ライフサイエンスコーパス: primary tumor

1 patient (i.e. cells already migrated outside primary tumor).

2 tested for somatic BRCA1/2 mutations of the primary tumor.

3 sociated macrophages to produce CXCL1 in the primary tumor.

4 ot known to have metastatic disease of their primary tumor.

5 through stromal compartments adjacent to the primary tumor.

6 rowth of invasive glioma cells away from the primary tumor.

7 are influenced by the site and stage of the primary tumor.

8 ho present with metastatic NET, but no known primary tumor.

9 ot targets for metastasis or affected by the primary tumor.

10 years, by receipt of initial surgery to the primary tumor.

11 tion tool was used to contour each patient's primary tumor.

12 asive properties that enable escape from the primary tumor.

13 the main breast cancer, without removing the primary tumor.

14 ume of contrast enhancement) and originating primary tumor.

15 hose with the same site, stage, and grade of primary tumor.

16 the same mutational processes active in the primary tumor.

17 y in the same patient after treatment of the primary tumor.

18 DNA damage in both precancerous lesions and primary tumors.

19 ly distinct state from normal epithelium and primary tumors.

20 d metastatic tumors were often distinct from primary tumors.

21 ical challenges limit comparable analyses in primary tumors.

22 m spatially localized to the leading edge of primary tumors.

23 metastatic sites is even higher than that in primary tumors.

24 tially driving and druggable gene fusions in primary tumors.

25 is but are infrequently found in the core of primary tumors.

26 ated to tumor sites, and robustly eradicated primary tumors.

27 tomes, for BCBM- CTCs that is different from primary tumors.

28 ploidy and genetic heterogeneity observed in primary tumors.

29 lencing in multiple malignant cell lines and primary tumors.

30 and CD44E expression levels in human gastric primary tumors.

31 a total of 1,056 cancer cell lines and 9,250 primary tumors.

32 faithfully represent the genomic features of primary tumors.

33 ablished CRC cell line are representative of primary tumors.

34 ave undergone an R0 or R1 resection of their primary tumor?

35 1.5, respectively), followed by the type of primary tumor (1.7), age (2.4), tumor burden (2.8), and

36 ors (13% v 64%, respectively) or right-sided primary tumors (36% v 81%, respectively).

37 he hypothesis that subsequent removal of the primary tumor after early detection would enhance surviv

38 ized uptake value (%SUVmax) remaining in the primary tumor after induction chemotherapy-%SUVremaining

39 There was no bleeding found within primary tumors after treatment.

40 values of cholinesterase, bilirubin, type of primary tumor, age at radioembolization, hepatic tumor b

41 tumors and predict pTR, using avidity of the primary tumor alone.

42 However, at that time, a cystoscopy of his primary tumor and a transurethral resection revealed res

43 chance of margin-free (R0) resection of the primary tumor and at least a macroscopic complete resect

44 c demands that accompany rapid growth of the primary tumor and colonization of distinct metastatic si

45 to assess the anatomic relationships of the primary tumor and for the presence of intra-abdominal me

46 c tool for the detection of c-Met-expressing primary tumor and has potential utility for the detectio

47 ion patterns were highly similar across each primary tumor and its associated metastases.

48 files, and no radiographic interface between primary tumor and mesenteric vasculature.

49 epresents combined genetic material from the primary tumor and metastases.

50 Heterogeneity in HER2 expression between primary tumor and metastasis has repeatedly been describ

51 did not compromise tracer uptake in residual primary tumor and metastatic lesions.

52 ell xenografts reduced the sizes of both the primary tumor and metastatic lung colonies.

53 control of B16 melanoma, or EL4 lymphoma, in primary tumor and metastatic settings.

54 ent Imaging Tomography (DLIT) for monitoring primary tumor and metastatic spreading in breast cancer

55 , fluorouracil, and radiation therapy to the primary tumor and regional lymph nodes (45 to 54 Gy) plu

56 ed CRT: 45 to 54 Gy radiation therapy to the primary tumor and regional lymph nodes plus eight once-w

57 by which cancer cells direct MDSC homing to primary tumor and suggests that targeting MDSC recruitme

58 Importantly, these changes in the primary tumor and the metastatic lung were all dependent

59 al/CT studies of 14 patients with inoperable primary tumors and 56 patients with metastatic and recur

60 In the KMC, all tumors were acquired from primary tumors and 65.7% (n = 105) were acral or mucosal

61 n deposits that are enriched in mice bearing primary tumors and are also present in vessels from huma

62 pecific immune-mediated tumor regressions in primary tumors and colorectal liver metastases.

63 ase (TERT) is overexpressed in 80% to 90% of primary tumors and contributes to sustaining the transfo

64 human breast cancer metastases compared with primary tumors and demonstrated that SNX9 expression in

65 and 4 were verified as genetically distinct primary tumors and did not harbor similar copy number al

66 romoters of these genes in a small cohort of primary tumors and distant metastases.

67 aving the potential to safely eradicate both primary tumors and distant metastatic foci.

68 ked lung and lymph node metastasis; however, primary tumors and established metastasis were less sens

69 The MKR mice developed larger primary tumors and greater number of pulmonary metastase

70 Using low passage cultures from primary tumors and liver metastases we show that ATM los

71 ion of chromosomal alterations in pancreatic primary tumors and liver metastases.

72 tagonist N6L strongly impaired the growth of primary tumors and liver metastasis in an orthotopic mou

73 quired for the growth and vascularization of primary tumors and lung metastases in a breast cancer xe

74 C) patients, including five matched pairs of primary tumors and lymph node metastases.

75 berration (CNA) landscapes with those of the primary tumors and lymph node metastasis, we establish t

76 re are intrinsic subtype differences between primary tumors and matched BrM and to uncover BrM-acquir

77 recent studies show independent evolution of primary tumors and metastases and in most cases mutation

78 bioinformatics, detecting rare mutations in primary tumors and metastases contributing to subclonal

79 olated pure populations of cancer cells from primary tumors and metastases from a genetically enginee

80 D1R-expressing primary tumors and metastases in mice were detected by f

81 Notably, growth of primary tumors and metastases was both strongly inhibite

82 Comparative genomic analyses of primary tumors and metastases within individuals with pa

83 setting, including 32 patients with matched primary tumors and metastases, and found a high level of

84 D8(+) T-cell-dependent tumor cell killing in primary tumors and metastases, and that these effects ca

85 t of targeted therapeutics effective against primary tumors and metastases.

86 Accumulating evidence from primary tumors and model systems supports a role for KDM

87 Xs is strikingly similar to that observed in primary tumors and recapitulates the heterogeneity of re

88 NK cell invasion of primary tumors and recruitment to the site of metastasis

89 ceptors (betaARs) to enhance metastasis from primary tumors and that beta-blockers may be protective

90 sults in the eradication of light-irradiated primary tumors and the complete inhibition of untreated

91 es (PMNs) result from communications between primary tumors and the microenvironment of future distan

92 unosuppressive myeloid cell populations into primary tumors and their ascites.

93 otoxicity against malignant T-cell lines and primary tumors and were protective in a mouse xenograft

94 in-fixed, paraffin-embedded samples of their primary tumors and were randomized to either a 5-year ta

95 of its somatic mutation repertoire with the primary tumor, and all samples from each patient grouped

96 , contains many of the same mutations as the primary tumor, and could be a tool for noninvasive disea

97 oncept of metabolic heterogeneity within the primary tumor, and how cancer cells are metabolically co

98 elop liver metastases after resection of the primary tumor, and surgical resection of the metastases

99 d SUVmean of healthy target organs, residual primary tumor, and up to 5 lesions with the highest SUVm

100 105 cases of neuroblastoma, complemented by primary tumor- and cell line-derived global histone modi

101 Primary tumors are known to constantly shed a large numb

102 Primary tumors are often heterogeneous, composed of ther

103 lorectal cancer (mCRC) is heterogeneous, and primary tumors arising from different regions of the col

104 lorectal cancer (mCRC) is heterogeneous, and primary tumors arising from different regions of the col

105 the relationship of (18)F-FDG uptake in the primary tumor at diagnosis, during therapy, and after th

106 apitulate underlying genomic aberrations and primary tumor biology.

107 estral subclone that was not detected in the primary tumor biopsy.

108 formed from formalin-fixed paraffin-embedded primary tumor blocks.

109 n, we hypothesized that high-intensity LT of primary tumor burden, defined as the receipt of radical

110 Despite a reduced primary tumor burden, Notch activation in Pten-null mice

111 helial cells, which collectively reduced the primary tumor burden.

112 dvantageous traits that may originate in the primary tumor but continue to evolve during disseminatio

113 cation is present in approximately 10-30% of primary tumors but in more than 70% of recurrent tumors,

114 oma patients, ARID1A was highly expressed in primary tumors but not in metastatic lesions, suggesting

115 metastasis or relapse disseminate late from primary tumors, but continue to acquire mutations, mostl

116 athogenesis of this disease, even before the primary tumor can be detected.

117 erfect, and less-oriented crystals) and that primary tumors can further increase HA immaturity even b

118 aintained at high viability and suitable for primary tumor cell culture, are comprehensively characte

119 re, we studied genomic alterations in single primary tumor cells and circulating tumor cells (CTCs) f

120 ene were observed only in a minor portion of primary tumor cells but were present in all CTCs, sugges

121 es occurred sporadically, whereas CNAs among primary tumor cells emerged accumulatively rather than a

122 ng-for example, with cancer therapies-viable primary tumor cells from patients with cancer.

123 were graded by estimating the percentage of primary tumor cells showing a positive staining of their

124 th in the majority of the MCL cell lines and primary tumor cells tested.

125 isms that result in the metastatic spread of primary tumor cells to distal organs.

126 lecular changes can promote the spreading of primary tumor cells to distant tissues.

127 We cultured primary tumor cells, isolated from EAC patient samples,

128 Results Of 152 patients, 125 had adequate primary tumor control after CCRT and entered follow-up (

129 fibers take a less tortuous path out of the primary tumor; conversely, cells that turn back upon enc

130 ved CDCP1) lead to increased LD abundance in primary tumors, decreased metastasis, and increased ACSL

131 Suppression of GnT-III in EOC cell lines and primary tumor-derived cells resulted in an inhibition of

132 tive extent to which factors from within the primary tumor disseminate to systemic tissues as well as

133 es acquired driver mutations not seen in the primary tumor, drawing from a wider repertoire of cancer

134 We show that a distant primary tumor drives the expansion of HSPCs within the b

135 , and OMI in tumor organoids correlates with primary tumor drug response.

136 Disease solidity and primary tumor energy from the co-occurrence matrix were

137 absence of BCMA, we maintained cytolysis of primary tumor expressing both BCMA and TACI in the prese

138 ally, endosialin-expressing pericytes in the primary tumor facilitate distant site metastasis by prom

139 delta (PyMT/p38delta(-/-)) exhibited delayed primary tumor formation and highly reduced lung metastat

140 Although primary tumor formation was similar between miR-23b/-27b

141 the primary tumor or is acquired well after primary tumor formation.

142 CD3(+) T cell infiltration in primary tumors from 77 metastatic melanoma patients was

143 metastatic tumor cells and was also found in primary tumors from colon cancer patients with distant m

144 in non-small cell lung cancer cell lines and primary tumors from multiple TCGA dataset with high EMT

145 We show that a high LOX expression in primary tumors from patients with colorectal cancer was

146 Moreover, MYCN-amplified and high-risk primary tumors from patients with neuroblastoma exhibite

147 MCPyV sequencing to distinguish independent primary tumors from related metastases.

148 ntly elevated on bone metastases relative to primary tumors from the same patient (n = 42).

149 uently develops years after the removal of a primary tumor, from a minority of disseminated cancer ce

150 We also integrated RNA-Seq data in various primary tumors, gene expression microarray data in over

151 Several CNAs recurrently observed in primary tumors gradually disappeared in PDXs, indicating

152 Tumor integrin beta1 (ITGB1) contributes to primary tumor growth and metastasis, but its specific ro

153 ordingly, EVs play an essential role in both primary tumor growth and metastatic evolution.

154 Furthermore, SI-2 can significantly inhibit primary tumor growth and reduce SRC-3 protein levels in

155 herapy induced CD8(+) T lymphocyte-dependent primary tumor growth delay and prolonged survival only i

156 eted therapy ("tumor cell debris") stimulate primary tumor growth when coinjected with a subthreshold

157 AFs at these early timepoints did not affect primary tumor growth, but instead increased the presence

158 Compared with vehicle, FPS-ZM1 inhibited primary tumor growth, inhibited tumor angiogenesis and i

159 eous subclonal populations emerge that drive primary tumor growth, regional spread, distant metastasi

160 suppresses bladder cancer metastasis but not primary tumor growth, which involves tumor-associated ma

161 ung metastasis formation while not affecting primary tumor growth.

162 attenuates lung metastasis without affecting primary tumor growth.

163 imental metastases in vivo without affecting primary tumor growth.

164 uces pulmonary metastasis, with no effect on primary tumor growth.

165 We find that each multicentric primary tumor harbors distinct oncogenic alterations, in

166 somatic alterations in muscle-invasive (MI) primary tumors, highlighting a major mechanism(s) contri

167 chromatin-immunoprecipitation sequencing of primary tumors, however, revealed clear differences, lea

168 ternative source to detect gene mutations in primary tumors; however, most previous studies have focu

169 ntinued attempts at >/= 90% resection of the primary tumor in high-risk neuroblastoma.

170 ry that evaluated the role of surgery of the primary tumor in patients with de novo stage IV breast c

171 s of metastases largely reflects that of the primary tumor in untreated patients, and PDAC driver mut

172 nd the dissemination of tumor cells from the primary tumor in vivo.

173 dentification of aberrant DNA methylation in primary tumors in humans more than 3 decades ago, progre

174 on of liver cancer organoids propagated from primary tumors in the genetic model was further develope

175 Primary tumors in the presacral (retrorectal) space are

176 iteria (INRC) require serial measurements of primary tumors in three dimensions, whereas the Response

177 lines mirrored the proteomic aberrations of primary tumors, in particular for intrinsic programs.

178 CC may develop a second genetically distinct primary tumor; in this case, the subsequent tumor is lik

179 n both carcinoma cell lines and a variety of primary tumors, independently of tumor microenvironment.

180 lower LD abundance than their corresponding primary tumors, indicating that LD abundance in primary

181 Emerging evidence suggests that the primary tumor influences the development of supportive m

182 BXO32 inhibits colony formation in vitro and primary tumor initiation and growth in vivo through targ

183 In HNSCC cell lines as well as primary tumors, integration into cancer-related genes le

184 aracteristically via direct extension of the primary tumor into nearby organs and the spread of exfol

185 Localization of the site of the unknown primary tumor is critical for surgical treatment of pati

186 Cancer cell invasion from primary tumors is mediated by a complex interplay betwee

187 ecades after initial successful treatment of primary tumors is well documented but poorly understood

188 hat inherited mitochondrial haplotypes alter primary tumor latency and metastatic efficiency.

189 rognostic information on the location of the primary tumor (left vs right location site of CC) indepe

190 dition, radioligand accumulation was seen in primary tumor lesions as well as in metastases.

191 In selected MCC patients with primary tumors less than 2 cm in diameter treated with s

192 g diverged at different time points from the primary tumor lineage.

193 significant interaction was observed between primary tumor location and treatment for OS (CRYSTAL: ha

194 rognostic role of left vs right-sidedness of primary tumor location in patients with CC.

195 rognostic role of left vs right-sidedness of primary tumor location in patients with CC.

196 amine the prognostic and predictive value of primary tumor location in patients with RAS wild-type (w

197 Primary tumor location is emerging as an important progn

198 Importance: Primary tumor location is emerging as an important progn

199 Left sided primary tumor location was associated with a significant

200 Primary tumor locations included the femur (n = 17; 50%)

201 xamine the evolutionary relationship between primary tumor, lymph node, and distant metastases in hum

202 Surgery, the mainstay of primary tumor management, also plays a role in the advan

203 hrough live imaging that LRC are leaving the primary tumor mass at a very early stage and disseminate

204 ns, these findings on initial surgery to the primary tumor may be of importance.

205 Thus, analyzing early-stage primary tumors may reveal the presence of T cells that a

206 and VEGFR2 rapidly formed tumors outside the primary tumor microenvironment in nude mice, exhibited s

207 mary tumors, indicating that LD abundance in primary tumor might serve as a prognostic marker for met

208 ding of how the cancer genome evolves as the primary tumor migrates from its origin in the pancreas t

209 osine kinase receptors was 10-fold higher in primary tumors of metastatic colorectal than in nonmetas

210 downregulation/methylation in cell lines and primary tumors of multiple carcinomas and lymphomas, inc

211 a landscape of genomic rearrangements in the primary tumors of ten ovarian cancer patients.

212 Injection of Mobilan into primary tumors of the prostate cancer-prone transgenic a

213 better SAR, and this benefit was limited to primary tumors of the proximal colon.

214 me measure was the effect of the site of the primary tumor on the association of biomarkers with SAR.

215 found among the uptake indices for residual primary tumor or any metastatic lesions in the liver, bo

216 and whether this ability is inherent to the primary tumor or is acquired well after primary tumor fo

217 Patients with node-negative primary tumors or a low clinical risk score seemed to be

218 expression in the microenvironment of either primary tumors or liver metastases triggered regression

219 In stromal leukocytes found in primary tumors or tumor-draining lymph nodes, which incl

220 t ECM protein signatures unique to fibrosis, primary tumors, or metastases.

221 Primary tumor organoids are a robust model of individual

222 Primary tumor organoids grown in three-dimensional cultu

223 were increased in metastases compared to the primary tumors (p = 0.031), independent of PIK3CA mutati

224 In NSCLC primary tumors, parametric and static baseline (18)F-FDG

225 PPP2R1A expression is elevated in high-grade primary tumor patients with papillary serous tumors of t

226 te a critical role for endosialin-expressing primary tumor pericytes in mediating metastatic dissemin

227 sition (EMT) is believed to be important for primary tumor progression and dissemination, whereas a m

228 process, as opposed to representing natural primary tumor progression.

229 At the primary tumor, PTX increased the abundance of the tumor

230 uppressing metastasis through effects on the primary tumor rather than the metastatic site.

231 or response (>/=10% vital tumor cells in the primary tumor) relative to marker levels.

232 3973 study evaluated the impact of extent of primary tumor resection on local progression and surviva

233 Adjuvant therapies were given after primary tumor resections to treat postsurgical regrowths

234 None of the methods of primary tumor response assessment was predictive of outc

235 Primary tumor response in children with high-risk neurob

236 idomic profile comparisons of LNM versus the primary tumor revealed a close association in contrast t

237 of skin cutaneous melanoma (SKCM) using 103 primary tumor samples from TCGA, and measured the expres

238 pression is reduced or absent in a subset of primary tumor samples.

239 ells acquire the ability to disseminate from primary tumors, seed distant organs, and grow into tissu

240 tial initial antitumor activity found in the primary tumor setting.

241 Analysis of TCR sequences from primary tumors showed about fourfold more overlap in tum

242 Five of 7 primary tumors showed focal (89)Zr-bevacizumab uptake (S

243 Analysis of the primary tumors showed significant increase in vimentin p

244 Local injection of CpG and polyI:C in a primary tumor significantly enhanced the activity of sys

245 lusion:(89)Zr-transferrin targets human TNBC primary tumors significantly better than (18)F-FDG, as s

246 the GBM tumor cells migrating away from the primary tumor site along the nanotopography of white mat

247 ound for MMR (P = .03) and KRAS (P = .02) by primary tumor site for SAR.

248 Management of the primary tumor site in patients with metastatic breast ca

249 ses (metastases that are in transit from the primary tumor site to the local nodal basin) in vivo.

250 py, platinum-refractory disease, mediastinal primary tumor site, nonseminoma histology, intermediate-

251 ile exhibiting increased angiogenesis at the primary tumor site, showed signs of shrinkage in the sin

252 central surgery review and resection of the primary tumor site.

253 t diagnosis with consideration for stage and primary tumor site.

254 Lack of p38delta resulted in reduced primary tumor size and blocked the metastatic potential

255 salt = 12 +/- 3, P < 0.05), without reducing primary tumor size.

256 ed INRC will integrate tumor response in the primary tumor, soft tissue and bone metastases, and bone

257 In vitro cultures of mouse primary tumor spheroids and human cancer cell lines disp

258 or papillary thyroid cancer as a function of primary tumor stage and number of LNs examined.

259 extracellular matrix that recapitulates the primary tumor stroma, adopt a basal-like phenotype.

260 of the DTCs to either the main tumor clone, primary tumor subclones, or subclones in an axillary lym

261 phosphorylation site mutations identified in primary tumors, supporting the confidence in their assoc

262 Of those 7600 women underwent primary tumor surgery although 8647 did not have any sur

263 Primary tumor surgery decreased from 62.0% in 1998 to 39

264 The benefit of primary tumor surgery increased from 1998 to 2009 for ov

265 Most importantly, the benefit of primary tumor surgery increased over time from 1998 to 2

266 s-provides evidence of a favorable impact of primary tumor surgery on mortality in metastatic breast

267 The effect of primary tumor surgery on overall and cancer-specific mor

268 Primary tumor surgery was associated with decreased over

269 netically more similar to their paired index primary tumors than metachronous recurrent tumors.

270 these models could be less representative of primary tumors than previously thought, particularly whe

271 is in human melanoma and is able to identify primary tumors that are likely to become metastatic.

272 direct apoptosis of lymphoma cell lines and primary tumors that otherwise were resistant to native I

273 In primary tumors the percentage of calcifications increase

274 Because of known primary tumor, the masses in the salivary glands were su

275 We analyzed the primary tumor, the sole treatment-resistant metastasis,

276 mutation burden is higher in metastases than primary tumors, the method described here may allow earl

277 tastases are seeded by single cells from the primary tumor, there is growing evidence that seeding re

278 stasis-relevant activities and thus help the primary tumor to adapt to the new microenvironment.

279 chanisms underlying the contributions of the primary tumor to premetastatic niche formation are not f

280 pared between clinically designated multiple primary tumors to characterize genetic relatedness and h

281 The spread of cancer cells from primary tumors to regional lymph nodes is often associat

282 Similar to the primary tumor, tumor cell cultures expressed very high l

283 status, time developing motor deficits, and primary tumor type.

284 in SM#1 is significantly associated with (i) primary tumor type; (ii) entropy in SM#2 (same malignant

285 abine in a preclinical model of PDAC reduces primary tumor volume and eliminates metastatic disease.

286 The median reduction in the size of the primary tumor was 14.4% (interquartile range, 1.4%-21.1%

287 C3 expression in primary tumors was predictive of leptomeningeal relapse.

288 From an initial 630 ILBC primary tumors, we interrogated oncogenic substitutions

289 , through the analysis of approximately 3000 primary tumors, we show that miR-424(322)/503 is commonl

290 -negative, and unconfirmed rates for unknown primary tumor were 38%, 7%, 50%, and 5%, respectively.

291 All negative scans for primary tumor were considered false-negative.

292 Results: The primary tumors were breast cancer (92 patients, 426 scan

293 The primary tumors were breast cancer (92 patients, 426 scan

294 The (11)C-MET-positive primary tumors were delineated semiautomatically on PET

295 ases arose from independent subclones in the primary tumor, whereas in 35% of cases they shared commo

296 y to recapitulate the heterogeneity found in primary tumors, which are referred to as cancer stem cel

297 abolism, which can endow rare cells within a primary tumor with metastatic potential.

298 n 2 of the KRAS proto-oncogene (KRAS) in the primary tumor with SAR in patients with stage III colon

299 Primary tumors with high GRPR expression were associated

300 hat the Kras(mut) allele was heterogenous in primary tumors yet homogenous in metastases, a pattern c