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

4 histological stages of hyperplasia, DCIS to invasive carcinoma.

5 omas and completely prevented progression to invasive carcinoma.

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

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

8 rom premalignant ductal carcinoma in situ to invasive carcinoma.

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

10 ence of documented associated progression to invasive carcinoma.

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

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

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

14 occurred during or after the progression to invasive carcinoma.

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

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

17 ociated with more frequent predisposition to invasive carcinoma.

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

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

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

21 from prostatic intra-epithelial neoplasia to invasive carcinoma.

22 pathways which proceeds the transition into invasive carcinoma.

23 ritical transition from carcinoma in situ to invasive carcinoma.

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

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

26 etected in lesions before the development of invasive carcinoma.

27 t during the transition from preneoplasia to invasive carcinoma.

28 MI phenotype in any CAHs without associated invasive carcinoma.

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

30 18 (22%) CAHs that were not associated with invasive carcinoma.

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

32 itions between intraepithelial neoplasia and invasive carcinoma.

33 premalignant lesions prior to development of invasive carcinoma.

34 plicate DCIS as a non-obligate precursor for invasive carcinoma.

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

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

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

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

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

40 lates with increasing disease progression to invasive carcinoma.

41 progression from ductal carcinoma in situ to invasive carcinoma.

42 ose breast tissue to eventual development of invasive carcinoma.

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

44 most benign lesion that rarely progresses to invasive carcinoma.

45 from prostatic intraepithelial neoplasia to invasive carcinoma.

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

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

48 ere 21.1% ductal carcinoma in situ and 78.9% 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 en they progress from preinvasive lesions to invasive carcinomas.

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

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

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

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

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

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

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

62 as important implications for development of invasive carcinomas.

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

64 proportion than we have previously noted for invasive carcinomas.

65 mammary lesions developed and progressed to invasive carcinomas.

66 gly expressed in the neoplastic epithelia of 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 nd with stromal fibroblasts surrounding many invasive carcinomas.

71 of the dysplastic lesions and in 67% of the invasive carcinomas.

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

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

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

75 ression and increasing histological grade in 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 llele losses in dysplasia (20% and 17%), and invasive carcinoma (40% and 48%) were detected in the sa

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

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

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

85 Invasive carcinoma after atypical lobular hyperplasia is

86 rade prostatic intraepithelial neoplasia and invasive carcinoma also showed down-regulation of p27Kip

87 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

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

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

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

91 %, with the highest level of concordance for invasive carcinoma and lower levels of concordance for D

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

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

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

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

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

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

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 yperplasia), the latter sharing LOH with the invasive carcinoma at some but not all chromosomal loci.

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

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

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

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

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

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

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

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

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

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

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

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

129 within ductal or lobular carcinoma in situ, invasive carcinoma, carcinoma-associated stroma, benign

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

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

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

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

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

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

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

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

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

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

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

141 Invasive carcinoma cells use specialized actin polymeriz

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

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

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

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

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

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

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

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

150 3CA mRNA levels were significantly higher in invasive carcinomas compared with benign and low maligna

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

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

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

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

155 Frankly invasive carcinoma developing subsequently showed occasi

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

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

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

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

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

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

162 Although all invasive carcinomas had elevated levels of p27 mRNA, 45

163 elevated levels of p27 mRNA, 45 (83%) of 54 invasive carcinomas had low p27 protein levels (<50% pos

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

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

166 In invasive carcinomas, HSF1 expression was associated with

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

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

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

170 Findings included invasive carcinoma in 17 patients, isolated ductal carci

171 IGCNBB demonstrated invasive carcinoma in 178 patients.

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

173 WLEBB confirmed carcinoma in situ in 54 and invasive carcinoma in 30 (65.4% sensitivity, 97.7% speci

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 the transformation from normal epithelium to invasive carcinoma in the majority of patients with IPMT

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

201 Early invasive carcinoma may be encountered in association wit

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

203 545; 3.6 %), dysplasia (n = 49; 0.4 %), and invasive carcinoma (n = 22; 0.2 %) were rare.

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

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

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

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

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

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

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

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

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

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 standard treatment for patients with muscle-invasive carcinoma of the urinary bladder is radical cys

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

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

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

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

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

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

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

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

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

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

236 ies resembling either benign fibroadenoma or invasive carcinoma samples.

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

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

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

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

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

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

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

244 Invasive carcinomas survive and evade apoptosis despite

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

263 Invasive carcinoma was detected significantly more often

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

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

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

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

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

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

270 Invasive carcinoma was present in 11 (46%) of 24 patient

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 23 in primary breast carcinomas, in situ and invasive carcinomas were analysed for allelic loss using

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

281 Invasive carcinomas were modestly underrepresented in MF

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

283 (atypical hyperplasia, carcinoma in situ, or invasive carcinoma) were evaluated by WLEBB.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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