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 atypical lobular hyperplasia and one lobular carcinoma in situ).

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

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

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

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

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

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

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

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

12 veloped mammary gland hyperplasia and ductal carcinoma in situ.

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

14 omal angiogenesis that resemble human ductal carcinoma in situ.

15 t urothelial carcinomas smaller than 2 cm or carcinoma in situ.

16 aging sensitivity in the detection of ductal carcinoma in situ.

17 ervical intraepithelial neoplasia grade 3 or carcinoma in situ.

18 uding atypical ductal hyperplasia and ductal carcinoma in situ.

19 umors than in normal breast tissue or ductal carcinoma in situ.

20 (1.72-4.63) and 1.56 (1.38-1.75) for ductal carcinoma in situ.

21 Most tumours are ductal and 10% are ductal carcinoma in situ.

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

23 etected at screening mammography were ductal carcinoma in situ.

24 cular invasion and intermediate grade ductal carcinoma in situ.

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

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

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

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

29 ancer in postmenopausal patients with ductal carcinoma in situ.

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

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

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

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

34 g susceptibility to AOM-induced adenomas and carcinomas in situ.

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

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

37 .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

38 mammary glands (10 of 10) but not all ductal carcinoma in situ [11 of 19 (57.9%), P = 0.018] and inva

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

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

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

42 computer simulation is used to model ductal carcinoma in situ, a form of non-invasive breast cancer.

43 ociated with malignant progression of ductal carcinoma in situ, a precancerous lesion.

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

45 Invasive ductal carcinoma and ductal carcinoma in situ account for about 85% of breast cancer

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

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

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

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

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

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

52 he physical status of HPV-16 in 126 cervical carcinoma in situ and 92 invasive cervical cancers.

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

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

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

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

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

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

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

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

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

62 integrated or episomal status estimated for carcinoma in situ and invasive cervical cancer cases was

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

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

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

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

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

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

69 , 2.73; P = 0.008) and higher grade lesions (carcinoma in situ and squamous cell carcinoma versus dys

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

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

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

73 was strongly expressed in a subset of breast carcinomas in situ and invasive ductal carcinomas ( appr

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

75 3%) had invasive cancer, 45 (19%) had ductal carcinoma in situ, and 125 (53%) had both; 11 patients h

76 denoma, 47 (32%) borderline tumors, 16 (11%) carcinoma in situ, and 16 (11%) invasive carcinoma.

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

78 py, ductal carcinoma with concurrent lobular carcinoma in situ, and DCIS in elderly people and in men

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

80 from reduction mammoplasty, adenosis, ductal carcinoma in situ, and infiltrating ductal carcinoma sho

81 tissues from patient-matched normal, ductal carcinoma in situ, and invasive ductal carcinoma reveale

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

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

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

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

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

87 found to have ductal cancer and one lobular carcinoma in situ at time of CDR.

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

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

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

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

92 s qRT-PCR assay, HPV-16 was characterized in carcinoma in situ cases as episomal (61.9%), mixed (i.e.

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

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

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

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

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

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

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

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

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

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

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

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

105 To determine whether residual ductal carcinoma in situ (DCIS) after completion of preoperativ

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

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

108 ncreased risk of recurrent disease in ductal carcinoma in situ (DCIS) and a poorer prognosis in node-

109 ssion reduced in approximately 50% of ductal carcinoma in situ (DCIS) and invasive breast cancers (IB

110 ia (ADH), are candidate precursors to ductal carcinoma in situ (DCIS) and invasive cancer.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 ht, and well-differentiated papillary ductal carcinoma in situ (DCIS) in two.

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

128 s, and clinical outcome indicate that ductal carcinoma in situ (DCIS) is a heterogeneous disease, mea

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

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

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

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

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

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

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

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

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

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

139 Ductal carcinoma in situ (DCIS) is the fourth leading cancer fo

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

141 d morphologic characteristics of pure ductal carcinoma in situ (DCIS) lesions depicted on dynamic con

142 Certain ductal carcinoma in situ (DCIS) lesions overexpress the HER-2/n

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

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

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

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

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

148 The current literature suggests that ductal carcinoma in situ (DCIS) of the breast is infrequently d

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

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

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

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

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

154 ng surgery (BCS) and radiotherapy for ductal carcinoma in situ (DCIS) reduced the absolute occurrence

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

156 2s expression in human primary breast ductal carcinoma in situ (DCIS) samples and found that SIM2s is

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

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

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

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

161 ial cells inhibit, the progression of ductal carcinoma in situ (DCIS) to invasive breast carcinomas b

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

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

164 Some women with unilateral ductal carcinoma in situ (DCIS) undergo contralateral prophylac

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

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

167 ontaining ducts distended with murine ductal carcinoma in situ (DCIS) were prepared for XFM.

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

169 panel of breast tumors, including 10 ductal carcinoma in situ (DCIS), 18 invasive breast carcinomas,

170 3 cases of invasive breast cancer, 73 ductal carcinoma in situ (DCIS), 72 with atypical hyperplasia (

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

191 ate treatment for small, grade 1 or 2 ductal carcinoma in situ (DCIS).

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

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

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

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

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

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

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

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

200 in tissue microarray cores from pure ductal carcinoma in situ (DCIS; n = 62), invasive breast cancer

201 herapy (BCT) for patients treated for ductal carcinoma-in-situ (DCIS) or invasive breast cancer at Na

202 ons underwent biopsy, of which 83 (16 ductal carcinoma in situ [DCIS] and 67 invasive cancers) were m

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

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

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

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

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

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

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

210 re in a manner that is reminiscent of ductal carcinoma in situ; however, motile cells do not invade t

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

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

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

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

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

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

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

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

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

220 Imaging of ductal carcinoma in situ, infiltrating cancer, and microcalcifi

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

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

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

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

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

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

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

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

229 R-145 expression in atypical hyperplasia and carcinoma in situ lesions suggests that this miRNA may h

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

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

232 ents had borderline neoplasms, and three had carcinoma in situ lesions.

233 borderline (malignant) neoplasms; and three, carcinoma in situ lesions.

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

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

236 Excisional findings included lobular carcinoma in situ (n=2), ductal carcinoma in situ (n=7),

237 uded lobular carcinoma in situ (n=2), ductal carcinoma in situ (n=7), papillary carcinoma (n=2), and

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

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

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

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

242 e (p=0.03), with a relative risk for lobular carcinoma in situ of 2.82 (1.72-4.63) and 1.56 (1.38-1.7

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

244 diotherapy after sector resection for ductal carcinoma in situ of the breast (DCIS) in patient groups

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

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

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

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

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

250 6]; P < .001), invasive cancer versus ductal carcinoma in situ (OR, 1.6 [95% CI: 1.0, 2.4]; P = .031)

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

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

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

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

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

256 We surveyed all ductal carcinoma in situ patients and a 20% random sample of in

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

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

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

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

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

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

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

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

265 ajor steps observed during the transition of carcinoma in situ to frank malignancy.

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

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

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

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

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

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

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

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

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

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

276 4 patients with low-risk invasive and ductal carcinoma in situ treated with breast-conserving surgery

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

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

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

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

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

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

283 Carcinoma in situ was accurately diagnosed in 11 cases,

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

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

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

287 Penetrance of ductal carcinomas in situ was also decreased.

288 including invasive breast cancers and ductal carcinomas in situ) was not significant (4.15 cases per

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

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

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

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

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

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

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

296 3/T4), inflammatory breast cancer, or ductal carcinoma in situ (when breast-conserving surgery is pla

297 ignant stage and were initially diagnosed as carcinoma in situ which rapidly progressed to squamous c

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

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

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