ライフサイエンスコーパス: ductal carcinoma

1 target in cancer, particularly in pancreatic ductal carcinoma.

2 ot benefit as much as patients with invasive ductal carcinoma.

3 (ER(+)) breast cancer and a triple-negative ductal carcinoma.

4 tomy with radiation for early-stage invasive ductal carcinoma.

5 0 regulates CSCs in luminal subtype invasive ductal carcinoma.

6 ed to manually annotated regions of invasive ductal carcinoma.

7 t and is more favorable than that of grade 1 ductal carcinoma.

8 Outcomes included invasive lobular or ductal carcinoma.

9 ents diagnosed with lobular carcinoma versus ductal carcinoma.

10 e been implicated in progression to invasive ductal carcinomas.

11 tor-positive and ErbB2-negative infiltrating ductal carcinomas.

12 and a relationship to lymph node invasion in ductal carcinomas.

13 in breast cancer cell lines and in invasive ductal carcinomas.

14 total of 24 lesions were imaged (15 invasive ductal carcinoma, 1 high-grade mammary carcinoma, 3 lobu

15 (ductal carcinoma in situ, 35%; infiltrating ductal carcinoma, 29%; infiltrating lobular carcinoma, 2

16 Methylation of FOXF1 in invasive ductal carcinoma (37.6% of 117 cases) correlated with hi

17 ransition, we used 80 biopsies from invasive ductal carcinoma, 8 from ductal carcinoma in situ, and 6

18 atients with lobular carcinoma vs those with ductal carcinoma (adjusted odds ratio, 1.44; 95% CI 1.06

19 stem, with Schizophrenia, HD, and pancreatic ductal carcinoma among the top five, suggesting that abe

20 ta overexpression also persisted in invasive ductal carcinoma and contributed to the further progress

21 ed a poorly differentiated, grade 3 invasive ductal carcinoma and ductal carcinoma in situ (largest f

22 Invasive ductal carcinoma and ductal carcinoma in situ account fo

23 ssible link between the presence of invasive ductal carcinoma and fatty acid fractions in breast adip

24 Immunohistochemical analysis of 53 invasive ductal carcinomas and their autologous metastatic lesion

25 mens of normal mammary gland versus invasive ductal carcinoma, and primary breast cancer versus BMBC.

26 of MRJ (DNAJB6) protein is lost in invasive ductal carcinoma, and restoration of MRJ(L) restricts ma

27 0% of breast adenocarcinomas, 18% of in situ ductal carcinomas, and all lactating breast cases, but n

28 lied SURVIV to TCGA RNA-seq data of invasive ductal carcinoma as well as five additional cancer types

29 evels significantly increase in infiltrating ductal carcinomas as well as in invasive breast cancer c

30 male Runx3(+/-) mice spontaneously developed ductal carcinoma at an average age of 14.5 months.

31 rapeutic resistance in human breast invasive ductal carcinoma by negatively regulating caspase-7 acti

32 ere confirmed in LCM-isolated human invasive ductal carcinomas compared with patient-matched normal t

33 methylation of upstream CpG islands in human ductal carcinomas, confers morphological, molecular, and

34 ith a stage II (T2N1), right-sided, invasive ductal carcinoma considered grade 2 of 3 on core biopsy,

35 sclosed a moderately differentiated invasive ductal carcinoma (diameter, 2.5 cm).

36 A core biopsy confirmed invasive ductal carcinoma, grade 2 of 3, that was estrogen recept

37 in situ (0.05-17.0 cm), 2.4 cm for invasive ductal carcinoma (IDC) (0.2-8.9 cm), 3.5 cm for lobular

38 T in newly diagnosed advanced local invasive ductal carcinoma (IDC) and invasive lobular carcinoma (I

39 The resulting mAb (RL21A) stained invasive ductal carcinoma (IDC) but not ductal carcinoma in situ,

40 l carcinoma in situ (DCIS), and 150 invasive ductal carcinoma (IDC) lesions.

41 cent normal tissue in patients with invasive ductal carcinoma (IDC) of the breast and determined that

42 The aggressiveness of invasive ductal carcinoma (IDC) of the breast is associated with

43 itu (DCIS) is a precursor lesion of invasive ductal carcinoma (IDC) of the breast.

44 noma (ILC) is less conspicuous than invasive ductal carcinoma (IDC) on (18)F-FDG PET, we hypothesized

45 Patients diagnosed with early-stage invasive ductal carcinoma (IDC) or classic invasive lobular carci

46 ious mass, and core biopsy confirms invasive ductal carcinoma (IDC) that is estrogen receptor moderat

47 logical breast cancer subtype after invasive ductal carcinoma (IDC), accounting for around 10% of all

48 cohort of 466 patients with primary invasive ductal carcinoma (IDC), the most frequent type of BC, by

49 e pattern was evaluated for ILC and invasive ductal carcinoma (IDC).

50 ance has been obtained in models of invasive ductal carcinoma (IDC).

51 of 512 breast cancer patients with invasive ductal carcinoma (IDC).

52 DCIS is considered a precursor to invasive ductal carcinoma (IDC); however, approximately half of D

53 ared with a cohort of 14 responding invasive ductal carcinomas (IDC) matched on clinicopathologic fea

54 and its presence in the nucleus of invasive ductal carcinomas (IDCs) is associated with decreased nu

55 Average tumor size was 2.8 cm for ductal carcinoma in situ (0.05-17.0 cm), 2.4 cm for inva

56 r (HR 0.66 [95% CI 0.54-0.81], p<0.0001) and ductal carcinoma in situ (0.65 [0.43-1.00], p=0.05), but

57 Ductal carcinoma in situ (21 of 87 lesions [24%]; 95% CI

58 erinterpreted and 8.6% underinterpreted) and ductal carcinoma in situ (DCIS) (18.5% overinterpreted a

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

60 Ductal carcinoma in situ (DCIS) accounts for 20% of all

61 fit with adjuvant tamoxifen in patients with ductal carcinoma in situ (DCIS) after lumpectomy and rad

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

63 1 expression reduced in approximately 50% of ductal carcinoma in situ (DCIS) and invasive breast canc

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

65 lecular events required for the formation of ductal carcinoma in situ (DCIS) and its progression to i

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

67 that investigates progression of early-stage ductal carcinoma in situ (DCIS) and report that compromi

68 nonpalpable invasive breast cancer (IBC) or ductal carcinoma in situ (DCIS) and to examine whether t

69 ion of atypical ductal hyperplasia (ADH) and ductal carcinoma in situ (DCIS) at magnetic resonance (M

70 surgery (BCS) is an effective treatment for ductal carcinoma in situ (DCIS) but women who undergo BC

71 s) after breast-conserving surgery (BCS) for ductal carcinoma in situ (DCIS) by approximately 50% aft

72 ew breast events of ipsilateral invasive and ductal carcinoma in situ (DCIS) compared with no radioth

73 st ultrasonography) in the identification of ductal carcinoma in situ (DCIS) components of biopsy-pro

74 Ductal carcinoma in situ (DCIS) constitutes a major publ

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

76 on of the overdiagnosis and overtreatment of ductal carcinoma in situ (DCIS) detected by mammography

77 The prevalence of ductal carcinoma in situ (DCIS) diagnoses has significan

78 nd in earlier detection of breast cancer and ductal carcinoma in situ (DCIS) in a transgenic mouse mo

79 [64%] vs 349 of 845 [41%], P < .0001), have ductal carcinoma in situ (DCIS) in the index breast (31%

80 atient-derived epithelial cells derived from ductal carcinoma in situ (DCIS) increased secretion of t

81 Ductal carcinoma in situ (DCIS) is a heterogeneous group

82 e value of screen detection and treatment of ductal carcinoma in situ (DCIS) is a matter of controver

83 Ductal carcinoma in situ (DCIS) is a noninvasive precurs

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

85 Ductal carcinoma in situ (DCIS) is a subtype of breast c

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

87 Ductal carcinoma in situ (DCIS) is characterized by duct

88 Ductal carcinoma in situ (DCIS) is defined as a prolifer

89 e tumor bed after whole-breast RT (WBRT) for ductal carcinoma in situ (DCIS) is largely extrapolated

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

91 Ductal carcinoma in situ (DCIS) is the fourth leading ca

92 orrelates with HER2-positive status in human ductal carcinoma in situ (DCIS) lesions and invasive bre

93 Certain ductal carcinoma in situ (DCIS) lesions overexpress the

94 at 271 invasive breast cancer tumors and 179 ductal carcinoma in situ (DCIS) lesions were overdiagnos

95 ital mammography depicted significantly more ductal carcinoma in situ (DCIS) lesions, irrespective of

96 f key lipogenic genes in clinical samples of ductal carcinoma in situ (DCIS) of breast cancer and fou

97 While the prevalence of ductal carcinoma in situ (DCIS) of the breast has increa

98 Ductal carcinoma in situ (DCIS) of the breast is a non-i

99 Ductal carcinoma in situ (DCIS) of the breast represents

100 A total of 486 cases of ductal carcinoma in situ (DCIS) of the breast were ident

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

102 ied that semaphorin 7a is a potent driver of ductal carcinoma in situ (DCIS) progression.

103 ic resonance (MR) images are associated with ductal carcinoma in situ (DCIS) recurrence risk after de

104 or recurrence (IBTR) after local excision of ductal carcinoma in situ (DCIS) remains a clinical conce

105 zed SIM2s expression in human primary breast ductal carcinoma in situ (DCIS) samples and found that S

106 he processes that control the progression of ductal carcinoma in situ (DCIS) to invasive breast cance

107 ular mechanisms mediating the progression of ductal carcinoma in situ (DCIS) to invasive breast cance

108 The transition from ductal carcinoma in situ (DCIS) to invasive breast cance

109 The transition from preinvasive ductal carcinoma in situ (DCIS) to invasive breast carci

110 epithelial cells inhibit, the progression of ductal carcinoma in situ (DCIS) to invasive breast carci

111 ilateral breast event (IBE) in patients with ductal carcinoma in situ (DCIS) treated with breast-cons

112 arding the optimal negative margin width for ductal carcinoma in situ (DCIS) treated with breast-cons

113 Some women with unilateral ductal carcinoma in situ (DCIS) undergo contralateral pr

114 oepithelial cells in a subset of preinvasive ductal carcinoma in situ (DCIS) upregulate expression of

115 , whereas they are increased in human breast ductal carcinoma in situ (DCIS) versus normal breast tis

116 lices containing ducts distended with murine ductal carcinoma in situ (DCIS) were prepared for XFM.

117 breast cancer and multicentric tumors, with ductal carcinoma in situ (DCIS) who will undergo mastect

118 uding 23 cases of invasive breast cancer, 73 ductal carcinoma in situ (DCIS), 72 with atypical hyperp

119 804 study identified good-risk patients with ductal carcinoma in situ (DCIS), a breast cancer diagnos

120 cer prevention is to reduce the incidence of ductal carcinoma in situ (DCIS), an early stage of breas

121 MR imaging database contained 132 benign, 71 ductal carcinoma in situ (DCIS), and 150 invasive ductal

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

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

124 e sequenced exons 9 and 20 of PIK3CA in pure ductal carcinoma in situ (DCIS), DCIS adjacent to invasi

125 use of radiation therapy (RT) in women with ductal carcinoma in situ (DCIS), despite prospective ran

126 to clinical presentation of that cancer, for ductal carcinoma in situ (DCIS), invasive breast cancer,

127 es showed no pathologic abnormality, 21% had ductal carcinoma in situ (DCIS), invasive carcinoma (IC)

128 Women with ductal carcinoma in situ (DCIS), or stage 0 breast cance

129 the majority of breast cancers diagnosed are ductal carcinoma in situ (DCIS), the most common lesion

130 opose aggressive and non-aggressive forms of ductal carcinoma in situ (DCIS), they cannot be identifi

131 cular alterations driving the progression of ductal carcinoma in situ (DCIS), we compared patients wi

132 Ductal carcinoma in situ (DCIS)--a significant precursor

133 e absence of any residual invasive cancer or ductal carcinoma in situ (DCIS).

134 and proportion of small invasive cancers and ductal carcinoma in situ (DCIS).

135 ere nine invasive cancers and three cases of ductal carcinoma in situ (DCIS).

136 oninvasive spheroids with characteristics of ductal carcinoma in situ (DCIS).

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

138 py after breast-conserving surgery (BCS) for ductal carcinoma in situ (DCIS).

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

140 of early-stage breast lesions, most commonly ductal carcinoma in situ (DCIS).

141 of life (QoL) are scarce among survivors of ductal carcinoma in situ (DCIS).

142 ndard treatment option for the management of ductal carcinoma in situ (DCIS).

143 fen for women with hormone-receptor-positive ductal carcinoma in situ (DCIS).

144 ncer, a benefit has not been demonstrated in ductal carcinoma in situ (DCIS).

145 ed in premalignant breast cancers, including ductal carcinoma in situ (DCIS); however, little is know

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

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

148 Ductal carcinoma in situ (n = 5) enhanced a mean of 59.6

149 1.3, 2.6]; P < .001), invasive cancer versus ductal carcinoma in situ (OR, 1.6 [95% CI: 1.0, 2.4]; P

150 size T3/T4), inflammatory breast cancer, or ductal carcinoma in situ (when breast-conserving surgery

151 67 lesions underwent biopsy, of which 83 (16 ductal carcinoma in situ [DCIS] and 67 invasive cancers)

152 o cancers were found by mammography alone (a ductal carcinoma in situ [DCIS] with microinvasion and a

153 nally shown to be true-positive (23 cases of ductal carcinoma in situ [DCIS], 43 invasive cancers) an

154 ive, close or positive for invasive tumor or ductal carcinoma in situ according to central pathology

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

156 Detected cancers with change were 21.1% ductal carcinoma in situ and 78.9% invasive carcinoma.

157 Detected cancers with no change were 19.3% ductal carcinoma in situ and 80.7% invasive carcinoma.

158 but is significantly reduced in precancerous ductal carcinoma in situ and all breast cancer subtypes.

159 detected at similar frequencies during early ductal carcinoma in situ and in the later invasive ducta

160 s associated with COX-2 expression levels in ductal carcinoma in situ and invasive cancer.

161 samples were separated from most noninvasive ductal carcinoma in situ and invasive carcinomas by incr

162 gnancy, specifically a 3.3 relative risk for ductal carcinoma in situ and invasive ductal carcinoma,

163 the incidence of early-stage breast cancer (ductal carcinoma in situ and localized disease) and late

164 e and metastatic breast cancer compared with ductal carcinoma in situ and nonmalignant breast, and ce

165 h tumor progression, with high expression in ductal carcinoma in situ and reduced expression in invas

166 Indolent non-progressive forms of ductal carcinoma in situ are managed according to simila

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

168 patients with node-negative breast cancer or ductal carcinoma in situ before final treatment is recom

169 Breast cancer or ductal carcinoma in situ developed in 373 patients, with

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

171 ll patient scans, including the detection of ductal carcinoma in situ in 1 case.

172 methods of estimation and the importance of ductal carcinoma in situ in overdiagnosis.

173 rwent mastectomy after cancellation, one had ductal carcinoma in situ in the same quadrant as the MR-

174 Ductal carcinoma in situ is a common finding in women ha

175 Ductal carcinoma in situ is currently managed with excis

176 c mutations or deletions of TP53 and PTEN in ductal carcinoma in situ lesions have been implicated in

177 ty and the development of estrogen-dependent ductal carcinoma in situ lesions.

178 Moreover, further genetic interrogation of ductal carcinoma in situ might lead to a reclassificatio

179 s of radiotherapy after sector resection for ductal carcinoma in situ of the breast (DCIS) in patient

180 = 955) compared with patients with residual ductal carcinoma in situ only (n = 309), no invasive res

181 mmon cause of death for women diagnosed with ductal carcinoma in situ or stage I disease and for wome

182 e identified 233,754 patients diagnosed with ductal carcinoma in situ or stage I to III unilateral br

183 ubsequent breast cancers in each subset were ductal carcinoma in situ or stage I.

184 omen aged 20 to 79 years diagnosed as having ductal carcinoma in situ or stages I to III invasive bre

185 t invasive tumor fronts, particularly within ductal carcinoma in situ samples, establishes that EMT-i

186 rs, six were invasive cancers and three were ductal carcinoma in situ stage Tis-T1c.

187 ompared with total tissue lysates from human ductal carcinoma in situ tissue loaded on basic immobili

188 e examined 296 breast adenocarcinomas and 38 ductal carcinoma in situ tissues that were represented i

189 urred during the transition from noninvasive ductal carcinoma in situ to invasive breast cancer.

190 tes with increasing disease progression from ductal carcinoma in situ to invasive carcinoma.

191 nt chemotaxis in vitro and for conversion of ductal carcinoma in situ to invasive ductal carcinoma in

192 The transition from ductal carcinoma in situ to invasive ductal carcinoma is

193 profile established for the normal breast to ductal carcinoma in situ transition was largely maintain

194 Postmenopausal women with hormone-positive ductal carcinoma in situ treated by lumpectomy with clea

195 Postmenopausal women with hormone-positive ductal carcinoma in situ treated by lumpectomy with clea

196 1184 patients with low-risk invasive and ductal carcinoma in situ treated with breast-conserving

197 ersus tamoxifen in postmenopausal women with ductal carcinoma in situ undergoing lumpectomy plus radi

198 Of these, 64.7% (11 of 17) were ductal carcinoma in situ versus 6.7% (two of 30) of canc

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

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

201 The incidence of ductal carcinoma in situ was higher in bisphosphonate us

202 f 18437 women with invasive breast cancer or ductal carcinoma in situ were enrolled as cases and matc

203 e, missing stage or treatment data, and with ductal carcinoma in situ were excluded, leaving 3729 pat

204 hyperplasia or lobular carcinoma in situ; or ductal carcinoma in situ with mastectomy.

205 2963 were diagnosed with invasive cancer or ductal carcinoma in situ within 12 months of screening.

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

207 nual incidence of invasive plus noninvasive (ductal carcinoma in situ) breast cancers was 0.35% on ex

208 as incidence of all breast cancer (including ductal carcinoma in situ) during a 10 year follow-up per

209 UK/ANZ DCIS (UK, Australia, and New Zealand ductal carcinoma in situ) trial suggested that radiother

210 alateral breast cancer, invasive disease, or ductal carcinoma in situ), analysed by intention to trea

211 of breast cancer (invasive breast cancer and ductal carcinoma in situ), analysed by intention to trea

212 rly stages of breast cancer (hyperplasia and ductal carcinoma in situ), in morphogenesis assays G1P3

213 ast cancer (invasive cancers or non-invasive ductal carcinoma in situ).

214 who were screened, eight were diagnosed with ductal carcinoma in situ, 16 with early stage disease (1

215 12% bilateral), with no dominant histology (ductal carcinoma in situ, 35%; infiltrating ductal carci

216 A computer simulation is used to model ductal carcinoma in situ, a form of non-invasive breast

217 are associated with malignant progression of ductal carcinoma in situ, a precancerous lesion.

218 ents (23%) had invasive cancer, 45 (19%) had ductal carcinoma in situ, and 125 (53%) had both; 11 pat

219 psies from invasive ductal carcinoma, 8 from ductal carcinoma in situ, and 6 from normal breast.

220 inoma compared to normal breast epithelia or ductal carcinoma in situ, and general loss of Nuc-pYStat

221 cimens from reduction mammoplasty, adenosis, ductal carcinoma in situ, and infiltrating ductal carcin

222 TA1s-TG mice revealed ductal hyperplasia and ductal carcinoma in situ, and low incidence of palpable

223 ge, menopausal status, presence of extensive ductal carcinoma in situ, clinical tumour size, nodal st

224 ined invasive ductal carcinoma (IDC) but not ductal carcinoma in situ, fibroadenoma, or normal breast

225 They occur in ductal carcinoma in situ, in breast cancers, and in brea

226 cuity of malignant breast lesions, including ductal carcinoma in situ, is significantly improved at c

227 aging depicted 60 additional breast cancers (ductal carcinoma in situ, n = 20; invasive carcinoma, n

228 = 1552) were identified (invasive, n = 1287; ductal carcinoma in situ, n = 270); in five, both kinds

229 r without a prior diagnosis of breast cancer,ductal carcinoma in situ, or lobular carcinoma in situ.

230 II invasive ductal or lobular breast cancer, ductal carcinoma in situ, or prophylaxis.

231 , and PI3K catalytic subunit (PIK3CA) in 110 ductal carcinoma in situ, primary tumor, and metastatic

232 d in healthy tissue but already prominent in ductal carcinoma in situ, together with ECM and cell-cel

233 In cellular models of breast ductal carcinoma in situ, we reveal a link between filop

234 breast cancer and multicentric tumors, with ductal carcinoma in situ, who will undergo mastectomy, w

235 edge of the specimen removed in the case of ductal carcinoma in situ.

236 e group of stakeholders on the management of ductal carcinoma in situ.

237 the kinase domain and overexpressed only in ductal carcinoma in situ.

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

239 till developed mammary gland hyperplasia and ductal carcinoma in situ.

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

241 ent stromal angiogenesis that resemble human ductal carcinoma in situ.

242 o MR imaging sensitivity in the detection of ductal carcinoma in situ.

243 s, including atypical ductal hyperplasia and ductal carcinoma in situ.

244 rom surgery for invasive breast carcinoma or ductal carcinoma in situ.

245 ncers detected at screening mammography were ductal carcinoma in situ.

246 mphovascular invasion and intermediate grade ductal carcinoma in situ.

247 from having a choice of effective agents for ductal carcinoma in situ.

248 al growth factor receptor 2, with associated ductal carcinoma in situ.

249 he management of both low-risk and high-risk ductal carcinoma in situ.

250 reast cancer in postmenopausal patients with ductal carcinoma in situ.

251 r widespread low-grade or intermediate-grade ductal carcinoma in situ.

252 nifested as calcifications and 28 (65%) were ductal carcinoma in situ.

253 nd 1.0 cm (range, 0 to 9.3) in patients with ductal carcinoma in situ.

254 hitecture in a manner that is reminiscent of ductal carcinoma in situ; however, motile cells do not i

255 de glioma, and 2 preinvasive breast cancers [ductal carcinoma in situ]); all but 1 required only rese

256 criptional events among subtypes of invasive ductal carcinoma in The Cancer Genome Atlas (TCGA) Breas

257 sion of ductal carcinoma in situ to invasive ductal carcinoma in vivo.

258 c analysis resulted in the diagnosis of four ductal carcinomas in situ and 10 invasive carcinomas (fi

259 cancers were diagnosed in 18 patients (nine ductal carcinomas in situ and 11 invasive breast cancers

260 Eleven breast cancers (four ductal carcinomas in situ and seven invasive cancers; al

261 d the number of intraductal hyperplasias and ductal carcinomas in situ by 50 days of age in Wistar-Fu

262 invasive breast cancer, which revealed that ductal carcinomas in situ show intratumor genetic hetero

263 Penetrance of ductal carcinomas in situ was also decreased.

264 ts A total of 45 cancers (33 invasive and 12 ductal carcinomas in situ) were diagnosed, 43 were seen

265 on from ductal carcinoma in situ to invasive ductal carcinoma is a key event in breast cancer progres

266 Ductal carcinoma is one of the most common cancers among

267 39 phosphorylation of PIPKIgamma in invasive ductal carcinoma lesions and suggested a positive correl

268 Results When compared with grade 1 ductal carcinoma (n = 212), TC (n = 102) was more likely

269 ,453) with that of risk factors and invasive ductal carcinomas (n = 7,525); in addition, we compared

270 58 years; range, 32-83 years) with invasive ductal carcinoma of at least 10 mm were recruited to und

271 al staining among 198 patients with invasive ductal carcinoma of the breast, using available clinical

272 t prognostic value in patients with invasive ductal carcinoma of the breast.

273 uencing data from 680 cases of TCGA invasive ductal carcinomas of the breast and correlated them to c

274 prognostic value of TC compared with grade 1 ductal carcinomas of the breast.

275 restin1 in human breast cancer (infiltrating ductal carcinoma or IDC and metastatic IDC) correlates w

276 results that showed in situ or infiltrating ductal carcinoma or infiltrating lobular carcinoma in th

277 of DCIS but lower risks of LCIS and invasive ductal carcinomas (P for heterogeneity < 0.01).

278 nohistochemical analysis of human pancreatic ductal carcinoma (PDAC) specimens, and in vitro validati

279 Fibrosis compromises pancreatic ductal carcinoma (PDAC) treatment and contributes to pat

280 psy of the breast mass diagnoses an invasive ductal carcinoma, poorly differentiated (grade 3), with

281 phosphorylation in the invasive human breast ductal carcinomas positively correlate with the levels o

282 h Slit2 in the vasculature of invasive human ductal carcinoma samples.

283 , ductal carcinoma in situ, and infiltrating ductal carcinoma showed down-regulation of COX-2 express

284 carcinoma in situ and in the later invasive ductal carcinoma stage.

285 Compared with grade 1 ductal carcinoma, TC was associated with longer disease-

286 9 +/- 0.11; P < .05) for women with invasive ductal carcinoma than for those with benign tissue.

287 r in vivo and to human specimens of invasive ductal carcinoma that express ErbB2 ex vivo.

288 raphically detected grade 3, 2.2-cm invasive ductal carcinoma that is sentinel lymph node negative, e

289 core needle biopsy revealed an infiltrating ductal carcinoma that was estrogen receptor (ER) positiv

290 ast cancers are mostly basal-like high-grade ductal carcinomas that frequently overexpress epidermal

291 old and in patients with high grade invasive ductal carcinoma, the boost dose reduced the local relap

292 sk for ductal carcinoma in situ and invasive ductal carcinoma, the most common early breast cancers i

293 argely maintained in the in situ to invasive ductal carcinoma transition.

294 or female patients with early-stage invasive ductal carcinoma treated with BCT, mastectomy alone, or

295 the PAXP1 gene in a matched clinical breast ductal carcinoma tumor sample; two of which are likely l

296 n multivariate analysis, high-grade invasive ductal carcinoma was associated with an increased risk o

297 0.6 x 0.5 cm Nottingham grade 1 infiltrating ductal carcinoma was removed from the right upper outer

298 Middle T antigen (PyMT) mouse model of human ductal carcinoma, we show that the specific ablation of

299 Women aged 45 years and older with invasive ductal carcinoma were enrolled and randomly assigned in

300 years) with a diagnosis of primary invasive ductal carcinoma were included.