ライフサイエンスコーパス: invasive carcinoma

1 derate dysplasia) and malignant (in situ and invasive carcinoma).

2 cal neoplasia (MFN) (high-grade dysplasia or invasive carcinoma).

3 from prostatic intraepithelial neoplasia to invasive carcinoma.

4 DCIS is a nonobligatory precursor for invasive carcinoma.

5 ma from an indolent in situ state to a frank invasive carcinoma.

6 ere 19.3% ductal carcinoma in situ and 80.7% invasive carcinoma.

7 ere 21.1% ductal carcinoma in situ and 78.9% invasive carcinoma.

8 histological stages of hyperplasia, DCIS to invasive carcinoma.

9 omas and completely prevented progression to invasive carcinoma.

10 rs, 16 (11%) carcinoma in situ, and 16 (11%) invasive carcinoma.

11 atients with non-high-grade DCIS will harbor invasive carcinoma.

12 edict progression from CIN1/CIN2 to CIN3 and invasive carcinoma.

13 rom premalignant ductal carcinoma in situ to invasive carcinoma.

14 ng of 12 IPMNs with or without an associated invasive carcinoma.

15 ence of documented associated progression to invasive carcinoma.

16 ductal carcinoma in situ (DCIS) and 341 were invasive carcinoma.

17 e marker for the presence of IPMN-associated invasive carcinoma.

18 pressing BRAF(V600E) in thyrocytes developed invasive carcinoma.

19 nstability and loss of cell cycle control in invasive carcinoma.

20 r estimating the presence of IPMN-associated invasive carcinoma.

21 breast carcinoma; five (83%) of the six had invasive carcinoma.

22 occurred during or after the progression to invasive carcinoma.

23 rmalities and to develop toward the stage of invasive carcinoma.

24 ic instability, can result in progression to invasive carcinoma.

25 ociated with more frequent predisposition to invasive carcinoma.

26 for telomerase activity, but only in foci of invasive carcinoma.

27 nsition from localized, carcinoma in situ to invasive carcinoma.

28 a in situ in all eight; two also had foci of invasive carcinoma.

29 from prostatic intra-epithelial neoplasia to invasive carcinoma.

30 pathways which proceeds the transition into invasive carcinoma.

31 ritical transition from carcinoma in situ to invasive carcinoma.

32 idase expression, but expression was seen in invasive carcinoma.

33 rostate intraepithelial neoplasia (PIN), and invasive carcinoma.

34 etected in lesions before the development of invasive carcinoma.

35 t during the transition from preneoplasia to invasive carcinoma.

36 MI phenotype in any CAHs without associated invasive carcinoma.

37 dysplasia/metaplasia, in situ carcinoma, and invasive carcinoma.

38 18 (22%) CAHs that were not associated with invasive carcinoma.

39 r epithelium are not directly related to the invasive carcinoma.

40 itions between intraepithelial neoplasia and invasive carcinoma.

41 premalignant lesions prior to development of invasive carcinoma.

42 is, especially in the absence of macroscopic invasive carcinoma.

43 nety-three IPMN patients (38%) suffered from invasive carcinoma.

44 lates with increasing disease progression to invasive carcinoma.

45 progression from ductal carcinoma in situ to invasive carcinoma.

46 ose breast tissue to eventual development of invasive carcinoma.

47 ted in the in situ and down-regulated in the invasive carcinoma.

48 most benign lesion that rarely progresses to invasive carcinoma.

49 cancers detected with MR imaging alone were invasive carcinomas.

50 cysts and microcysts, as well as in situ and invasive carcinomas.

51 B-Chr Y(FVB-Tg(Ela-KRASG12D)) mice developed invasive carcinomas.

52 wild-type allele of Trp53 and progression to invasive carcinomas.

53 papillary bladder tumors, without eliciting invasive carcinomas.

54 aperones as valuable therapeutic targets for invasive carcinomas.

55 en they progress from preinvasive lesions to invasive carcinomas.

56 in cancer cell motility, a key phenotype of invasive carcinomas.

57 lesions (LSIL), high-grade SILs (HSIL), and invasive carcinomas.

58 and a substantive reduction in the number of invasive carcinomas.

59 and is very strongly expressed in nearly all invasive carcinomas.

60 ant lesions, of nascent solid tumors, and of invasive carcinomas.

61 cells as tumors progressed to comedo-DCIS or invasive carcinomas.

62 s DCIS lesions progressed to comedo-DCIS and invasive carcinomas.

63 as important implications for development of invasive carcinomas.

64 s benign or in situ proliferative lesions to invasive carcinomas.

65 proportion than we have previously noted for invasive carcinomas.

66 mammary lesions developed and progressed to invasive carcinomas.

67 82 large (> or =1 cm) adenomas, and 1 of 72 invasive carcinomas.

68 hologic findings included six in situ and 20 invasive carcinomas.

69 ng progression to expansive solid tumors and invasive carcinomas.

70 gly expressed in the neoplastic epithelia of invasive carcinomas.

71 Cancer Imaging Archive (TCIA) for 91 breast invasive carcinomas.

72 ated NOTCH1 protein and increased TICs in TN invasive carcinomas.

73 tion is present in all the models developing invasive carcinomas.

74 ression and increasing histological grade in invasive carcinomas.

75 ients at risk for IOPNs and their associated invasive carcinomas.

76 N: 57 adenomas (39 advanced adenomas) and 12 invasive carcinomas.

77 lesions, and in 89% of in situ and in 83% of invasive carcinomas.

78 Eleven primary invasive carcinomas (10 masses, one case of microcalcifi

79 s (40% vs 16%; OR, 3.5; 95% CI, 2.0-6.1) and invasive carcinomas (12% vs 5%; OR, 2.9; 95% CI, 1.2-6.9

80 2%) had either high-grade dysplasia (33%) or invasive carcinoma (39%).

81 l activity was only confirmed in a number of invasive carcinomas (5/26).

82 +ve), expression is usually lost in adjacent invasive carcinoma (8/30 Rad+ve; P < 0.0001).

83 sults in effects ranging from hyperplasia to invasive carcinoma accompanied by metastasis, depending

84 Invasive carcinoma after atypical lobular hyperplasia is

85 e intrinsic molecular subtypes that exist in invasive carcinoma also exist in DCIS with prognostic im

86 as 1.1 cm (range, 0 to 6.5) in patients with invasive carcinoma and 1.0 cm (range, 0 to 9.3) in patie

87 Of the 57 breast lesions, 39 were invasive carcinoma and 18 were postbiopsy inflammation.

88 Immunostaining showed increased L12-LOX in invasive carcinoma and approximately one-half of metasta

89 yielded carcinoma, of which five (50%) were invasive carcinoma and five (50%) were DCIS.

90 %, with the highest level of concordance for invasive carcinoma and lower levels of concordance for D

91 DATS administration prevents progression to invasive carcinoma and lung metastasis in TRAMP mice.

92 les the relationship of borderline tumors to invasive carcinoma and provides a morphological and mole

93 continuous progression from premalignant to invasive carcinoma and seven (77.7%) of these cases show

94 of these lesions, of which seven (78%) were invasive carcinoma and two (22%) were ductal carcinoma i

95 umors, allelic loss may predate the onset of invasive carcinoma and, in some cases, cellular atypia (

96 Of the 55 lesions evaluated, 35 were invasive carcinomas and 20 were benign.

97 2/39 (30.8%) malignancies in 12 women: seven invasive carcinomas and five ductal carcinoma in situ.

98 instability drives tumorigenic processes in invasive carcinomas and premalignant breast lesions, and

99 D326) is a surface glycoprotein expressed by invasive carcinomas and some epithelia.

100 noma in situ, but was expressed in 36 of 118 invasive carcinomas and strongly correlated with tumor s

101 ion for the heightened decorin levels around invasive carcinomas and suggest that decorin may functio

102 vasive DCIS cells enhances the transition to invasive carcinomas and suggests that three-dimensional

103 sease-specific survival (P = 0.01) in widely invasive carcinomas and the Ki-67(+)/Bcl-2(-) phenotype

104 patients correlated strongly with high-grade invasive carcinomas and with chromosome instability, par

105 h-grade prostatic intraepithelial neoplasia, invasive carcinoma, and a lung metastasis exhibited sign

106 l carcinoma in situ (DCIS), DCIS adjacent to invasive carcinoma, and invasive ductal breast carcinoma

107 ic intraepithelial neoplasia, microinvasion, invasive carcinoma, and poorly or undifferentiated carci

108 atypical hyperplasia, carcinoma in situ, or invasive carcinoma, and the remaining 8% exhibited histo

109 n, defining the relation between in situ and invasive carcinomas, and identifying clinically useful m

110 appears hormone-responsive at early stages, invasive carcinomas are hormone-independent, which corre

111 acterize the clinicopathological features of invasive carcinomas arising in intraductal papillary muc

112 Two distinct histological subtypes of invasive carcinomas arising in IPMNs have been described

113 spontaneously, and tumor lesions, including invasive carcinoma, arose in the inflamed region of the

114 as likely to progress to larger adenomas and invasive carcinomas as other adenomas, however, with the

115 e recurrence and progression and to identify invasive carcinoma at an earlier stage, when it may be m

116 bout 12 weeks of age with the development of invasive carcinomas at about 16 weeks of age in 100% of

117 elopment of preneoplastic fundic lesions and invasive carcinoma attributable to the deletion of one p

118 ors other than tumor biology associated with invasive carcinoma based on final pathologic findings ma

119 sis of non-high-grade DCIS, 8320 (22.2%) had invasive carcinoma based on final pathologic findings.

120 tly associated with an upgraded diagnosis of invasive carcinoma based on final pathologic findings.

121 s, and recently updated staging criteria for invasive carcinoma based on the Cancer Staging Manual, e

122 plications to DNA methylation data of breast invasive carcinoma (BRCA) and kidney renal clear cell ca

123 oma in The Cancer Genome Atlas (TCGA) Breast Invasive Carcinoma (BRCA) cohort.

124 IPNB is a recognized precursor of invasive carcinoma, but its pathogenesis and natural his

125 r neoplasia by 3 months, which progressed to invasive carcinoma by 6-10 months.

126 ost noninvasive ductal carcinoma in situ and invasive carcinomas by increased miR-21 (the most abunda

127 develop adenomas and inevitably progress to invasive carcinomas by the age of 40.

128 Progression to invasive carcinoma can occur years after the surgical re

129 We propose that invasive carcinomas can arise by different genetic and b

130 NA methylation array data of the four breast invasive carcinoma cancer subtypes from The Cancer Genom

131 Among invasive carcinoma cases (663 interpretations), 96% (95%

132 havbeta6 have been linked to more aggressive invasive carcinoma cell behavior and poorer clinical pro

133 We found that when highly invasive carcinoma cells (MDA-MB-231) were placed in con

134 in's activity, we restored its expression in invasive carcinoma cells and analyzed the resulting chan

135 (6)beta(4) integrin exists on the surface of invasive carcinoma cells and that hepatocyte growth fact

136 ivo invasion assay, it was demonstrated that invasive carcinoma cells are a unique subpopulation of t

137 Invasive carcinoma cells form invadopodia, F-actin-rich

138 Given that only invasive carcinoma cells gain permanent access to type I

139 s to identify the gene expression profile of invasive carcinoma cells in primary mammary tumors.

140 depletion of beta(4) by RNA interference in invasive carcinoma cells that express both receptors red

141 Invadopodia, actin-based protrusions of invasive carcinoma cells that focally activate extracell

142 Invasive carcinoma cells use specialized actin polymeriz

143 the glycosylation of alpha-DG is altered in invasive carcinoma cells, and this modification causes c

144 edge, as well as in invadopodia formation of invasive carcinoma cells, where it is activated at the b

145 are matrix-degrading membrane protrusions in invasive carcinoma cells.

146 ation previously shown to be associated with invasive carcinoma cells.

147 n normal cells, and is deregulated in highly invasive carcinoma cells.

148 smosomes but it also plays a dynamic role in invasive carcinoma cells.

149 80) revealed frequent loss of Nuc-pYStat5 in invasive carcinoma compared to normal breast epithelia o

150 t of MRI was not significantly different for invasive carcinoma compared with ductal carcinoma-in-sit

151 3CA mRNA levels were significantly higher in invasive carcinomas compared with benign and low maligna

152 errogation of the Cancer Genome Atlas breast invasive carcinoma data set indicates that alterations o

153 We apply JDINAC to a Breast Invasive Carcinoma dataset, which includes 114 patients

154 ) of invasive carcinomas; smaller subsets of invasive carcinoma demonstrated moderate telomere shorte

155 the tissue recombinants responded by forming invasive carcinomas, demonstrating mixed, predominantly

156 Frankly invasive carcinoma developing subsequently showed occasi

157 ming that only a single lesion progresses to invasive carcinoma during the life of an individual, and

158 d animals, histopathologically heterogeneous invasive carcinomas exhibiting up-regulation of the Igf1

159 sis of four ductal carcinomas in situ and 10 invasive carcinomas (five at stage I).

160 tions of cases with an upgraded diagnosis of invasive carcinoma from final surgical pathologic findin

161 mples from IPMNs, MCNs, and small associated invasive carcinomas from 18 patients using whole exome o

162 growing, highly motile cancer cells and late invasive carcinomas, GIV is highly expressed and has an

163 However, a dose-response reduction in invasive carcinoma growth was observed for both DFMO, an

164 advanced neoplasia [high grade dysplasia or invasive carcinoma (HGD/IC)] was determined.

165 High-risk PCLs were those with invasive carcinomas, high-grade dysplasia, or intestinal

166 carcinoma, increasing size and percentage of invasive carcinoma, histologic type of invasive carcinom

167 ly expressed by the stromal cells within the invasive carcinoma; however, 1 (collagen 1alpha1) was ex

168 In invasive carcinomas, HSF1 expression was associated with

169 ty, 21% had ductal carcinoma in situ (DCIS), invasive carcinoma (IC), or lymphovascular invasion (LVI

170 carcinoma in situ (DCIS) is a progenitor of invasive carcinoma (IDC).

171 e frequent in DCIS than previously noted for invasive carcinoma implicates signaling by HER-2/neu as

172 IGCNBB demonstrated invasive carcinoma in 178 patients.

173 high-grade intraepithelial neoplasia and 12 invasive carcinoma in 30 (23.3%) patients.

174 ere essential to promote the preneoplasia to invasive carcinoma in an LTbeta receptor (LTbetaR)-depen

175 he commensal Escherichia coli NC101 promoted invasive carcinoma in azoxymethane (AOM)-treated Il10(-/

176 d point was pathologic complete response (no invasive carcinoma in breast or axilla).

177 ancy rate including high-grade dysplasia and invasive carcinoma in IPMNs with MPD involvement was 68%

178 ers to predict the presence of an associated invasive carcinoma in IPMNs.

179 sion from ductal breast carcinoma in situ to invasive carcinoma in mouse xenograft models.

180 cyte ratio (PLR) values, and the presence of invasive carcinoma in patients with intraductal papillar

181 or the development of an IPMN with HGD or an invasive carcinoma in the remnant pancreas.

182 E was defined as local recurrence of DCIS or invasive carcinoma in the treated breast.

183 cancer in 22 lesions, and the diagnosis was invasive carcinoma in the two other cancers.

184 ne, which was sufficient to enable growth of invasive carcinoma in vivo.

185 ctable in human biopsies from aggressive and invasive carcinomas in comparison with in situ carcinoma

186 and cooperated with oncogenic Ras to produce invasive carcinomas in vivo.

187 ntation with elevated bilirubin, presence of invasive carcinoma, increasing size and percentage of in

188 erwent resection for IPMN with an associated invasive carcinoma (IPMN-INV).

189 The progression from preinvasive lesion to invasive carcinoma is a critical step contributing to br

190 An IGCNBB diagnosis of invasive carcinoma is also associated with nearly 100% s

191 Tumor progression to invasive carcinoma is associated with activation of SRC

192 table derivative of this dogma is that every invasive carcinoma is in fact a missed intraepithelial t

193 st cancer varies among histological types of invasive carcinoma is unknown.

194 Among the invasive carcinoma lesions, 33 (85%) showed an increase

195 higher than that of p53 loss in mPIN but not invasive carcinoma lesions.

196 A total of 70 small IPMN-associated invasive carcinomas (</=20-mm invasion) were identified,

197 ines reveals that certain lines derived from invasive carcinomas maintain expression of Delta Np63, a

198 Biopsy results revealed eight early stage invasive carcinomas (malignant group) and 73 benign lesi

199 from two institutions providing consecutive invasive carcinomas manifesting as noncalcified masses s

200 Early invasive carcinoma may be encountered in association wit

201 Minimally invasive carcinomas ([MIC] n = 23) had one focus of intr

202 545; 3.6 %), dysplasia (n = 49; 0.4 %), and invasive carcinoma (n = 22; 0.2 %) were rare.

203 intraductal papillary mucinous neoplasms as invasive carcinoma (n = 40) or as noninvasive neoplasms

204 rgery on the basis of histologic findings of invasive carcinoma (n = 7), ductal carcinoma in situ (n

205 ssed selectively in IPMNs with an associated invasive carcinoma (n = 7), we also identified a panel o

206 rray analysis on a cohort of 139 consecutive invasive carcinomas (n = 417 tissue samples) immunostain

207 t cancers (ductal carcinoma in situ, n = 20; invasive carcinoma, n = 40) for an overall supplemental

208 48) and high-risk (high-grade dysplasia and invasive carcinoma: n = 30) groups.

209 ry B cells (Bregs) were observed in PBMCs of invasive carcinoma of breast (IBCa) patients compared wi

210 disease without an intervening recurrence as invasive carcinoma of different histologic type.

211 ndard treatment for all patients with muscle-invasive carcinoma of the bladder.

212 Patients aged at least 18 years with invasive carcinoma of the breast (pT1-3, pN0-1, M0) afte

213 ently positive for DNA-PKcs and Ku80, except invasive carcinoma of the breast.

214 cancer; operable, histologically confirmed, invasive carcinoma of the breast; adequate tumour specim

215 The remaining 19 patients proved to have invasive carcinoma of the cervix.

216 creased expression of 12/15-LOX in HGPIN and invasive carcinoma of the LPB-Tag model is similar to th

217 ation, of a renal transplant patient with an invasive carcinoma of the vulva for which postoperative

218 or loss of CCN6 protein has been reported in invasive carcinomas of the breast with lymph node metast

219 a mixture of adenomas, squamous papillomas, invasive carcinomas of the forestomach, as well as tumor

220 Invasive progression was defined as invasive carcinoma on pathology and/or positive cytopath

221 ed the safety of both guidelines, describing invasive carcinoma or carcinoma in situ in 67% of BD-IPM

222 Ns, 24.6% (17/69) showed malignant features (invasive carcinoma or carcinoma in situ) upon histologic

223 Positive margins (ink on invasive carcinoma or ductal carcinoma in situ) are asso

224 Patients with invasive carcinoma or with follow-up < 6 months were exc

225 Many women with DCIS will develop actual invasive carcinoma over time, whereas others-especially

226 ly elevated in patients with IPMN-associated invasive carcinoma (P < 0.001).

227 her hand, LOH was observed in 40% (17/42) of invasive carcinomas (P = 0.0005).

228 sing Omics Pipe, we analyzed 100 TCGA breast invasive carcinoma paired tumor-normal datasets based on

229 eading us to term them poorly differentiated invasive carcinomas (PDICs).

230 lesions of all histological grades, although invasive carcinomas per se were not seen.

231 ge of invasive carcinoma, histologic type of invasive carcinoma, positive lymph nodes, and vascular i

232 ma); for papillary tumors, the proportion of invasive carcinoma present was determined.

233 The size of invasive carcinomas ranged from 0.6-1.0 cm (mean, 0.5 cm

234 Seventeen (85%) of 20 primary invasive carcinomas recurred invasively: 16 (94%) with s

235 promotes the growth of poorly differentiated invasive carcinomas remains to be defined.

236 e-grade dysplasia, high-grade dysplasia, and invasive carcinoma, respectively (P < 0.001).

237 ies resembling either benign fibroadenoma or invasive carcinoma samples.

238 Of the invasive carcinomas smaller than 1 cm, RhoC was highly s

239 lomere shortening in the majority (52.5%) of invasive carcinomas; smaller subsets of invasive carcino

240 tory analysis revealed a distinctive primary invasive carcinoma subclass featuring extreme global met

241 ice showed a higher incidence of in situ and invasive carcinoma, suggesting that endometrial tumorige

242 noma in situ exhibited similar expression as invasive carcinoma, suggesting that GKLF is activated pr

243 cancer progression from in situ carcinoma to invasive carcinoma, suggesting that loss of tumor HEVs i

244 helial neoplasia and DCIS, and progressed to invasive carcinoma, suggesting the model provides a rigo

245 Invasive carcinomas survive and evade apoptosis despite

246 of breast cancer survival (P < 0.05, n = 80 invasive carcinoma; TCGA RNA-sequences).

247 s were significantly higher in patients with invasive carcinoma than those patients with either benig

248 Ductal carcinoma in situ is a non-invasive carcinoma that is unlikely to recur if complete

249 s from precursor intraepithelial lesions, to invasive carcinoma that metastasizes to lymph nodes, liv

250 e is no robust marker capable of identifying invasive carcinomas that despite their small size have a

251 epithelial cadherin (E-cad) is a hallmark of invasive carcinomas that have acquired epithelial-mesenc

252 In 221 assessable cores of invasive carcinoma, the Mcm-2 LI showed a positive assoc

253 On WLEBB, 173 of the remaining 175 had invasive carcinoma; the other 2 patients had carcinoma i

254 Given their significant risk of harboring invasive carcinoma, they should be treated with complete

255 se to cervical intraepithelial neoplasia and invasive carcinoma through the expression and activity o

256 an breast cancer cell lines and human breast invasive carcinoma tissue compared with a human non-tumo

257 Furthermore, low CCN6 expression in invasive carcinoma tissue samples correlates with reduce

258 vascular growth especially at the in situ to invasive carcinoma transition.

259 ve series of 173 patients (176 cancers) with invasive carcinoma underwent SSM and immediate breast re

260 to limit the progression of preneoplasms to invasive carcinoma unless circumvented by the acquisitio

261 Patients with an upgraded diagnosis of invasive carcinoma vs those with a diagnosis of DCIS bas

262 alence of NP-CRNs with in situ or submucosal invasive carcinoma was 0.82% (95% CI, 0.46%-1.36%; n = 1

263 iation of NP-CRNs with in situ or submucosal invasive carcinoma was also observed in subpopulations f

264 Invasive carcinoma was detected significantly more often

265 al abnormality at US; in two (12%) patients, invasive carcinoma was diagnosed at US-guided biopsy (9

266 idual in situ mammographically and US occult invasive carcinoma was found at histopathologic examinat

267 n 31, carcinoma in situ was found in 25, and invasive carcinoma was found in 11 (100% sensitivity, 88

268 reater than 3 cm, it was 8.8%, and 1 case of invasive carcinoma was found.

269 ay be underestimated at SDVAB; in our study, invasive carcinoma was later discovered in 25% of patien

270 The presence of histopathologic invasive carcinoma was noted at subsequent surgical biop

271 Invasive carcinoma was present in 30 patients (48%).

272 Invasive carcinoma was seen in 29/39 (74%) IPNBs.

273 tal mammography in the detection of DCIS and invasive carcinoma was substantially better than that of

274 quamous cell carcinomas to undifferentiated, invasive carcinomas was increased.

275 gnancy rate of 18% (high-grade dysplasia and invasive carcinoma) was found.

276 Because PLK1 is up-regulated in many invasive carcinomas, we asked whether it may also play a

277 thologic differentiation grades for DCIS and invasive carcinoma were similar with both modalities.

278 " trial showed that young age and high-grade invasive carcinoma were the most important risk factors

279 Invasive carcinomas were found only in Eralpha(+/-)Min/+

280 Invasive carcinomas were modestly underrepresented in MF

281 nistration of 1,2-dimethylhydrazine and DSS, invasive carcinomas were observed exclusively in Spdef(-

282 ial structures, corresponding to in situ and invasive carcinoma, were not consistently altered by NAF

283 erplasia, metaplasia, carcinoma in situ, and invasive carcinoma, were observed.

284 p-STAT3, IL-6R, and SNAIL and progressed to invasive carcinomas, which was not observed in WT animal

285 MAD4 and TGFBR2 are frequently restricted to invasive carcinoma, while RNF43 alterations are largely

286 Widely invasive carcinomas ([WIC] n = 33) demonstrated more tha

287 st cancer risk factors, the RRs (95% CIs) of invasive carcinoma with a favorable histology were 4.42

288 of ever HRT use was associated with risk of invasive carcinoma with a favorable histology, with an R

289 inal polyps in 6-8 months that progressed to invasive carcinomas with a similar pattern of dysplasia

290 hyrocytes become transformed and progress to invasive carcinomas with a very short latency, a process

291 as (SCCs), but the mice still develop highly invasive carcinomas with EMT properties, reduced levels

292 The tumors resemble human invasive carcinomas with increased vascularization and o

293 RhoC had high specificity (88%) in detecting invasive carcinomas with metastatic potential.

294 one of the top genes with low expression in invasive carcinomas with poor clinical outcome.

295 pancreatic neuroendocrine tumors (PNET) and invasive carcinomas with varying degrees of aggressivene

296 rol rabbits receiving vector alone developed invasive carcinoma within 8 to 13 months.

297 n circulating EV can predict the presence of invasive carcinoma within IPMN.

298 t many of these lesions will not progress to invasive carcinoma within the lifetime of a patient.

299 thology revealed an 8-mm well-differentiated invasive carcinoma without lymphovascular invasion and i

300 progress through a flat adenomatous stage to invasive carcinoma without transit through an intermedia

301 ial cell-BM interaction is often impaired in invasive carcinomas, yet roles and underlying mechanisms