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

162 f tumor-infiltrating lymphocytes begins when tumor antigens reach the lymph node (LN) to stimulate T

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

164 n individual's cancer are the most important tumor antigens recognized by T cells.

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

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

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

168 -2 (TRP-2, Dct) harbor T cells that maintain tumor antigen responsiveness but lack the ability to con

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

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

171 ed vaccine to generate a large population of tumor antigen specific T cells but found that the presen

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

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

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

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

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

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

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

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

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

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

182 They efficiently prime tumor antigen-specific CD8 T cells in vivo, induce CD8 T

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

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

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

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

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

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

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

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

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

192 robust cross-presentation and activation of tumor antigen-specific CD8(+) T cells.

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

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

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

196 conventional DCs (cDCs) in generating potent tumor antigen-specific CD8+ T cell responses.

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

198 and increased infiltration of both viral and tumor antigen-specific CD8+ T cells, as well as oHSV int

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

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

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

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

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

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

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

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

207 , which indicate control of cancer growth by tumor antigen-specific IgE that recruit and re-educate T

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

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

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

211 on contains the necessary signals to promote tumor antigen-specific immune responses, priming T cells

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

233 levels of Tregs while specifically enhancing 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 or- and memory-precursor-like TILs contained tumor-antigen-specific cells, exhibited proliferative an

238 47nb-expressing bacteria stimulates systemic tumor-antigen-specific immune responses that reduce the

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

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

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

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

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

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

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

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

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

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

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

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

253 However, the tumor antigens targeted in successful treatments remain

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

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

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

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

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

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

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

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

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

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

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

265 teins from PDAC patient plasmas and identify tumor antigens that induce antibody response together wi

266 that exosomes display a large repertoire of tumor antigens that induce autoantibodies and exert a de

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

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

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

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

271 lls were further engineered with a surrogate tumor antigen to facilitate assays of T cell activity.

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

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

274 Cell surface MHC-I can present tumor antigens to CD8(+) T cells.

275 ary for cross-presentation of many viral and tumor antigens to CD8(+) T cells.

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

277 be a liposomal vaccine carrier that delivers tumor antigens to human CD169/Siglec-1(+) antigen-presen

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

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

280 ntigen presenting cells for cross-presenting tumor antigens to T cells, subsequent PD-L1 upregulation

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

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

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

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

285 provide sites of tumor cell spread, whereas tumor antigen transfer into and presentation in tumor-dr

286 iscuss molecular identification of different tumor antigen types, and the clinical safety and efficac

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

288 d primary human T cells against a variety of tumor antigens via the addition of SpyTag-labeled target

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

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 ptors (PARs) allowing selective targeting of tumor antigens while incorporating a dissociation mechan

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

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

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

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

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