ライフサイエンスコーパス: tumor-associated

1 d distinct biophysicochemical properties for tumor-associated 4-mers within each cancer type.

2 e tissue, the impact of lymphangiogenesis on tumor-associated adipose tissue (AT) has not yet been in

3 ting the release of endogenous adjuvants and tumor-associated Ags.

4 that are recognized by the immune system as tumor-associated Ags.

5 s melanoma are used to extract a snapshot of tumor-associated alteration in the serum.

6 suggest that anti-inflammatory TAMs promote tumor-associated angiogenesis and immunosuppression by a

7 novel biomarkers and mechanisms involved in tumor-associated angiogenesis.

8 s potent immune modulatory effects, inducing tumor-associated antigen (TAA) cross-priming with antitu

9 tients with advanced melanoma that is of low tumor-associated antigen (TAA) expression often respond

10 ession of PD-1, TIM3, and LAG3 was higher on tumor-associated antigen (TAA)-specific CD8(+) TIL, comp

11 Tumor-associated antigen cytotoxic T cells (TAA-Ts) repr

12 gen spreading and a reduction in circulating tumor-associated antigen DNA levels in patients with rel

13 This suggests IL1RAP as a tumor-associated antigen for immunotherapy cell targetin

14 antigen receptor directed against a specific tumor-associated antigen like CD19 in lymphoma.

15 Clinically, the exploitation of tumor-associated antigen mimics may contribute to the de

16 Here, TCRs against the tumor-associated antigen NY-ESO-1 were isolated either f

17 g cancer patients, CAR-T cells targeting the tumor-associated antigen receptor tyrosine kinase-like o

18 g lymphodepletion, CAR-T cells targeting the tumor-associated antigen ROR1 lysed tumors in mice but i

19 in situ so that the cancer cells can act as tumor-associated antigen-presenting cells (tAPCs) by ind

20 ands, cationic W-TBP mediates PDT to release tumor associated antigens and delivers immunostimulatory

21 r inducing clinical regressions by targeting tumor-associated antigens (TAA).

22 Tumor-associated antigens (TAAs) are monomorphic self-an

23 apeutic monoclonal antibodies (mAbs) against tumor-associated antigens (TAAs) is that their mechanism

24 to naturally occurring tumor peptides (both tumor-associated antigens and neoantigens), as well as t

25 u tumor vaccine, induce CD8+ T cells against tumor-associated antigens and provide a viable oncologic

26 e and elicit robust immune responses against tumor-associated antigens and/or neoantigens.

27 proven challenging, as the vast majority of tumor-associated antigens are also expressed in normal t

28 This requires indirect presentation of tumor-associated antigens on surrounding antigen-present

29 The release of tumor-associated antigens then promotes the maturation o

30 g to additional T cell responses to nonviral tumor-associated antigens through epitope spreading.

31 The process through which tumor-associated antigens trigger humoral response is no

32 gen spreading and a reduction in circulating tumor-associated antigens using digital droplet polymera

33 ed from mucin MUC1 are an important class of tumor-associated antigens.

34 pecific memory T cells that cross-react with tumor-associated antigens.

35 ation shapes an inflammatory response within tumor-associated AT by facilitating accumulation of tumo

36 eneration of an inflammatory response within tumor-associated AT was studied.

37 Here we show that tumor associated B cells are vital to melanoma associate

38 Tumor associated B cells therefore orchestrate and susta

39 that PI3K-gamma was also highly expressed in tumor-associated B cells.

40 microenvironment, which is mediated by human tumor-associated B cells.

41 strong evidence for the pivotal role of the tumor-associated blood and lymphatic vasculature in supp

42 TORC1 versus mTORC2 in cancer, their role in tumor-associated blood vessels and tumor immunity, and p

43 Tumor-associated blood vessels differ from normal vessel

44 , we sought an alternative therapy to reduce tumor-associated bone destruction.

45 ession modulated drug vector distribution in tumor-associated capillaries.

46 n of immune responses after vaccination with tumor-associated carbohydrate antigen (TACA)-containing

47 highly express the disialoganglioside GD2, a tumor-associated carbohydrate antigen, which is only spa

48 er treatment, similar progress in exploiting tumor-associated carbohydrate antigens, such as sLeA, ha

49 on of microbial antigens, self-antigens, and tumor-associated carbohydrate antigens.

50 high levels of natural IgM reactive against tumor-associated carbohydrate antigens.

51 s, as they showed to selectively inhibit the tumor-associated CAs IX/XII over ubiquitous CAs.

52 Tumor-associated CD8+ T-lymphocytes and macrophages of c

53 rapamycin treatment further inhibited these tumor-associated cellular processes.

54 auge the selectivity of ligands for specific tumor-associated chaperome pools.

55 med on 20 matched blood and aqueous samples; tumor-associated chromosomal changes were found in 0/20

56 Here we show that tumor-associated CK1alpha mutations exclusively localize

57 known drivers of PPBC progression including tumor-associated COX-2 expression and fibroblast-mediate

58 ng tumor burden and increasing the number of tumor-associated cytotoxic T cells.

59 Also, evolving are the strategies to alter tumor-associated dysbiosis and move it toward eubiosis w

60 icacy and reduce toxicity; (2) targeting the tumor-associated endothelium for specific delivery of th

61 Tumor-associated enzyme-activated prodrugs can potential

62 However, the paucity of tumor-associated enzymes which are essential for prodrug

63 all into question the conventional view that tumor-associated epigenomic alterations are primarily on

64 CD47 KO increased tumor-associated extracellular matrix protein tenascin C

65 regulatory capacity, and oncogenic nature of tumor-associated extrachromosomal DNA.

66 rophages resulting in decreased abundance of tumor-associated fibroblasts (TAF) and robustly reduced

67 The tumor-promoting fibrotic stroma rich in tumor-associated fibroblasts (TAF) is drawing increased

68 e microenvironment with increased stroma and tumor-associated fibroblasts.

69 In contrast, patient tumor-associated G(12/13) mutations characterized to dat

70 PSCs that have been genome-edited to contain tumor-associated genetic driver mutations revealed by Th

71 gning synthetic tools to explore the role of tumor-associated glycans of MUC1 in the formation of met

72 These tumor-associated glycans trigger inhibitory signaling in

73 led with the alpha-emitter (225)Ac to target tumor-associated glycoprotein 72-positive xenografts in

74 scaffold to obtain potent inhibitors of the tumor-associated human carbonic anhydrases (hCAs) IX and

75 r hallmark of IBC is high infiltration of M2 tumor-associated (immune-suppressing) macrophages.

76 raction between tumor metabolic activity and tumor associated immunocytes may be a critical driver of

77 atients by anti-CD20 immunotherapy decreases tumor associated inflammation and CD8(+) T cell numbers.

78 Tumor associated inflammation predicts response to immun

79 In many settings, tumor-associated inflammation, supported mainly by innat

80 ion and the development of hypercalcemia and tumor-associated inflammation.

81 For gliomas, the tumor-associated inflammatory response is pivotal to sup

82 ssion by restricting numbers of bacteria and tumor-associated inflammatory responses.

83 enotype characterized by low infiltration of tumor-associated leukocytes, particularly macrophages an

84 alyses of transcriptomes of human colorectal tumors associated lower levels of RNase H2 with shorter

85 Tumor-associated lymphangiogenesis correlates with lymph

86 their role in mediating LEC migration during tumor-associated lymphangiogenesis is not well defined.

87 t tumor cell growth, motility, invasion, and tumor-associated lymphangiogenesis, all of which are als

88 er (BC) patients, and it directly depends on tumor-associated lymphatic vessels.

89 A subset of tumor-associated lymphocytes, most prominent in uveal me

90 Here, using human peripheral and tumor-associated lymphocytes, we investigated how tumor-

91 lso detected in the mitochondria of isolated tumor-associated lymphocytes.

92 -derived xenograft model showed reduction of tumor-associated M2 macrophages and favored polarization

93 eolin protein family, increases M1-polarized tumor-associated macrophage (TAM) and CD8 T cell infiltr

94 t and therapeutic resistance are linked with tumor-associated macrophage (TAM) and myeloid-derived su

95 h reflected high vascularization and greater tumor-associated macrophage (TAM) levels.

96 opulation increased while the populations of tumor-associated macrophage and regulatory T cell declin

97 First, systemic methods for targeting tumor-associated macrophage are summarized and limitatio

98 ler tumors, prolonged survival and a reduced tumor-associated macrophage content.

99 Here, we report that caspase-1 promotes tumor-associated macrophage differentiation by cleaving

100 endogenous regulatory mechanisms underlying tumor-associated macrophage differentiation remain large

101 accumulation of lipid droplets and promoting tumor-associated macrophage differentiation.

102 xpression by T cells is necessary for proper tumor-associated macrophage expression of IFNgamma-induc

103 lular matrix (ECM) in response to injury and tumor-associated macrophage microenvironmental cues faci

104 mune checkpoints other than PD-1; modulating tumor-associated macrophage phenotype from tumor-promoti

105 for OC progression principally by promoting tumor-associated macrophage recruitment and activation v

106 o localized, biomaterial-based modulation of tumor-associated macrophage.

107 approaches that rely on immune modulation of tumor associated macrophages (TAMs) from a pro-tumorigen

108 Within the TME, tumor associated macrophages (TAMs) mediate angiogenesis

109 Tumor associated macrophages (TAMs) play a critical role

110 s to IH accelerated tumor progression with a tumor associated macrophages (TAMs) shift towards a pro-

111 ration, NHWD-870 blocks the proliferation of tumor associated macrophages (TAMs) through multiple mec

112 that elicits recruitment and polarization of tumor associated macrophages (TAMs).

113 ecreased the suppressive lymphocytes such as tumor associated macrophages and myeloid derived suppres

114 Such adaptive response is mediated by tumor associated macrophages, whose blockage improves th

115 Absence of miR-21 expression in tumor- associated macrophages (TAMs), caused a global re

116 arizes M0-macrophages into Gas6-secreting M2-tumor-associated macrophages (M2-TAMs).

117 egulatory networks of mesenchymal-associated tumor-associated macrophages (MA-TAMs), which drive the

118 cells restored activation of proinflammatory tumor-associated macrophages (TAM) and intratumoral immu

119 Tumor-associated macrophages (TAM) are highly expressed

120 Tumor-associated macrophages (TAM) are important tumor-p

121 myeloid-derived suppressor cells (MDSC) and tumor-associated macrophages (TAM) in tumor tissue has b

122 r (NSCLC), accumulation of anti-inflammatory tumor-associated macrophages (TAM) is associated with wo

123 Tumor-associated macrophages (TAM) promote triple-negati

124 In glioblastoma (GBM), tumor-associated macrophages (TAM) represent up to one h

125 myeloid-derived suppressor cells (MDSC) and tumor-associated macrophages (TAM) that inhibit T cells

126 ntitumoral and protumoral roles of M1 and M2 tumor-associated macrophages (TAM) typify the complexity

127 nt creates an immunosuppressive signature on tumor-associated macrophages (TAM), which favors express

128 reased numbers of lymphatic vessels (LV) and tumor-associated macrophages (TAM).

129 decreased the immunosuppressive function of tumor-associated macrophages (TAM).

130 eg-attracting chemokine Ccl17 by MHCII(high) tumor-associated macrophages (TAM).

131 Furthermore, it is likely that TANs and tumor-associated macrophages (TAMs) act in tandem within

132 The roles of tumor-associated macrophages (TAMs) and circulating mono

133 Tumor-associated macrophages (TAMs) are a complex and he

134 Tumor-associated macrophages (TAMs) are essential compon

135 Tumor-associated macrophages (TAMs) are the most abundan

136 Tumor-associated macrophages (TAMs) are the most promine

137 Herein, we identify tumor-associated macrophages (TAMs) as the primary sourc

138 Tumor-associated macrophages (TAMs) can exist in pro- an

139 Tumor-associated macrophages (TAMs) can have protumor pr

140 M2 polarization of tumor-associated macrophages (TAMs) correlates with poor

141 However, tumor-associated macrophages (TAMs) express cytokines an

142 Tumor-associated macrophages (TAMs) have a significant p

143 Of the cell types in the TME, tumor-associated macrophages (TAMs) have gained attentio

144 ut to test the hypothesis that morphology of tumor-associated macrophages (TAMs) in colorectal liver

145 iptolide conjugate that specifically targets tumor-associated macrophages (TAMs) in glioblastoma from

146 Recent studies of the role of tumor-associated macrophages (TAMs) in the progression o

147 Tumor-associated macrophages (TAMs) isolated from Camkk2

148 Tumor-associated macrophages (TAMs) play an important ro

149 become a prominent therapeutic target, with tumor-associated macrophages (TAMs) playing a critical r

150 ile anti-inflammatory M2 macrophages such as tumor-associated macrophages (TAMs) promote tumor growth

151 y between glioblastoma stem cells (GSCs) and tumor-associated macrophages (TAMs) promotes progression

152 ntially differentiate into immunosuppressive tumor-associated macrophages (TAMs) rather than immunost

153 Tumor-associated macrophages (TAMs) recruited from blood

154 Tumor-associated macrophages (TAMs) represent the most a

155 an increase in CD1C(+) dendritic cells, the tumor-associated macrophages (TAMs) showed pro-tumoral f

156 Tumor-associated macrophages (TAMs) support tumor growth

157 Among tumor-infiltrating immune cells, tumor-associated macrophages (TAMs) take a center stage

158 e (MSS) phenotypes and had a high density of tumor-associated macrophages (TAMs) that expressed CD274

159 mor microenvironment, where they mature into tumor-associated macrophages (TAMs) that promote disease

160 ccine activates the NF-kappaB pathway in the tumor-associated macrophages (TAMs) through the TLR2 and

161 factors, secreted by cancer cells, polarize tumor-associated macrophages (TAMs) to a tumorigenic M2

162 ling pathway responsible for polarization of tumor-associated macrophages (TAMs) to immunosuppressive

163 Tumor-associated macrophages (TAMs) usually display an a

164 Tumor-associated macrophages (TAMs) usually express an M

165 We found that the number of tumor-associated macrophages (TAMs) was not affected by

166 t exhibited distinct transcriptional states, tumor-associated macrophages (TAMs) were associated with

167 ions between exhausted T cells and SLAMF7(+) tumor-associated macrophages (TAMs), and a unique subset

168 eath-1 ligand (PD-L1)-positive HRS cells and tumor-associated macrophages (TAMs), which associate wit

169 mmunosuppressive microenvironment created by tumor-associated macrophages (TAMs).

170 finity for cognate Fc receptors expressed by tumor-associated macrophages (TAMs).

171 cid synthesis in immunosuppressive (M2-like) tumor-associated macrophages (TAMs).

172 Iron deposits are a phenotypic trait of tumor-associated macrophages (TAMs).

173 ionable, given the well-known limitations of tumor-associated macrophages (TAMs).

174 eath, leading to an increase in inflammatory tumor-associated macrophages (TAMs).

175 eritoneally (i.p.) selectively accumulate in tumor-associated macrophages (TAMs).

176 t by promoting the survival of both GSCs and tumor-associated macrophages (TAMs).

177 Furthermore, we found increased tumor-associated macrophages and an enhanced effect of a

178 Cassetta and Pollard introduce tumor-associated macrophages and discuss their origin, d

179 eveal that inflammatory niches consisting of tumor-associated macrophages and fibroblasts contribute

180 poor prognosis, and enhanced recruitment of tumor-associated macrophages and fibroblasts, we propose

181 Tumor-associated macrophages and microglia (TAMs) have b

182 sociated immune infiltrates are dominated by tumor-associated macrophages and microglia (TAMs), which

183 Hence, modulation and reeducation of tumor-associated macrophages and microglia in GBM is con

184 newal and induces the recruitment of M2-like tumor-associated macrophages and regulatory T cells, thu

185 ctivity suppresses alternative activation of tumor-associated macrophages and the growth of colon can

186 mary tumors in proximity to CD206(+)CD163(+) tumor-associated macrophages and vessels.

187 Tumor-associated macrophages are major contributors to m

188 tion in type 1 regulatory T cells and PD-L1+ tumor-associated macrophages at this early time point of

189 Tumor-associated macrophages contribute to tumor progres

190 secrete stimulating factors, which polarize tumor-associated macrophages from an antitumor M1 phenot

191 -derived xenograft resulted in a shift among tumor-associated macrophages from the immunosuppressive

192 Tumor-associated macrophages have been shown to promote

193 e of Immunity, Zhu et al. (2017) report that tumor-associated macrophages in a mouse model of pancrea

194 and to reduce monocyte differentiation into tumor-associated macrophages in an MCA-203 fibrosarcoma

195 ters PRMT1 expression in blood monocytes and tumor-associated macrophages in human HCC.

196 promotes the protumoral M2-like phenotype of tumor-associated macrophages in the tumor microenvironme

197 ombination with cisplatin; and reprogramming tumor-associated macrophages into a proinflammatory stat

198 pression of fibroblast-activating factors in tumor-associated macrophages resulting in decreased abun

199 data show that MCMV infection and sensing in tumor-associated macrophages through STING signaling is

200 immunosuppressive gene expression program in tumor-associated macrophages to a proinflammatory one, w

201 mic tumor-specific CD8 + T cells, repolarize tumor-associated macrophages towards an inflammatory M1-

202 d molecular similarities between obesity and tumor-associated macrophages, and assessed the regulator

203 production of IFNalpha by activated MHCII(+) tumor-associated macrophages, and enables tumor regressi

204 is mediated by its effect on tumor cells and tumor-associated macrophages, and not directly over T ce

205 4-deficient mice contained higher numbers of tumor-associated macrophages, as well as more lymphatic

206 n E-R72 mice also had an increased influx of tumor-associated macrophages, contributing to angiogenes

207 ion of mast cells suppresses accumulation of tumor-associated macrophages, reduces tumor cell prolife

208 ced acquisition of procancerous phenotype by tumor-associated macrophages, resulting in activation of

209 cell types in glioblastoma tumors, including tumor-associated macrophages, tumor-infiltrating dendrit

210 on depends on an interplay between Tregs and tumor-associated macrophages, which can be reversed by A

211 s promotes a macrophage phenotype similar to tumor-associated macrophages, which may contribute to th

212 obese versus lean women are more similar to tumor-associated macrophages.

213 ating macrophages from inflamed synovium and tumor-associated macrophages.

214 y "cold" tumors by recruiting and modulating tumor-associated macrophages.

215 and/or immune cells, the most critical being tumor-associated macrophages.

216 to notable efforts to deplete or repolarize tumor-associated macrophages.

217 We present evidence that tumor-associated macrophages/microglia (TAMs) can promot

218 and murine models correlates with increased tumor-associated macrophages/monocytes/microglia.

219 In both models, CCX872 decreased tumor associated MDSCs and increased these cells within

220 oduce a synthetic reporter on adopting an M2 tumor-associated metabolic profile by coupling luciferas

221 hat was robustly and specifically cleaved by tumor-associated metalloproteinases in the Hi-Myc model.

222 Fecal and tumor-associated microbiota were assessed by 16s ribosom

223 tion in studying recruitment of cells by the tumor-associated microenvironment.

224 n-like growth factor 1 (IGF1) is produced by tumor-associated microglia in response to interleukin-4

225 cytosis and increased recruitment of M2-like tumor-associated microglia/macrophages (TAM).

226 ts in ASPN-null mice had a reduced number of tumor-associated MSCs, fewer cancer stem cells, decrease

227 rove the potential of these glycopeptides as tumor-associated MUC1 antigen mimics, the derivative bea

228 The Muc-1 oncoprotein is a tumor-associated mucin often overexpressed in pancreatic

229 Accordingly, administration of tumor-associated murine MSC-derived exosomes accelerates

230 mologous ING4, and that two of three primary tumor-associated mutants in the N-terminal domain strong

231 Tumor-associated mutants reveal how constitutive activat

232 Liquid biopsy and detection of tumor-associated mutations in cell-free circulating DNA

233 er, including selective loss of function for tumor-associated mutations.

234 ne interaction, are highly activated in TNBC tumor associated myeloid cells.

235 Tumor-associated myeloid cells (TAMCs) are key drivers o

236 wth in multiple organs in vivo and implicate tumor-associated myeloid cells and associated signals as

237 ether, this work identifies Hyal2-expressing tumor-associated myeloid cells as key players in the acc

238 nal activation of this costimulatory axis in tumor-associated myeloid cells is poorly understood.

239 This study identifies Hyal2-expressing tumor-associated myeloid cells of monocyte-macrophage li

240 Collectively, these data reveal that tumor-associated myeloid cells provide signals critical

241 Tumor-associated myeloid cells regulate tumor growth and

242 Here we describe a novel function of tumor-associated myeloid cells related to the enhanced b

243 Thus, we hypothesized that tumor-associated myeloid cells would support T-ALL in vi

244 ted by additional costimulatory signals from tumor-associated myeloid cells,v leading to enhanced TIL

245 se (PERK) in the immunoinhibitory actions of tumor-associated myeloid-derived suppressor cells (tumor

246 to alphaVbeta3 integrins present in both the tumor-associated neovasculature and on the surface of ov

247 However, the diversity of tumor-associated neutrophils (TANs) remains elusive.

248 ifferent terms, including N1/N2 neutrophils, tumor-associated neutrophils, and polymorphonuclear neut

249 is by impairing survival and mobilization of tumor-associated neutrophils.

250 However, tumor-associated NK cells become dysfunctional; thus, st

251 sion in primary tumors may be complicated by tumor-associated or normal stromal blood vessels yet its

252 Tumor-associated peptide-human leukocyte antigen complex

253 anistic insight on proteasomal regulation of tumor-associated peptide/HLA antigen complexes, and yiel

254 he identification of pathogen-associated and tumor-associated peptides.

255 tudying the effect of ICMT overexpression on tumor-associated phenotypes in vitro and in vivo, and an

256 ultifunctional nanoparticles takes ~10 h for tumor-associated platelet regulation and 16 h for PSC re

257 By regulating tumor-associated platelets and pancreatic stellate cells

258 ence that hypoxia is a potent determinant of tumor-associated PMN phenotypes and direct PMN-tumor cel

259 On exposure to tumor-associated proteases, such as matrix metalloprotei

260 While progress in antibodies targeting tumor-associated protein antigens resulted in an impress

261 Tumor-associated radioactivity was significantly higher

262 dies (n = 294) or from within canine mammary tumor associated regions (n = 471).

263 Here we report on Mammary Tumor Associated RNA 25 (MaTAR25), a nuclear enriched an

264 Tumor-associated Schwann cells, therefore, can have a si

265 primed CD8(+) T cells recognizing nonmutated tumor-associated self-antigens.

266 esponses capable of cross-reacting on native tumor-associated self.

267 ings provide insights into the dual roles of tumor-associated senescence and can potentially impact t

268 Here, we investigate the roles of tumor-associated signals in regulating endothelial cell

269 However, most tumor-associated sites, predominantly in noncoding regio

270 Cancer cells exert mastery over the local tumor-associated stroma (TAS) to configure protective im

271 , it remains unclear whether activity in the tumor-associated stroma contributes to malignancy.

272 due to the presence of an immunosuppressive tumor-associated stroma.

273 A higher density of tumor-associated T cells correlates with improved Merkel

274 We considered that tumor-associated T cells might promote malignancy via di

275 Comparing scRNA-seq profiles of tumor-associated T cells to our dataset reveals predomin

276 findings demonstrate that the quality of the tumor-associated T-cell infiltrate informs patient progn

277 imaging of cancers using probes specific for tumor-associated target proteins offers a powerful solut

278 ucosylated GSLs were recognized as potential tumor-associated targets.

279 for terminal GalNAc residues present in the tumor-associated Tn antigen (alphaGalNAc-Ser/Thr) and it

280 We detected increased expression of both tumor-associated truncated O-linked glycans and their re

281 tudies herein present a novel mouse model of tumor-associated USP22 overexpression and implicate USP2

282 Here, in vivo characterization of tumor-associated USP22 upregulation and unbiased interro

283 tic transcriptional up-regulation of Pfn1 in tumor-associated vascular endothelial cells in the clini

284 ation into tumors and restored blood flow in tumor-associated vasculature.

285 ment model under the influence of functional tumor-associated vasculature.

286 impairs virus function, and we suggest that tumor-associated viruses may be more likely to contain D

287 We found a high prevalence of known tumor-associated viruses such as Epstein-Barr virus (EBV

288 Glioblastoma is a hostile brain tumor associated with high infiltration leading to poor

289 Kaposi's sarcoma (KS) is a rare vascular tumor associated with human herpesvirus (HHV)-8 infectio

290 HV interactions.IMPORTANCE KS is a prevalent tumor associated with infections with two distinct virus

291 is a key microenvironmental stress in solid tumors associated with acquired resistance to convention

292 rus Ags induces complete regression of large tumors associated with an influx of Ag-specific CD8 T ce

293 MSI-H tumors associated with diminished intra-tumoral heteroge

294 ge; unfortunately they can become aggressive tumors associated with distant metastasis, shortening su

295 n extend beyond the fibrous capsule; desmoid tumors associated with the implants; and breast implant-

296 pancreatic cancer xenografts, compared with tumors associated with the nervous system, including GTM

297 en (HPV+) OPSCC, a significant subset of HPV tumors associated with tobacco exposure have diminished

298 arcinomas and bladder urothelial carcinomas, tumors associated with TSC gene mutations.

299 umor progression, compared to saline-treated tumors associated with wild-type prostatic fibroblasts.

300 These NEPC tumors, associated with aggressive disease and poor prog