ライフサイエンスコーパス: invasive tumor

1 ihood of progression of superficial tumor to invasive tumor.

2 PSCC can occur as either an in situ or invasive tumor.

3 oclonal transformed cells to develop into an invasive tumor.

4 s than in patients with concomitant DCIS and invasive tumor.

5 ular evidence for the progression of DCIS to invasive tumor.

6 in the clonal progression to the synchronous invasive tumor.

7 nd messenger RNA, or mRNA, expression in the invasive tumor.

8 AC6 in vivo led to a more circumscribed less invasive tumor.

9 sion from APC-mutant neoplasia to submucosal invasive tumor.

10 oenvironment, ultimately resulting in a more invasive tumor.

11 enetic pathways, resulting in noninvasive or invasive tumors.

12 ficial tumors that are likely to progress to invasive tumors.

13 logy in the absence of features of malignant invasive tumors.

14 articularly estrogen receptor (ER) -positive invasive tumors.

15 found in poorly differentiated, later-staged invasive tumors.

16 tu melanomas, and from the RGP and VGP of 29 invasive tumors.

17 junction/cytoskeletal axis is a hallmark of invasive tumors.

18 unger, had higher stage tumors, and had more invasive tumors.

19 erentially expressed between superficial and invasive tumors.

20 st during the cells' transition to malignant invasive tumors.

21 ors have different propensity to progress to invasive tumors.

22 ugh the benefit was more pronounced for less invasive tumors.

23 duced apoptosis that is a hallmark of highly invasive tumors.

24 to a single phenotype at advanced stages of invasive tumors.

25 TAg-expressing cells in preinvasive foci and invasive tumors.

26 gnant epithelial cells in late-stage, highly invasive tumors.

27 -grade lesions but not in those derived from invasive tumors.

28 invariably integrate into the host genome in invasive tumors.

29 f the ACVR1C signaling, was observed in most invasive tumors.

30 eptide, reduced or absent staining in muscle invasive tumors.

31 ally increased in human gliomas, notoriously invasive tumors.

32 oplastic stages and a decreased incidence of invasive tumors.

33 pattern of staining to that observed for the invasive tumors.

34 uitary tumor growth and expansion into large invasive tumors.

35 ved in the invasiveness of gliomas and other invasive tumors.

36 Human malignant gliomas are highly invasive tumors.

37 of the end point of carcinomas and number of invasive tumors.

38 nase A on cell surfaces and are expressed in invasive tumors.

39 The bladder remains at risk for new invasive tumors.

40 croscopic manifestations of disease, such as invasive tumors.

41 CA1d cells outcompeted MCF10A, forming invasive tumors.

42 varian cancer, including both borderline and invasive tumors.

43 focus upon their role in high-risk nonmuscle invasive tumors.

44 hroughout tumor progression, and absent from invasive tumors.

45 scription factor that synergizes with FOS in invasive tumors.

46 2 and IL13 were increased and IL13 predicted invasive tumors.

47 differentiate between superficial and muscle-invasive tumors.

48 ring mutant p53, leading to the formation of invasive tumors.

49 i alone were lowest in localized and locally invasive tumors (1/14 and 2/12, respectively) and highes

50 18.5%; P < .001), and margin involvement by invasive tumor (12.3% vs 6.3%; P = .046) compared with t

51 Of 29 invasive tumors, 16 exhibited RGP mutations (55.2%); 22

52 %) relapsed in the bladder with a new muscle-invasive tumor, 18 (53%) were successfully treated with

53 Higher median AI scores were observed for invasive tumors (62 [IQR, 39-88]) than for noninvasive t

54 f 16 (100%) HNSCC cell lines, 26 of 29 (90%) invasive tumors, 7 of 7 (100%) dysplastic lesions, and 5

55 y of having an in situ tumor (rather than an invasive tumor) [95% CI: 3.48-4.61], compared to sites o

56 SVER expression resulted in hyperplasias or invasive tumors affecting particular visceral smooth mus

57 ped hyperplastic ductal trees and multifocal invasive tumors after several pregnancies, some of which

58 icial bladder tumors, the tumors progress to invasive tumors after treatment.

59 the probability of having an in situ versus invasive tumor among SCCA cases.

60 ne signature distinguishing invasive and non-invasive tumors among esLUAD.

61 quencies in 5,724 subjects with at least one invasive tumor and 1,943 subjects with in situ tumors on

62 Eligibility included 1 cm or larger invasive tumor and gBRCA-positive disease.

63 unger than the screening age, found that 711 invasive tumors and 180 cases of DCIS were overdiagnosed

64 D3S1300, was found in 6 of 16 microdissected invasive tumors and 3 of 6 ductal in situ carcinomas.

65 960 breast invasive tumors and 56 human breast cancer cell lines we

66 It is likely that 1 in every 3 invasive tumors and cases of DCIS diagnosed in women off

67 lioma model, PDZ1i resulted in smaller, less invasive tumors and enhanced survival.

68 e small GTPase RhoC is overexpressed in many invasive tumors and is essential for metastasis.

69 longer survival with only 20% penetrance of invasive tumors and no apparent lung or liver metastases

70 have demonstrated that proteases secreted by invasive tumors and pathological microorganisms are capa

71 uld predict the likelihood of progression to invasive tumors and to test the robustness of the expres

72 These sinusoids arose around locally invasive tumors and were associated with more advanced i

73 al cells of the desmoplastic response to the invasive tumor, and four of these genes were specificall

74 ven ovarian carcinoma cell lines, 71% of the invasive tumors, and 92% of the borderline tumor tissues

75 Advanced AJCC T-stage, locally invasive tumors, and more pathologically aggressive tumo

76 Non-muscle-invasive tumors are treated with endoscopic resection an

77 n which fingerlike shapes, characteristic of invasive tumor, are observed.

78 sociated form of RalGEF (RalGDS-CAAX) formed invasive tumors as well, demonstrating that activation o

79 omparatively resistant to the development of invasive tumors, as are RT2 C3HB6(F1) hybrid mice.

80 al complete response or the disappearance of invasive tumor at surgery.

81 generally present with small, unresectable, invasive tumors at a site traditionally considered progn

82 ts undergoing surgical resection for grossly invasive tumors at UT Southwestern Kidney Cancer Program

83 Glioblastoma multiforme is a highly invasive tumor bearing a dismal prognosis.

84 clear the breast and axillary lymph nodes of invasive tumor before surgery.

85 early-stage breast cancer treatment via non-invasive tumor burden assessment.

86 ygosity at this locus was observed in 50% of invasive tumors but in none of the borderline tumors.

87 endothelial, and tumor cells in a variety of invasive tumors but is undetectable in the majority of n

88 n family, N-cadherin, is expressed in highly invasive tumor cell lines that lacked E-cadherin express

89 tumor cells and their revertants from highly invasive tumor cell populations, indicating how phenotyp

90 and studying the gene expression profile of invasive tumor cell subpopulations would be a crucial st

91 Based on the hypothesis that invasive tumor cells are released more readily upon dige

92 cancer, 3p loss of heterozygosity occurs in invasive tumor cells as well as in morphologically norma

93 that archazolid induced apoptosis in highly invasive tumor cells at nanomolar concentrations which w

94 The invasive tumor cells collected from PyMT mouse mammary t

95 ndogenous APCN showed elevated expression in invasive tumor cells compared with intratumoral cells.

96 show a pattern like that seen previously in invasive tumor cells from the MTLn3 cell line-derived tu

97 activity significantly reduces migration of invasive tumor cells in vitro.

98 yonic development and for progression of non-invasive tumor cells into malignant, metastatic carcinom

99 To test the hypothesis that invasive tumor cells may block the formation of the fibr

100 cell behavior, which were identified in the invasive tumor cells of cell line-derived tumors, are co

101 ll line-derived tumors, are conserved in the invasive tumor cells of PyMT-derived mouse mammary tumor

102 ng that the enforced expression of PEA-15 in invasive tumor cells reduced invasion.

103 The nuclei in 11 invasive tumor cells were typically round with finely di

104 iform, intense membrane staining of > 30% of invasive tumor cells), a fluorescent in situ hybridizati

105 analogously to the process of chemotaxis in invasive tumor cells, axonal growth cones of Xenopus spi

106 r conductance versus those derived from less invasive tumor cells, based on dielectrophoresis measure

107 herefore, CD147, which is itself elevated on invasive tumor cells, may make a major contribution to t

108 anched polylactosamine sugars that appear on invasive tumor cells.

109 n of EPLIN may contribute to the motility of invasive tumor cells.

110 ild type is expressed in G2/G3 tumors and in invasive tumor cells.

111 in, p38 MAPK activity, and uPA expression in invasive tumor cells.

112 ucial role in the promotion of glycolysis in invasive tumor cells.

113 on of CXCR4 and activated AKT in primary and invasive tumor cells.

114 d beta1 integrin may serve as a biomarker of invasive tumor cells.

115 ovide a means of targeting mesenchymal-like, invasive tumor cells.

116 several-fold lower than in the corresponding invasive tumors; cells throughout these multilayered pro

117 Invasive tumor characteristics did not differ significan

118 ficient mice resulted in development of less-invasive tumors compared with mice given vehicle.

119 glutamate release leads to smaller and less invasive tumors compared with saline-treated controls.

120 umors and widespread hypermethylation in the invasive tumors, confirming that the two pathways differ

121 gemistocytic astrocytomas, typically highly invasive tumors, contained high numbers of PLP-positive

122 Invasive tumors demonstrating loss of VHL consistently d

123 The mean diameter of the invasive tumors detected was 10.9 mm.

124 plus synthesized mammography (SM) increases invasive tumor detection compared with digital mammograp

125 bed that PPARgamma activation suppresses non-invasive tumor development and induces ER-positivity wit

126 and induces ER-positivity without affecting invasive tumor development.

127 combined mammography and MR imaging, median invasive tumor diameters at diagnosis decreased to 1.9,

128 from normal to preinvasive and ultimately to invasive tumors, discovering a potential structural bott

129 Interestingly, in situ lesions found in invasive tumors displayed LOH.

130 lesions and subgroups within early-stage and invasive tumors displaying different overall survival.

131 TWIST1 and C3 colocalized at the invasive tumor edges, and in the neural crest and limb b

132 Invasive tumors, even if completely resected, require ad

133 risk factors were similar for borderline and invasive tumors, except for age at diagnosis.

134 Invasive tumors exhibit aberrations in recruitment and a

135 Overall, 112 of 161 (69.5%) invasive tumors exhibited elevated expression.

136 Highly angiogenic and poorly invasive tumors expressed low levels of beta8 integrin,

137 Mammography depicted 39 (81%) of 48 invasive tumor foci and 14 (88%) of 16 foci of DCIS.

138 US depicted 45 (94%) of 48 invasive tumor foci and seven (44%) of 16 foci of ductal

139 m low- and high-grade dysplastic lesions and invasive tumor foci from 10 fully embedded esophageal re

140 for Ras mutation, and Ras is sufficient for invasive tumor formation in Rb1 family mutant mouse embr

141 lysine demethylase KDM6A were present in non-invasive tumors from females than males.

142 using gene array analysis of preinvasive and invasive tumors from mice, which were then evaluated in

143 vasion of HCC cells in the livers, with more invasive tumor front and increased incidence of venous i

144 ivated in a small subset of SCC cells at the invasive tumor front and predicts for poor prognosis of

145 with a compact core lesion surrounded by an invasive tumor front.

146 inated elevation of Twist and Glu-tubulin at invasive tumor fronts, particularly within ductal carcin

147 MAGL expression is increased in invasive tumors, furnishing free fatty acids as pro-tumo

148 o isoforms of bFGF may have implications for invasive tumor growth and chemoresistance.

149 red for many pathologic processes, including invasive tumor growth as well as physiologic organ/tissu

150 th a history of previous debulking), lack of invasive tumor growth, and minimal residual disease afte

151 will further facilitate in-depth analysis of invasive tumor growth, angiogenesis, metastasis and tumo

152 This disease is characterized by invasive tumor growth, leading to extensive bone destruc

153 including proliferative fibrotic disorders, invasive tumor growth, rheumatoid arthritis, and atheros

154 including proliferative fibrotic disorders, invasive tumor growth, rheumatoid arthritis, and atheros

155 ol and identify Alk as a genetic modifier of invasive tumor growth.

156 ted in development, tissue regeneration, and invasive tumor growth.

157 teinase (MT1-MMP) mediates proteolysis-based invasive tumor growth.

158 LIN28 expression levels were associated with invasive tumor growth.

159 ed through screening were at risk for a more invasive tumor (>/=T3: relative risk [RR] = 1.96; P < .0

160 ly pattern of loss while all foci of CIS and invasive tumor had an advanced pattern.

161 However, all invasive tumors had evidence of ss-galactosidase express

162 ive breast carcinomas than in normal breast; invasive tumors have significantly higher numbers than D

163 luding targeted intervention therapy and non-invasive tumor imaging in vivo.

164 ete response (pCR) defined as no evidence of invasive tumor in breast and axilla.

165 age of pathologic complete response (pCR; no invasive tumor in breast and axillary nodes).

166 pCR was defined as no evidence of invasive tumor in the breast and axillary lymph nodes.

167 plete response was defined as the absence of invasive tumor in the breast.

168 resection of the mass showed large masses of invasive tumor in the resection site, with small foci of

169 cinoma in situ (DCIS) of the breast is a non-invasive tumor in which cells proliferate abnormally, bu

170 , Notch1 loss could accelerate the growth of invasive tumors in a manner associated with increased ex

171 which TbetaRIII had been knocked down formed invasive tumors in athymic nude mice, whereas the contro

172 lized MCF-7 cells overexpressing IQGAP1 form invasive tumors in immunocompromised mice, whereas tumor

173 s are transformed in vivo, forming large and invasive tumors in immunocompromised mice.

174 rprisingly, were fully capable of initiating invasive tumors in NOD SCID gamma (NSG) mice.

175 ferative, poorly differentiated, and locally invasive tumors in nude mice compared with WT EREG-expre

176 genes, grow in soft agar and develop ectopic invasive tumors in recipient mice, indicating that the c

177 vival with a bladder, frequency of recurrent invasive tumors in the bladder, and survival after salva

178 senchymal transition, and production of more invasive tumors in xenograft assays.

179 Invasive tumors, including gliomas, utilize proteinases

180 carcinomas revealed a new categorization of invasive tumors into basal-like (positive for DeltaNp63

181 high (A2b2) SPARC-secreting clones produced invasive tumors, invading with fingerlike projections an

182 The switch from a quiescent tumor to an invasive tumor is accompanied by the acquisition of angi

183 recently-proposed genus Versteria causing an invasive, tumor-like hepatic infection with regional and

184 In invasive tumors, low-level 3q amplification (3 to 4 X co

185 scent dextran and efficiently accumulated in invasive tumor margins and brain-invading cells.

186 These spaces surrounded only locally invasive tumors (mean diameter, 0.85 mm) that had obstru

187 oportion of detected tumors that were large (invasive tumors measuring >/=2 cm) decreased from 64% to

188 n of detected breast tumors that were small (invasive tumors measuring <2 cm or in situ carcinomas) i

189 We show that not all invasive tumors metastasize and identify determinants of

190 0 with fibroblasts and observed also in this invasive tumor model with stroma components a decreased

191 with the corresponding patient tumors, with invasive tumors more likely to successfully engraft.

192 ell nutrients, driving shape instability and invasive tumor morphologies, and stabilizing mechanical

193 rms was detected in paraffin sections in all invasive tumors, most prominently in moderately differen

194 s (n=54), carcinoma is situ (CIS) (n=15) and invasive tumors (n=12).

195 aIgTrkB NCM-1 cells form rapidly growing and invasive tumors necessitating euthanasia of all mice by

196 d within one of five distinct regions of the invasive tumors (neoplastic epithelium; angioendothelium

197 In 9 cases, the invasive tumor nests were surrounded by an intact BM; in

198 Glioblastoma is an aggressive, invasive tumor of the central nervous system (CNS).

199 positive SLNs was found in patients who had invasive tumors of increasing size: 18 of 112 patients (

200 thod to automatically identify the extent of invasive tumor on digitized images.

201 nal neural network for detecting presence of invasive tumor on whole slide images.

202 n was scored negative, close or positive for invasive tumor or ductal carcinoma in situ according to

203 lance is eventually overwhelmed by a growing invasive tumor, our findings suggest that productive tum

204 chymal transition and migration and promoted invasive tumor outgrowth within mouse mammary ducts.

205 ete loss of Pten was not sufficient to cause invasive tumors, over two thirds of the mutant females d

206 Invasive tumors overexpress the short progesterone recep

207 sk stratification of patients with nonmuscle-invasive tumors permits appropriate timing of intravesic

208 Carcinogen-treated RDEB mice developed invasive tumors phenocopying human RDEB-cSCC, whereas wi

209 ng short hairpin RNA technology to mimic the invasive tumor phenotype and also RAD51 knockdown (RAD51

210 icroenvironment affect the proliferative and invasive tumor phenotype of the earliest stages of tumor

211 hat promote the switch from a noninvasive to invasive tumor phenotype remain obscure.

212 or expression of MMP3 is co-incident with an invasive tumor phenotype.

213 Whether invasive tumor phenotypes like EMT arise from oncogenic

214 therapy may be more effective for minimally invasive tumors rather than advanced-stage disease.

215 Ras/Raf pathway in the eye, or in malignant invasive tumors resulting when Raf activation is combine

216 s with concentrations substantially lower in invasive tumor rim (intact BBB) compared to glioblastoma

217 kely than first melanomas to be in situ; for invasive tumors, second melanomas were more likely to be

218 low-up, while the effect of DCIS adjacent to invasive tumor seemed to remain stable.

219 Therefore, patients with high-grade invasive tumors should be monitored closely, especially

220 for IDC + DCIS was limited to patients with invasive tumor size < 4 cm or with node negative disease

221 significantly associated with sex (P < .01), invasive tumor size (P < .01), T status (P < .01), N sta

222 Median invasive tumor size and proportion of cancers detected a

223 Fourteen cancers (10 invasive, tumor size range 4-15 mm, median 9 mm) were di

224 tion of unedited miR-376a* and the extent of invasive tumor spread as measured by magnetic resonance

225 th the presence of lymph node metastases and invasive tumor stages.

226 overexpressed at least 1.5-fold in the more invasive tumor subtype.

227 ALT were present in both intraepithelial and invasive tumors, suggesting that an ATRX mutation is an

228 greater degree in higher grade node-positive invasive tumors than in normal breast tissue or ductal c

229 ncy of copy number alterations was higher in invasive tumors than that in DCIS, with several of them

230 luminal-like cells generated larger and more invasive tumors than their basal-like counterparts.

231 Ductal carcinoma in situ (DCIS) is a pre-invasive tumor that can progress to invasive breast canc

232 Patients with high-risk non-muscle invasive tumors that do not respond to adjuvant therapy

233 lood vessels, and arterioles and to identify invasive tumor through distinctive patterns in OCME imag

234 based on molecular mutations, which require invasive tumor tissue sampling.

235 f exon 2 solely in the cancer cell lines and invasive tumor tissues.

236 ension (ENE) or positive margins (<5 mm from invasive tumor to the resected margin).

237 tic tumors and other differentiated and less invasive tumor types.

238 We observed complete loss of KiSS-1 in all invasive tumors under study as compared to their respect

239 This surgery is best suitable for locally invasive tumors unresectable because of location and vas

240 enotypic pathways (superficial papillary non-invasive tumors versus flat carcinoma in situ lesions),

241 Induction of M-severin in an invasive tumor was directly observed in human colon aden

242 No invasive tumor was found in the tracheobronchial tree or

243 Invasive tumors were also divided into 2 groups (>10 mm

244 Invasive tumors were found at significantly higher frequ

245 Fifteen cases were pure DCIS; most invasive tumors were smaller than 1.0 cm.

246 with germ-line mutations in BRCA1 and BRCA2, invasive tumors were studied from 58 Jewish women ascert

247 ncident breast cancer cases (including 5,245 invasive tumors) were ascertained among 89,902 women.

248 oes not express BEHAB/brevican and forms non-invasive tumors when grown as intracranial grafts, can f

249 ls still form progressively growing, locally invasive tumors when injected into mammary fat pads but

250 when grown as intracranial grafts, can form invasive tumors when transfected with a 5' cDNA fragment

251 ults suggest that 10p losses may define less invasive tumors, whereas 10q losses may play a role in t

252 PIK3CA mutations occur almost exclusively in invasive tumors, whereas upstream mutations occur as fre

253 The less common but more aggressive invasive tumors, which have a higher mortality rate, are

254 The association of high-grade invasive tumor with IBTR diminished during follow-up, wh

255 assified normal urothelium, superficial, and invasive tumors with 82.2% accuracy, and stratified blad

256 risk of relapse (P = .04) and patients with invasive tumors with both shorter relapse-free (P = .004

257 ssociations were evident for the majority of invasive tumors with ductal histology and regardless of

258 erm invasive surveillance, to aggressive and invasive tumors with high disease-specific mortality.

259 low levels of beta8 integrin, whereas highly invasive tumors with limited neovascularization expresse

260 hiCD49flo cells, some of which progressed to invasive tumors with luminal features.

261 loci in 49 noninvasive urothelial tumors, 38 invasive tumors with matched normal-appearing urothelium

262 hnic minority groups more often have larger, invasive tumors with positive lymph nodes.

263 us cell carcinomas (SCCas) are heterogeneous invasive tumors with proliferating outer layers and inne

264 gnef-C-expressing cells formed smaller, less invasive tumors with reduced tyrosine phosphorylation of

265 Rnd3 expression was significantly lower in invasive tumors with satellite nodules.