ライフサイエンスコーパス: carcinoma in situ

1 cer (invasive cancers or non-invasive ductal carcinoma in situ).

2 ion (LVI), and 8% lobular neoplasia (lobular carcinoma in situ).

3 al ductal or lobular hyperplasia and lobular carcinoma in situ).

4 ving a choice of effective agents for ductal carcinoma in situ.

5 th factor receptor 2, with associated ductal carcinoma in situ.

6 ement, and 14.0% and 6.0% were identified as carcinoma in situ.

7 gement of both low-risk and high-risk ductal carcinoma in situ.

8 ancer in postmenopausal patients with ductal carcinoma in situ.

9 pread low-grade or intermediate-grade ductal carcinoma in situ.

10 d as calcifications and 28 (65%) were ductal carcinoma in situ.

11 cm (range, 0 to 9.3) in patients with ductal carcinoma in situ.

12 n: seven invasive carcinomas and five ductal carcinoma in situ.

13 f the specimen removed in the case of ductal carcinoma in situ.

14 of stakeholders on the management of ductal carcinoma in situ.

15 teroscopy and its potential for detection of carcinoma in situ.

16 ent measure) or women diagnosed with lobular carcinoma in situ.

17 cancer,ductal carcinoma in situ, or lobular carcinoma in situ.

18 nase domain and overexpressed only in ductal carcinoma in situ.

19 elial carcinoma, resembling human high-grade carcinoma in situ.

20 early stage breast cancer, including ductal carcinoma in situ.

21 One (4%) of the 23 patients had ductal carcinoma in situ.

22 veloped mammary gland hyperplasia and ductal carcinoma in situ.

23 the transition from pre-malignancy to ductal carcinoma in situ.

24 omal angiogenesis that resemble human ductal carcinoma in situ.

25 revious diagnosis of breast cancer or ductal carcinoma in situ.

26 ncidence of invasive breast cancer or ductal carcinoma in situ.

27 without preexisting breast cancer or ductal carcinoma in situ.

28 in progressed to high grade dysplasia and to carcinoma in situ.

29 gery for invasive breast carcinoma or ductal carcinoma in situ.

30 etected at screening mammography were ductal carcinoma in situ.

31 cular invasion and intermediate grade ductal carcinoma in situ.

32 ssed in the stroma of cervical squamous cell carcinomas in situ.

33 IL23 in the stroma of cervical squamous cell carcinomas in situ.

34 118 cancers were invasive and 21 were ductal carcinomas in situ.

35 Average tumor size was 2.8 cm for ductal carcinoma in situ (0.05-17.0 cm), 2.4 cm for invasive du

36 .66 [95% CI 0.54-0.81], p<0.0001) and ductal carcinoma in situ (0.65 [0.43-1.00], p=0.05), but no eff

37 e screened, eight were diagnosed with ductal carcinoma in situ, 16 with early stage disease (1.5%), t

38 Ductal carcinoma in situ (21 of 87 lesions [24%]; 95% CI: 15, 3

39 lateral), with no dominant histology (ductal carcinoma in situ, 35%; infiltrating ductal carcinoma, 2

40 The latter comprised eight ductal carcinomas in situ (88% intermediate or high grade [seve

41 ose or positive for invasive tumor or ductal carcinoma in situ according to central pathology review

42 ma, and 2 preinvasive breast cancers [ductal carcinoma in situ]); all but 1 required only resection f

43 l breast cancer, invasive disease, or ductal carcinoma in situ), analysed by intention to treat.

44 st cancer (invasive breast cancer and ductal carcinoma in situ), analysed by intention to treat.

45 There were 3553 patients with carcinoma in situ and 39,941 with clinical stage I cance

46 tected cancers with change were 21.1% ductal carcinoma in situ and 78.9% invasive carcinoma.

47 ted cancers with no change were 19.3% ductal carcinoma in situ and 80.7% invasive carcinoma.

48 sed guidelines, 76% of resected BD-IPMN with carcinoma in situ and 95% of resected BD-IPMN with invas

49 significantly reduced in precancerous ductal carcinoma in situ and all breast cancer subtypes.

50 transgenic mice expressing HRAS* resulted in carcinoma in situ and basal-subtype MIUCB with focal squ

51 elopment of lesions resembling squamous cell carcinoma in situ and elevated expression of Fbxw7 targe

52 d hyperplasia that progresses to endometrial carcinoma in situ and endometrial adenocarcinoma as evid

53 rocess, from low-grade dysplastic lesions to carcinoma in situ and eventually to metastatic disease.

54 t al. characterize this genetic diversity in carcinoma in situ and in invasive regions from 3 types o

55 d at similar frequencies during early ductal carcinoma in situ and in the later invasive ductal carci

56 iated with COX-2 expression levels in ductal carcinoma in situ and invasive cancer.

57 were separated from most noninvasive ductal carcinoma in situ and invasive carcinomas by increased m

58 specifically a 3.3 relative risk for ductal carcinoma in situ and invasive ductal carcinoma, the mos

59 cidence of early-stage breast cancer (ductal carcinoma in situ and localized disease) and late-stage

60 etastatic breast cancer compared with ductal carcinoma in situ and nonmalignant breast, and cellular

61 Intravesical treatment is used for carcinoma in situ and other high grade non-muscle-invasi

62 ly, immunohistochemical analyses of cervical carcinoma in situ and primary tumors have shown a statis

63 progression, with high expression in ductal carcinoma in situ and reduced expression in invasive duc

64 , 2.73; P = 0.008) and higher grade lesions (carcinoma in situ and squamous cell carcinoma versus dys

65 ncologically equivalent to major surgery for carcinoma in situ and T1 rectal cancer, but inferior for

66 sis resulted in the diagnosis of four ductal carcinomas in situ and 10 invasive carcinomas (five at s

67 s were diagnosed in 18 patients (nine ductal carcinomas in situ and 11 invasive breast cancers).

68 Eleven breast cancers (four ductal carcinomas in situ and seven invasive cancers; all T1N0

69 3%) had invasive cancer, 45 (19%) had ductal carcinoma in situ, and 125 (53%) had both; 11 patients h

70 rom invasive ductal carcinoma, 8 from ductal carcinoma in situ, and 6 from normal breast.

71 ompared to normal breast epithelia or ductal carcinoma in situ, and general loss of Nuc-pYStat5 in ly

72 mice revealed ductal hyperplasia and ductal carcinoma in situ, and low incidence of palpable tumors.

73 fied by age, sex, center, stage, presence of carcinoma in situ, and prior low-risk bladder cancer.

74 or severe dysplasia; 52% were classified as carcinoma in situ; and 11% were graded as squamous cell

75 Indolent non-progressive forms of ductal carcinoma in situ are managed according to similar surgi

76 margins (ink on invasive carcinoma or ductal carcinoma in situ) are associated with a two-fold increa

77 nded to highlight the relationship of ductal carcinoma in situ as a precursor to breast cancer and em

78 biopsy findings, two were upgraded to ductal carcinoma in situ at surgery (n = 5); none of the cases

79 esions (atypical ductal hyperplasia, lobular carcinoma in situ, atypical lobular hyperplasia).

80 s with node-negative breast cancer or ductal carcinoma in situ before final treatment is recommended.

81 cidence of invasive plus noninvasive (ductal carcinoma in situ) breast cancers was 0.35% on exemestan

82 umber of intraductal hyperplasias and ductal carcinomas in situ by 50 days of age in Wistar-Furth rat

83 Conclusion Ductal carcinoma in situ calcifications are more extensive at d

84 Because early breast cancer lesions such as carcinoma in situ, characterized by ducts exhibiting lum

85 profiled the expression of miRNAs in bladder carcinoma in situ (CIS) and distinct cell compartments o

86 cystitis with reactive urothelial atypia and carcinoma in situ (CIS) can be difficult, particularly a

87 Lung carcinoma in situ (CIS) lesions are the pre-invasive pre

88 mice developed invasive cancer directly from carcinoma in situ (CIS), bypassing the noninvasive papil

89 s the first line of treatment for urothelial carcinoma in situ (CIS), the precursor lesion of most mu

90 ls); conjunctival intraepithelial neoplasia, carcinoma in situ (CIS); and conjunctival squamous cell

91 clinically distinguish between balanitis and carcinoma in situ (CIS); thus, a biopsy may be needed to

92 ll SCCA stages and was the greatest for anal carcinoma in situ (CIS; APC, 14.2; 95% CI, 10.2 to 18.4)

93 ls from women with a prior history of breast carcinomas in situ (CIS) and in healthy controls.

94 Literature on familial risk of carcinomas in situ (CISs) is limited because many cancer

95 opausal status, presence of extensive ductal carcinoma in situ, clinical tumour size, nodal status, a

96 riates included age, sex, stage, presence of carcinoma in situ, completeness of TURBT, and protocol.

97 presents alone or with a co-existing ductal carcinoma in situ component (IDC + DCIS).

98 preted and 8.6% underinterpreted) and ductal carcinoma in situ (DCIS) (18.5% overinterpreted and 11.8

99 Young age (P < .001) and presence of ductal carcinoma in situ (DCIS) (HR, 2.15; 95% CI, 1.36-3.38; P

100 Ductal carcinoma in situ (DCIS) accounts for 20% of all newly d

101 h adjuvant tamoxifen in patients with ductal carcinoma in situ (DCIS) after lumpectomy and radiation.

102 (RT) after a local excision (LE) for ductal carcinoma in situ (DCIS) aims at reduction of the incide

103 events required for the formation of ductal carcinoma in situ (DCIS) and its progression to invasive

104 , in a large population of women with ductal carcinoma in situ (DCIS) and long follow-up, the relatio

105 vestigates progression of early-stage ductal carcinoma in situ (DCIS) and report that compromised myo

106 pable invasive breast cancer (IBC) or ductal carcinoma in situ (DCIS) and to examine whether the risk

107 r differentiation and perturbation in ductal carcinoma in situ (DCIS) are poorly understood.

108 Primary endocrine therapy for ductal carcinoma in situ (DCIS) as a potential alternative to s

109 atypical ductal hyperplasia (ADH) and ductal carcinoma in situ (DCIS) at magnetic resonance (MR) imag

110 y (BCS) is an effective treatment for ductal carcinoma in situ (DCIS) but women who undergo BCS remai

111 r breast-conserving surgery (BCS) for ductal carcinoma in situ (DCIS) by approximately 50% after 10 t

112 mean = 8.4 y), 2,225 invasive and 623 ductal carcinoma in situ (DCIS) cases were identified.

113 st events of ipsilateral invasive and ductal carcinoma in situ (DCIS) compared with no radiotherapy,

114 asonography) in the identification of ductal carcinoma in situ (DCIS) components of biopsy-proven inv

115 Ductal carcinoma in situ (DCIS) constitutes a major public heal

116 Previously, we found that basal-like ductal carcinoma in situ (DCIS) contains cancer stem-like cells

117 he overdiagnosis and overtreatment of ductal carcinoma in situ (DCIS) detected by mammography has led

118 The prevalence of ductal carcinoma in situ (DCIS) diagnoses has significantly inc

119 Ductal carcinoma in situ (DCIS) encompasses a highly heterogene

120 Testing of ductal carcinoma in situ (DCIS) for ER is recommended to determ

121 expression was lost in microdissected ductal carcinoma in situ (DCIS) from patients with luminal and

122 arlier detection of breast cancer and ductal carcinoma in situ (DCIS) in a transgenic mouse model [FV

123 vs 349 of 845 [41%], P < .0001), have ductal carcinoma in situ (DCIS) in the index breast (31% [27 of

124 The recalls yielding ductal carcinoma in situ (DCIS) increased from 0.3 per 1000 scr

125 derived epithelial cells derived from ductal carcinoma in situ (DCIS) increased secretion of the proi

126 Ductal carcinoma in situ (DCIS) is a heterogeneous group of non

127 of screen detection and treatment of ductal carcinoma in situ (DCIS) is a matter of controversy.

128 Ductal carcinoma in situ (DCIS) is a noninvasive precursor lesi

129 Ductal carcinoma in situ (DCIS) is a precursor lesion of invasi

130 Ductal carcinoma in situ (DCIS) is a subtype of breast cancer e

131 Breast ductal carcinoma in situ (DCIS) is being found in great numbers

132 Ductal carcinoma in situ (DCIS) is characterized by ductal epit

133 Ductal carcinoma in situ (DCIS) is defined as a proliferation o

134 bed after whole-breast RT (WBRT) for ductal carcinoma in situ (DCIS) is largely extrapolated from in

135 While the mortality associated with ductal carcinoma in situ (DCIS) is minimal, the risk of ipsilat

136 es with HER2-positive status in human ductal carcinoma in situ (DCIS) lesions and invasive breast can

137 Background Most ductal carcinoma in situ (DCIS) lesions are first detected on s

138 invasive breast cancer tumors and 179 ductal carcinoma in situ (DCIS) lesions were overdiagnosed in 2

139 mmography depicted significantly more ductal carcinoma in situ (DCIS) lesions, irrespective of screen

140 ipogenic genes in clinical samples of ductal carcinoma in situ (DCIS) of breast cancer and found that

141 A subset of patients with ductal carcinoma in situ (DCIS) of the breast develop ipsilater

142 Historically, ductal carcinoma in situ (DCIS) of the breast has been managed

143 While the prevalence of ductal carcinoma in situ (DCIS) of the breast has increased sub

144 Ductal carcinoma in situ (DCIS) of the breast is a non-invasive

145 Ductal carcinoma in situ (DCIS) of the breast represents a dise

146 A total of 486 cases of ductal carcinoma in situ (DCIS) of the breast were identified d

147 r older who were newly diagnosed with ductal carcinoma in situ (DCIS) or breast cancer.

148 t semaphorin 7a is a potent driver of ductal carcinoma in situ (DCIS) progression.

149 nance (MR) images are associated with ductal carcinoma in situ (DCIS) recurrence risk after definitiv

150 rrence (IBTR) after local excision of ductal carcinoma in situ (DCIS) remains a clinical concern.

151 Ductal Carcinoma In Situ (DCIS) represents a significant fracti

152 2s expression in human primary breast ductal carcinoma in situ (DCIS) samples and found that SIM2s is

153 of biopsy, using invasive cancer and ductal carcinoma in situ (DCIS) to define a positive reference

154 The transition from ductal carcinoma in situ (DCIS) to invasive breast cancer (IBC)

155 esses that control the progression of ductal carcinoma in situ (DCIS) to invasive breast cancer remai

156 chanisms mediating the progression of ductal carcinoma in situ (DCIS) to invasive breast cancer remai

157 The transition from preinvasive ductal carcinoma in situ (DCIS) to invasive breast carcinoma is

158 ers progress from relatively indolent ductal carcinoma in situ (DCIS) to invasive ductal carcinoma (I

159 the optimal negative margin width for ductal carcinoma in situ (DCIS) treated with breast-conserving

160 l breast event (IBE) in patients with ductal carcinoma in situ (DCIS) treated with breast-conserving

161 he re-intervention rate in women with ductal carcinoma in situ (DCIS) undergoing breast-conserving su

162 lial cells in a subset of preinvasive ductal carcinoma in situ (DCIS) upregulate expression of the in

163 as they are increased in human breast ductal carcinoma in situ (DCIS) versus normal breast tissues.

164 ry for node-negative breast cancer or ductal carcinoma in situ (DCIS) were randomly assigned to radio

165 cancer and multicentric tumors, with ductal carcinoma in situ (DCIS) who will undergo mastectomy, wh

166 3 cases of invasive breast cancer, 73 ductal carcinoma in situ (DCIS), 72 with atypical hyperplasia (

167 dy identified good-risk patients with ductal carcinoma in situ (DCIS), a breast cancer diagnosis foun

168 Ductal carcinoma in situ (DCIS), although often diagnosed as br

169 vention is to reduce the incidence of ductal carcinoma in situ (DCIS), an early stage of breast cance

170 ing database contained 132 benign, 71 ductal carcinoma in situ (DCIS), and 150 invasive ductal carcin

171 cluding invasive breast cancer (IBC), ductal carcinoma in situ (DCIS), and adjacent benign tissue (AB

172 detected with mammography alone were ductal carcinoma in situ (DCIS), and the third was DCIS with mi

173 Purpose To compare detection rates of ductal carcinoma in situ (DCIS), classified according to nuclea

174 nced exons 9 and 20 of PIK3CA in pure ductal carcinoma in situ (DCIS), DCIS adjacent to invasive carc

175 radiation therapy (RT) in women with ductal carcinoma in situ (DCIS), despite prospective randomized

176 ical presentation of that cancer, for ductal carcinoma in situ (DCIS), invasive breast cancer, and al

177 ed no pathologic abnormality, 21% had ductal carcinoma in situ (DCIS), invasive carcinoma (IC), or ly

178 Women with ductal carcinoma in situ (DCIS), or stage 0 breast cancer, ofte

179 ority of breast cancers diagnosed are ductal carcinoma in situ (DCIS), the most common lesion associa

180 ggressive and non-aggressive forms of ductal carcinoma in situ (DCIS), they cannot be identified with

181 lterations driving the progression of ductal carcinoma in situ (DCIS), we compared patients with pure

182 Ductal carcinoma in situ (DCIS)--a significant precursor to inv

183 believed to evolve from non-invasive ductal carcinoma in situ (DCIS).

184 e (QoL) are scarce among survivors of ductal carcinoma in situ (DCIS).

185 reatment option for the management of ductal carcinoma in situ (DCIS).

186 women with hormone-receptor-positive ductal carcinoma in situ (DCIS).

187 benefit has not been demonstrated in ductal carcinoma in situ (DCIS).

188 portion of small invasive cancers and ductal carcinoma in situ (DCIS).

189 e invasive cancers and three cases of ductal carcinoma in situ (DCIS).

190 ive spheroids with characteristics of ductal carcinoma in situ (DCIS).

191 ce of any residual invasive cancer or ductal carcinoma in situ (DCIS).

192 ductal hyperplasia (UDH) or malignant ductal carcinoma in situ (DCIS).

193 r breast-conserving surgery (BCS) for ductal carcinoma in situ (DCIS).

194 ductal hyperplasia and low/high grade ductal carcinoma in situ (DCIS).

195 y-stage breast lesions, most commonly ductal carcinoma in situ (DCIS).

196 remalignant breast cancers, including ductal carcinoma in situ (DCIS); however, little is known about

197 ion between risk factors and incident ductal carcinoma in situ (DCIS; n = 1,453) with that of risk fa

198 rs were found by mammography alone (a ductal carcinoma in situ [DCIS] with microinvasion and a DCIS w

199 hown to be true-positive (23 cases of ductal carcinoma in situ [DCIS], 43 invasive cancers) and 287 (

200 uring the past 2 decades, whereas the ductal carcinoma in situ detection rate increased less rapidly,

201 Breast cancer or ductal carcinoma in situ developed in 373 patients, with a stan

202 dence of all breast cancer (including ductal carcinoma in situ) during a 10 year follow-up period.

203 vasive ductal carcinoma (IDC) but not ductal carcinoma in situ, fibroadenoma, or normal breast tissue

204 onation in patients with non-low-risk ductal carcinoma in situ following breast-conserving surgery an

205 ated with tumor grade, size, and presence of carcinoma in situ for miR-222, recurrence (miR-222 and m

206 The heterogeneous nature of ductal carcinoma in situ has been emphasised by data for breast

207 , 2.73; 95% CI, 1.66 to 4.49) but not ductal carcinoma in situ (HR, 1.48; 95% CI, 0.72 to 3.05).

208 metaplasia in 47.8%, dysplasia in 15.7%, and carcinoma in situ in 0.6%.

209 ent scans, including the detection of ductal carcinoma in situ in 1 case.

210 guidelines, describing invasive carcinoma or carcinoma in situ in 67% of BD-IPMN smaller than 3 cm an

211 s of estimation and the importance of ductal carcinoma in situ in overdiagnosis.

212 astectomy after cancellation, one had ductal carcinoma in situ in the same quadrant as the MR-depicte

213 The high-grade carcinoma in situ in the UPK II-SV40 mice is associated

214 n cancer cells and in noninvasive colorectal carcinomas in situ in which EGFR signaling favors mitosi

215 ting breast cancer (both invasive and ductal carcinoma in situ) in the post-treatment period.

216 ges of breast cancer (hyperplasia and ductal carcinoma in situ), in morphogenesis assays G1P3 enhance

217 They occur in ductal carcinoma in situ, in breast cancers, and in breast canc

218 Ductal carcinoma in situ is a common finding in women having ma

219 Ductal carcinoma in situ is currently managed with excision, ra

220 f malignant breast lesions, including ductal carcinoma in situ, is significantly improved at contrast

221 grade 3 invasive ductal carcinoma and ductal carcinoma in situ (largest focus, 3.5 cm).

222 cer risk conferred by a diagnosis of lobular carcinoma in situ (LCIS) is poorly understood.

223 association between risk factors and lobular carcinoma in situ (LCIS; n = 186) with that of risk fact

224 pithelial tissue and hormone-negative ductal carcinoma in situ lesions but were uncoupled in triple-n

225 ions or deletions of TP53 and PTEN in ductal carcinoma in situ lesions have been implicated in progre

226 Analysis of bladder-associated microRNAs in carcinoma in situ lesions reveals a pro-angiogenic profi

227 s (TCC), 31 pTa high-grade TCCs, and 17 pTis carcinoma in situ lesions.

228 the development of estrogen-dependent ductal carcinoma in situ lesions.

229 ver, further genetic interrogation of ductal carcinoma in situ might lead to a reclassification of so

230 nvasive lobular carcinoma (n = 5), or ductal carcinoma in situ (n = 4).

231 Ductal carcinoma in situ (n = 5) enhanced a mean of 59.6 HU +/-

232 epicted 60 additional breast cancers (ductal carcinoma in situ, n = 20; invasive carcinoma, n = 40) f

233 were identified (invasive, n = 1287; ductal carcinoma in situ, n = 270); in five, both kinds of brea

234 ped breast cancer (invasive, n = 129; ductal carcinoma in situ,n = 47) over a median follow-up time o

235 tage Ta or T1); HGN = high grade (grade 3 or carcinoma in situ), nonmuscle invading (stage Ta, T1, or

236 urvival (lymphovascular invasion, associated carcinoma in situ, nonuse of bacillus Calmette-Guerin, t

237 There was carcinoma in situ of the bladder, and 42 nodes were nega

238 compared with patients with residual ductal carcinoma in situ only (n = 309), no invasive residuals

239 use of death for women diagnosed with ductal carcinoma in situ or stage I disease and for women aged

240 ified 233,754 patients diagnosed with ductal carcinoma in situ or stage I to III unilateral breast ca

241 nt breast cancers in each subset were ductal carcinoma in situ or stage I.

242 ed 20 to 79 years diagnosed as having ductal carcinoma in situ or stages I to III invasive breast can

243 6]; P < .001), invasive cancer versus ductal carcinoma in situ (OR, 1.6 [95% CI: 1.0, 2.4]; P = .031)

244 aningful initial complete response rate (for carcinoma in situ) or recurrence-free rate (for papillar

245 Patients with stage 0 (carcinoma in situ) or stage I (T1/2N0M0) adenocarcinoma

246 ut a prior diagnosis of breast cancer,ductal carcinoma in situ, or lobular carcinoma in situ.

247 sive ductal or lobular breast cancer, ductal carcinoma in situ, or prophylaxis.

248 cal ductal or lobular hyperplasia or lobular carcinoma in situ; or ductal carcinoma in situ with mast

249 breast cancer or extensive/high-grade ductal carcinoma in situ planned for standard radioactive-label

250 I3K catalytic subunit (PIK3CA) in 110 ductal carcinoma in situ, primary tumor, and metastatic BC samp

251 repair pathway and provides a link in ductal carcinoma in situ progression to invasive ductal carcino

252 co-expression of EGFR and MET marking ductal carcinoma in situ regions of normal-like tumors and lend

253 ive tumor fronts, particularly within ductal carcinoma in situ samples, establishes that EMT-induced

254 Squamous cell carcinoma in situ (SCCIS) is a prevalent precancerous le

255 al epithelial-mesenchymal transition status, carcinoma in situ scores, histologic features, and survi

256 ve breast cancer, which revealed that ductal carcinomas in situ show intratumor genetic heterogeneity

257 were invasive cancers and three were ductal carcinoma in situ stage Tis-T1c.

258 lson comorbidity score, treatment date, age, carcinoma in situ status, and hydronephrosis) with prope

259 ation was found in the independent cohort of carcinoma in situ, suggesting that loss or low expressio

260 ntroduces this month's special Breast Ductal Carcinoma in Situ Theme Issue, a series of reviews inten

261 with total tissue lysates from human ductal carcinoma in situ tissue loaded on basic immobilized pH

262 ned 296 breast adenocarcinomas and 38 ductal carcinoma in situ tissues that were represented in tissu

263 uring the transition from noninvasive ductal carcinoma in situ to invasive breast cancer.

264 matrices, and conversion from ductal breast carcinoma in situ to invasive carcinoma in mouse xenogra

265 h increasing disease progression from ductal carcinoma in situ to invasive carcinoma.

266 otaxis in vitro and for conversion of ductal carcinoma in situ to invasive ductal carcinoma in vivo.

267 The transition from ductal carcinoma in situ to invasive ductal carcinoma is a key

268 tors to delay progression of indolent ductal carcinoma in situ to invasive ductal carcinoma.

269 mouse urothelium expressing SV40T converted carcinoma-in-situ to high-grade papillary urothelial car

270 althy tissue but already prominent in ductal carcinoma in situ, together with ECM and cell-cell adhes

271 established for the normal breast to ductal carcinoma in situ transition was largely maintained in t

272 enopausal women with hormone-positive ductal carcinoma in situ treated by lumpectomy with clear resec

273 enopausal women with hormone-positive ductal carcinoma in situ treated by lumpectomy with clear resec

274 4 patients with low-risk invasive and ductal carcinoma in situ treated with breast-conserving surgery

275 DCIS (UK, Australia, and New Zealand ductal carcinoma in situ) trial suggested that radiotherapy red

276 ysplasia showed recurrence, whereas 12.8% of carcinoma in situ tumors and 22.2% of squamous cell carc

277 amoxifen in postmenopausal women with ductal carcinoma in situ undergoing lumpectomy plus radiotherap

278 ed malignant features (invasive carcinoma or carcinoma in situ) upon histological examination of the

279 Of these, 64.7% (11 of 17) were ductal carcinoma in situ versus 6.7% (two of 30) of cancers det

280 , for identifying invasive cancer and ductal carcinoma in situ versus benign breast tissue.

281 Carcinoma in situ was accurately diagnosed in 11 cases,

282 Local tumor excision for carcinoma in situ was associated with equivalent CSS com

283 The rate of screening-detected ductal carcinoma in situ was higher (P = .019) while the rate o

284 The incidence of ductal carcinoma in situ was higher in bisphosphonate users (HR

285 A 59% reduction in ductal carcinoma in situ was observed (0.41, 0.22-0.79, p=0.008

286 Penetrance of ductal carcinomas in situ was also decreased.

287 In cellular models of breast ductal carcinoma in situ, we reveal a link between filopodia fo

288 women with invasive breast cancer or ductal carcinoma in situ were enrolled as cases and matched to

289 my reconstruction for invasive cancer and/or carcinoma in situ were enrolled at 11 sites.

290 scle-invasive bladder cancer (NMIBC) without carcinoma in situ were enrolled in a randomized phase II

291 ing stage or treatment data, and with ductal carcinoma in situ were excluded, leaving 3729 patients i

292 with completely excised non-low-risk ductal carcinoma in situ were randomly assigned, by use of a mi

293 ar of diagnosis, and the presence of lobular carcinoma in situ were significantly associated with hig

294 tal of 45 cancers (33 invasive and 12 ductal carcinomas in situ) were diagnosed, 43 were seen with MR

295 3/T4), inflammatory breast cancer, or ductal carcinoma in situ (when breast-conserving surgery is pla

296 cancer and multicentric tumors, with ductal carcinoma in situ, who will undergo mastectomy, who prev

297 asia or lobular carcinoma in situ; or ductal carcinoma in situ with mastectomy.

298 55 (53.4%) of 103 patients with carcinoma in situ (with or without a high-grade Ta or T1

299 mplete response at any time in patients with carcinoma in situ (with or without a high-grade Ta or T1

300 ere diagnosed with invasive cancer or ductal carcinoma in situ within 12 months of screening.