ライフサイエンスコーパス: primary tumor

1 ndary organ conducive to the metastasis of a primary tumor.

2 the first capillary bed downstream from the primary tumor.

3 are highly genetically divergent from their primary tumor.

4 C phenotypes are spatially segregated in the primary tumor.

5 incised and imaged with CLI to visualize the primary tumor.

6 growth signaling as cancer cells within the primary tumor.

7 cancer cells without impact on growth of the primary tumor.

8 involves a small fraction of cells from the primary tumor.

9 rily by metastasis rather than growth of the primary tumor.

10 e and three-dimensional spheroids grown from primary tumors.

11 atched expression profiles of more than 9000 primary tumors.

12 higher levels in BCBM specimens compared to primary tumors.

13 d that CDK5 is dispensable for the growth of primary tumors.

14 ent therapies on genetic characterization of primary tumors.

15 s stroma, have higher tumor cellularity than primary tumors.

16 often occurs prior to clinical detection of primary tumors.

17 tochondrial functionality than nonmetastatic primary tumors.

18 a higher-level expression of KS compared to primary tumors.

19 ll lines are equal in their ability to model primary tumors.

20 IFNalpha/beta and rejection of transplanted primary tumors.

21 tion group, including in Miettinen high-risk primary tumors.

22 stand the differences between cell lines and primary tumors.

23 d numerous genes with recurrent mutations in primary tumors.

24 n combination with an aromatase inhibitor in primary tumors.

25 ative PCR for prostate cancer cell lines and primary tumors.

26 ssociated transcription factors than non-SCN primary tumors.

27 viral replication or T cell infiltration in primary tumors.

28 to trace migrations from metastases back to primary tumors.

29 as a metabolic vulnerability against CSCs in primary tumors.

30 xidant defenses, is often suppressed in many primary tumors.

31 h impaired M2 macrophage infiltration of the primary tumors.

32 ve DeltaNp63-high EMT cells in heterogeneous primary tumors.

33 hty-four patients underwent resection of the primary tumor (20%), after a median duration of 5 months

34 dentified, 38 (62.3%) are initiated from the primary tumors, 22 (36.1%) from LNMs, and 1 from liver m

35 (149 metastatic breast cancers, 63 untreated primary tumors, 29 local relapses, and 11 longitudinal p

36 ebral gliomas (9 low-grade, 34 high-grade; 9 primary tumors, 34 recurrent tumors) who had preoperativ

37 element of teratoma was present in 82 NSGCT primary tumors (42%).

38 detected 10 months later (91%) than with the primary tumor (79%), suggesting that early-disseminating

39 clopedia to evaluate cell lines as models of primary tumors across 22 tumor types.

40 Among them, 32 patients have primary tumors, adjacent normal tissues, and matched liv

41 of CD8(+) T cells increased significantly in primary tumors after combination therapy.

42 Proteomic and phosphoproteomic profiling of primary tumors alone successfully distinguishes cases wi

43 ifferences between immune populations in the primary tumor and ALNs(-) were associated with the lumin

44 h the primary cancer cells spread beyond the primary tumor and disseminate to other organs.

45 ng (gross and microscopic examination of the primary tumor and draining lymph nodes) require the infr

46 hanges that enable cancer cells to leave the primary tumor and establish inoperable and lethal metast

47 roduce a cell that is capable of leaving the primary tumor and growing in a distant organ?

48 high-risk regions within or adjacent to the primary tumor and hence potentially impact therapeutic o

49 atment-induced tumor dormancy at the site of primary tumor and in distant organs before and after can

50 ated whether patterns of immune cells in the primary tumor and in the axillary lymph nodes without me

51 approach was used to spatially partition the primary tumor and involved lymph nodes into subregions (

52 +/- 24.84 months following resection of the primary tumor and metastasis, respectively.

53 ts remodel the extracellular matrix (ECM) in primary tumor and metastatic microenvironments, exerting

54 -exome sequencing (WES) data from 457 paired primary tumor and metastatic samples from 136 patients w

55 an additional 223 cancer patients, plus 200 primary tumor and normal tissues.

56 omes of patients with or without teratoma in primary tumor and postchemotherapy retroperitoneal lymph

57 ry adenocarcinoma, HT29 from a more advanced primary tumor and SW620 from lymph-node metastasis.

58 including the accumulation of CTCs from the primary tumor and the extravasation of tumor cells from

59 The patient's primary tumor and the mouse xenografts were histological

60 Both the patient primary tumor and the xenograft tumors had a significant

61 x patients (68%) underwent pneumonectomy for primary tumors and 12 (32%) for metastases.

62 of immune markers compared with luminal A in primary tumors and ALNs(-).

63 ely based on the genetic characterization of primary tumors and are ineffective for metastatic diseas

64 systemic myeloid cell expansion, both in the primary tumors and at the distant organ sites.

65 evidence that cytochrome c deficiency in AA primary tumors and cancer cells abrogates apoptosome-med

66 ighlights transcriptomic differences between primary tumors and colorectal adenocarcinoma metastases

67 therapy can inhibit the tumor growth of both primary tumors and distant tumors, prolonging the surviv

68 umor cells can modify the immune response in primary tumors and in the axillary lymph nodes with meta

69 ression of MT1-MMP in wildtype cells of both primary tumors and lung metastases, but, surprisingly, M

70 pairs of non-small cell lung cancer (NSCLC) primary tumors and matched distant metastases.

71 an intimate signaling communication between primary tumors and metastases through the ITGBL1-loaded

72 ptor CXCR4 is highly expressed in both human primary tumors and metastases.

73 ces distinct sets of vulnerabilities between primary tumors and metastatic cancer, even in the same p

74 and posttreatment aromatase availability in primary tumors and metastatic lesions.

75 en injections of LS174T cells, and growth of primary tumors and numbers of liver and lung metastases

76 rity of somatic mutations are shared between primary tumors and paired distant metastases although mu

77 oth genetic inhibition of sEV secretion from primary tumors and pharmacologic inhibition of sEV uptak

78 PIMs were abundantly expressed in primary tumors and PMBL cell lines.

79 nd "high" immune signals, were identified in primary tumors and replicated in metastatic tumors.

80 wnstream of E6/E7 expression and analyses of primary tumors and The Cancer Genome Atlas (TCGA) data r

81 -Terminal motif (BET) inhibitor GS-626510 on primary tumors and xenografts harboring c-MYC amplificat

82 of seeding of new metastasis by clones from primary tumors and/or existing metastases.

83 ollowing attempted curative resection of the primary tumor, and up to 66% of local recurrences are as

84 t-derived glioblastoma stem cells (GSCs), 50 primary tumors, and 10 neural stem cells (NSCs) to ident

85 arcinoma, 30% (38 of 126) were invasive lung primary tumors, and 22% (28 of 126) were metastases.

86 promoter hypermethylation in cell lines and primary tumors, and a high frequency of GULP1 promoter m

87 vivo, DC3s infiltrated luminal breast cancer primary tumors, and DC3 infiltration correlated positive

88 clones, has a clonal architecture similar to primary tumors, and is dependent upon the Jak/Stat pathw

89 in lymph node metastases compared to matched primary tumors, and that TGLI1 was expressed at higher l

90 atic dissemination from early lesions before primary tumors appear are poorly understood.

91 Children with NF1 who develop a primary tumor are at increased risk of SN when compared

92 Unlike other human cancers, in which all primary tumors arise de novo, ovarian epithelial cancers

93 pathways, consistent with our findings that primary tumors arising from Rab27a knockdown cells were

94 RI (mpMRI) was performed, and the SUV in the primary tumor, as delineated by mpMRI, was measured by 2

95 onclusion: SUV measurements from uPAR PET in primary tumors, as delineated by mpMRI, showed a signifi

96 ighly homologous ING4, and that two of three primary tumor-associated mutants in the N-terminal domai

97 tatic tissues exhibit high similarities with primary tumors at the genetic but not the proteomic leve

98 al (OS) was examined by percentage TR in the primary tumor bed and pathologic nodal stage (ypN0) usin

99 lity therapy, in addition to >=90% TR in the primary tumor bed.

100 re the miRNA and gene expression profiles of primary tumors between two groups of patients (with and

101 astasis allows for the identification of the primary tumor, blood vessel, and lymphatic metastasis.

102 s, reduced expression of Aqp7 caused reduced primary tumor burden and lung metastasis.

103 maintains the pro-metastatic cluster within primary tumors but ablates pro-metastatic neutrophils.

104 ls (CTCs) are shed into the bloodstream from primary tumors, but only a small subset of these cells g

105 irculating tumor cells (CTCs) derived from a primary tumor can be detected in the venous blood of can

106 le cells, then some genetic diversity in the primary tumor can be transmitted.

107 During the growth of various cancers, primary tumors can escape antitumor immune responses of

108 associated with worse OS were node-positive primary tumor, carcinoembryonic antigen (CEA) >200 mug/L

109 s possible and associated with node-negative primary tumors, CEA <= 200 mug/L and CRS < 4.

110 Primary tumor cell lines lacking Atm expression also dem

111 During the multistep process of metastasis, primary tumor cells acquire cellular and phenotypic plas

112 east-to-lung metastasis model, we found that primary tumor cells activated vimentin and N-cadherin in

113 hich enables a more immediate study of fresh primary tumor cells and minimizes adaptive changes that

114 Functional profiling of primary tumor cells could circumvent these limitations,

115 r phenotypic heterogeneity in cell lines and primary tumor cells from bladder cancer patients.

116 uptake in secondary organs or secretion from primary tumor cells may be promising therapeutic strateg

117 The ability of primary tumor cells to invade into adjacent tissues, fol

118 Cultured A5(+/-);Kras primary tumor cells were resistant to induction and inhi

119 ted 10x higher TNF-alpha induction than with primary tumor cells.

120 "Achilles heel" in cancer therapies based on primary tumor characterization and suggests targeting DN

121 y ablative radiation therapy (RT) results in primary tumor cure, upregulation of a cytotoxic immune r

122 s (BMSCs) as a novel mechanism through which primary tumor-derived exosomes promote premetastatic nic

123 While not affecting primary tumor development and growth, FAK deletion signi

124 risk factors, adjusting for type and age at primary tumor diagnosis and therapeutic exposures.

125 ccurately reconstructs tumor evolution, with primary tumors differentiated from metastases.

126 umors exhibited decreased growth compared to primary tumors, due to high local M1-induced cytotoxicit

127 be able to detect treatment response in the primary tumor during NAC, and future studies with larger

128 The resulting PyMT(2c44) mice developed more primary tumors earlier than PyMT mice, with increased ly

129 epithelial-to-mesenchymal transition in the primary tumors, elevated levels of circulating tumor cel

130 Data were collected on the extent of primary tumor excision, severe operative complications,

131 f local endogenous inflammatory signaling in primary tumor formation.

132 After resection of the primary tumor from the patient liver, excess viable tumo

133 Primary tumors from Cyp2c44-deficient mice contained hig

134 tered in metastases compared with the paired primary tumors from which they arose.

135 Primary tumor gene expression is a good predictor of can

136 ons with the loss of VHL through analysis of primary tumor genomic and transcriptomic data.

137 n patients with higher-grade and lower-grade primary tumors (Gleason score of >=4 + 3 vs. <3 + 4).

138 rrelated with PSA, PSA kinetics and original primary tumor grade.

139 related with PSA, PSA kinetics, and original primary tumor grade.

140 oncogenic in a variety of cancers, promoting primary tumor growth and invasiveness.

141 ious differentiation pathways that attenuate primary tumor growth and metastasis formation.

142 poor clinical outcomes, but also facilitated primary tumor growth and metastasis in vivo.

143 racrine signaling pathway that mediates both primary tumor growth and metastasis, specifically, metas

144 ference in colon cancer cell lines decreased primary tumor growth and metastasis.

145 ablation of T cell steroidogenesis restricts primary tumor growth and metastatic dissemination in mou

146 ancer progresses in a multistep process from primary tumor growth and stroma invasion to metastasis.

147 models, Angpt2(443) differentially affected primary tumor growth and vascularization; these varying

148 himeric extracellular vesicles that suppress primary tumor growth by activating tumor-eliminating mac

149 AT-RvD1 and AT-RvD3) or AT-LXA(4) inhibited primary tumor growth by enhancing macrophage phagocytosi

150 cancer distant metastasis without affecting primary tumor growth in mice.

151 s of Coronin 1C in this model increases both primary tumor growth rates and distant metastases.

152 te-containing liposomes dramatically inhibit primary tumor growth via long-term down-regulation of mi

153 Primary tumor growth was similar between conditions, lik

154 veral stages of tumor progression, including primary tumor growth, angiogenesis, invasion and metasta

155 prisingly, MT1-MMP deficiency did not affect primary tumor growth, bone degradation or the formation

156 a deficiency in macrophages had no impact on primary tumor growth, but was essential for dectin-1-med

157 genetic inhibition of MTA2 suggested that in primary tumor growth, independent of IKK2, MTA2/NuRD cor

158 strongly suggest a prominent role of MTA2 in primary tumor growth, lung metastasis, and NF-kappaB sig

159 e and invasive cells that coordinately drive primary tumor growth, progression, and recurrence after

160 or cell-expressed Angpt2 was dispensable for primary tumor growth, yet in-depth analysis of primary t

161 tasis in vivo without significantly altering primary tumor growth.

162 to anti-PD1 immunotherapy, despite unchanged primary tumor growth.

163 and metastasis, despite having no effect on primary tumor growth.

164 ced metastasis in vivo, but had no effect on primary tumor growth.

165 ients died from tumor metastasis, instead of primary tumor growth.

166 associated with worse RFS were node-positive primary tumor, >=4 CRLM, and positive hepatic margin.

167 Patients with RB1 loss in the primary tumor had a worse prognosis.

168 ead and neck squamous cell carcinoma (HNSCC) primary tumors had significantly more heterogeneity acro

169 While primary tumor high-risk features were associated with im

170 e methylation pattern of ctDNA shed from the primary tumor; however, to realize the full clinical uti

171 P = 0.013), chemotherapy as treatment of the primary tumor (HR: 2.07 P = 0.027) and adjuvant chemothe

172 The role of early resection of the primary tumor in metastatic small bowel neuroendocrine (

173 lic tumor volume (MTV), and IMH index of the primary tumor in patients with biopsy-proven adenocarcin

174 Here we show that surgical dissection of primary tumors in mice under anesthesia with sevoflurane

175 ty are predominant in the invasive fronts of primary tumors in proximity to CD206(+)CD163(+) tumor-as

176 ed infiltrated CD8(+) T cells, compared with primary tumors, in two independent cohorts.

177 t the evolutionary histories of 56 pediatric primary tumors, including 24 neuroblastomas, 24 Wilms tu

178 study shows that high values of TILs in the primary tumor independently seem to reduce the risk for

179 microRNAs in cervical cancer cell lines and primary tumors, indicating dysregulation of these two mi

180 mesenchymal-epithelial transition (MET), in primary tumor initiation, progression, and metastasis.

181 Finally, Prkd1 knockdown in vivo blocked primary tumor invasion and distant metastasis in a mouse

182 asive cancer cells into adipocytes repressed primary tumor invasion and metastasis formation in mouse

183 ) at key points during metastasis, including primary tumor invasion, intravasation, and extravasation

184 Complete surgical resection of the primary tumor is an important part of NBL treatment, but

185 a, particularly mature teratoma, in an NSGCT primary tumor is associated with a higher CIDD, consiste

186 e responded to induction therapy, CME of the primary tumor is associated with improved survival and l

187 The invasion of tumor cells from the primary tumor is mediated by invadopodia, actin-rich pro

188 s, only a fraction of genetic diversity in a primary tumor is passed on to metastases.

189 We assume that the primary tumor is resected at a given size and study the

190 g cell, so that none of the diversity in the primary tumor is transmitted to the metastasis.

191 Our results show that fewer primary tumor lineages seed distant metastases than lymp

192 In multivariate analysis, PDAC primary tumor location (isthmus vs head: hazard ratio [H

193 tudy aimed to clarify the prognostic role of primary tumor location in NSCLC.

194 ed in 31.4% of patients, was correlated with primary tumor location in the right colon (P = 0.006).

195 Following a therapeutic excision of the primary tumor, longitudinal tracking of immune phenotype

196 resected extrahepatic disease, patient age, primary tumor lymph node metastasis, tumor number, and c

197 structure of 94 tumor samples, covering the primary tumors, lymph node metastases (LNMs), and liver

198 esults: The highest contrast was achieved in primary tumors, lymph nodes, and distant metastases at 1

199 tatus was confirmed by molecular analysis of primary tumor material.

200 Higher MCAM expression in primary tumors may be complicated by tumor-associated or

201 that can eradicate the CSC subcompartment in primary tumors may prevent metastatic disease, thus repr

202 n cancer cells from patients with detectable primary tumors, mechanisms for early metastatic dissemin

203 Y537S ESR1 mutant primary tumors metastasized efficiently in the absence o

204 ex, age, AJCC stage, primary tumor site, and primary tumor mitotic rate in multivariable and conditio

205 High primary tumor mitotic rate was significantly associated

206 The results highlight the importance of primary tumor mitotic rate.

207 -nucleotide polymorphism (SNP) genotyping of primary tumors (n = 914).

208 Re-engraftment of these primary tumor neurospheres generates secondary tumors wi

209 Osteosarcoma is the most frequent primary tumor of bone and is characterized by its high t

210 Localization of the study drug in primary tumors of 5 patients was observed, with favorabl

211 The primary tumors of colorectal cancer (CRC) often metastas

212 nificantly associated with poor prognosis in primary tumors of neuroblastoma patients with high-risk

213 easing local dose of radiation to a residual primary tumor on the cumulative incidence of local progr

214 We profiled the transcriptome of primary tumors on a clinical grade assay from the SweBCG

215 ts were stratified by presentation status as primary tumor only (PRIM), primary with synchronous meta

216 umor recurrence, using molecular data of the primary tumor only.

217 rom the same patient obtained at the time of primary tumor operation and at recurrence) from patients

218 1:1 between standard RT dose 68.0 Gy to the primary tumor or dose escalation to 73.1 Gy.

219 astasis during inflammation triggered by the primary tumor or environmental stimuli.

220 based on the following sites: local lesion (primary tumor or prostate bed after radical prostatectom

221 dual characteristics, characteristics of the primary tumor, or treatment.

222 ng, randomly distributed leader cells within primary tumor organoids use CXCR4 and DDR2 to polarize t

223 c for breast cancer metastasis regardless of primary tumor origin.

224 ion glycolysis (TLG) were determined for the primary tumor, pelvic lymph nodes, and PALNs.

225 ncer metastases in contrast to its impact on primary tumor progression.

226 re 30 times more metastatic to the lung than primary tumor (PT) cells, similar to cells derived from

227 the tumors exhibited genetic variation among primary tumor regions.

228 how that in a colorectal cancer (CRC) model, primary tumors release integrin beta-like 1 (ITGBL1)-ric

229 Surgical resection of the primary tumor remains controversial among women with sta

230 or a stage II OCC in a curative intent (with primary tumor resection) between January 2000 and Decemb

231 In vivo, SEMA7A conferred primary tumor resistance to fulvestrant and induced lung

232 imary tumor growth, yet in-depth analysis of primary tumors revealed enhanced intratumoral necrosis u

233 nfiltrating immune cells from transplant and primary tumors, revealing striking differences in their

234 fying subclones using stage III colon cancer primary tumor samples as well as simulated data.

235 expression at the mRNA and protein levels in primary tumor samples of TNBC and NSCLC patients.

236 At pathologic examination, primary tumor samples were studied in detail.

237 ferent components of the ATR-CHK1 pathway in primary tumor samples.

238 SHH-MB model, targeted ablation of Abcc4 in primary tumors significantly reduced tumor burden and ex

239 ich breast cancer cells disseminate from the primary tumor site to bone.

240 MCF7b cells grew poorly in the primary tumor site when reinoculated in vivo, suggesting

241 For detecting residual disease at the primary tumor site, 12 studies evaluated endoscopic biop

242 influenced by patient sex, age, AJCC stage, primary tumor site, and primary tumor mitotic rate in mu

243 ltiple Cox regression adjusted for age, sex, primary tumor site, and tumor grade, the SUV(max) cutoff

244 In the pre-imatinib era, primary tumor site, size, and mitotic rate predicted out

245 ean body mass (SUL(max)) was measured at the primary tumor site.

246 tumor xenografts from mice were placed into primary tumor sites and either human bone stromal cells

247 In comparison with primary tumor sites, there were increased levels of CXCR

248 ignificantly associated with clinical stage, primary tumor size, and response to treatment.

249 sion calls for a more precise measurement of primary tumor size, best assessed with imaging.

250 icantly reduces metastasis without affecting primary tumor size, however, the precise molecular mecha

251 itiated prostate tumorigenesis by increasing primary tumor size, potentiating visceral organ metastas

252 ent-based analysis, sensitivity in detecting primary tumors, soft-tissue metastases, and bone or bone

253 based analysis, the sensitivity in detecting primary tumors, soft-tissue metastases, and bone or bone

254 f patients, that multiple subclones from the primary tumor spread very rapidly from the primary site

255 ative, or followed by ND if positive, during primary tumor surgery).

256 The primary tumor systemically recruits IFNgamma-producing i

257 aneous metastasis from significantly smaller primary tumors than PTEN(NULL), implying an enhanced abi

258 harness the intrinsic spatial information in primary tumors that can be exploited to optimize prognos

259 Among NF1-affected children with a primary tumor, therapeutic radiation, but not alkylating

260 Within the basal primary tumors, there was increased immune dysregulation

261 We apply SpAn to primary tumor tissue samples from a cohort of 432 chemo-

262 ved an increased expression of KS epitope on primary tumor tissues compared to uninvolved normal and

263 ls using gene expression data from patients' primary tumor tissues to predict whether a patient will

264 it to study EMT gene activity from the local primary tumor to a distant metastatic site in vivo.

265 n vitro model of tumor cell migration from a primary tumor to a distant site that allows use of tissu

266 c cancer is the adaptability of cells from a primary tumor to create new niches and survive in multip

267 i.e., the spreading of tumor cells from the primary tumor to distant organs, is responsible for the

268 Peritumoral lymphatic vessels connect the primary tumor to lymph nodes, facilitating tumor entry i

269 in reconstructing clone migrations from the primary tumor to new metastases as well as between metas

270 , responded to collagen I stimulation at the primary tumor to promote local invasion and utilized the

271 and less than 2 years from resection of the primary tumor to transplantation.

272 ellular targets in mediating the response of primary tumors to high-dose radiotherapy in vivo These s

273 ncer driver genes, 77% were transmitted from primary tumors to metastatic tumors, and 80% from primar

274 rodeoxyglucose PET texture features from the primary tumor, tumor penumbra, and bone marrow predicts

275 The most common primary tumor types were breast (n = 18), lung (n = 18),

276 atients received 21.6 Gy to the preoperative primary tumor volume.

277 al metastasis after initial diagnosis of the primary tumor was 17 months (interquartile range: 6-41).

278 Resection of the primary tumor was associated with longer survival in syn

279 Skeletal dissemination from the primary tumor was reversed with PREX1 knockdown, indicat

280 The primary tumor was semiautomatically delineated in the PE

281 Although the growth of the primary tumors was unaffected by activating mAbs, CTCs a

282 high levels of both Claudin-2 and Afadin in primary tumors were associated with poor disease-specifi

283 The most common primary tumors were breast (33.3%), urothelial (12.5%),

284 trial and The Cancer Genome Atlas (TCGA) of primary tumors were compared.

285 All primary tumors were positive with both agents (n = 33 ea

286 aries of metastasizing and non-metastasizing primary tumors were readily defined, leading to the iden

287 ple metastatic tumors from 39 patients whose primary tumors were unavailable (n = 271 tumors).

288 oted epithelial-to-mesenchymal transition in primary tumors, whereas SERPINB5 and CSTB enhanced late

289 led to a dramatic decrease in the growth of primary tumors, which exhibited reduced PD-L1 expression

290 k between the germ line and the epigenome of primary tumors, which may help identify germline biomark

291 Those with intact primary tumors who were alive 12 months after diagnosis

292 according to the pathologic response of the primary tumor with associated pathologic axillary outcom

293 TAC-operated mice developed larger primary tumors with a higher proliferation rate and disp

294 multiple BRCA1-mutant cancer cell lines and primary tumors with low levels of RNF168 protein express

295 t regulations, where one group was closer to primary tumors with metastasis than the other group.

296 Supervised analysis of 77 primary tumors with paired metastases revealed that the

297 In contrast, primary tumors with RhoA knockdown efficiently invaded s

298 Utilizing pre-ranked GSEA, we showed that primary tumors with Survivors were associated with anti-

299 Thirteen patients have primary tumors without distant metastasis and matched no

300 ge ratio was significantly different between primary tumors without distant metastatic recurrence (DM