ライフサイエンスコーパス: ductal carcinoma

1 (18)F-FDG PET than the more common invasive ductal carcinoma.

2 Outcomes included invasive lobular or ductal carcinoma.

3 ents diagnosed with lobular carcinoma versus ductal carcinoma.

4 target in cancer, particularly in pancreatic ductal carcinoma.

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

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

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

8 0 regulates CSCs in luminal subtype invasive ductal carcinoma.

9 because of a risk of progression to invasive ductal carcinoma.

10 ndolent ductal carcinoma in situ to invasive ductal carcinoma.

11 r histologies, invasive lobular and invasive ductal carcinoma.

12 cancer, is a potential precursor to invasive ductal carcinoma.

13 ng of FFPE sections of human breast invasive ductal carcinoma.

14 ed to manually annotated regions of invasive ductal carcinoma.

15 e been implicated in progression to invasive ductal carcinomas.

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

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

18 clinically diverse cohort of invasive breast ductal carcinomas.

19 an models of both luminal and basal invasive ductal carcinomas.

20 tes metastasis in diverse models of invasive ductal carcinomas.

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

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

23 ductal carcinoma (33.33%) and 7 infiltrating ductal carcinoma (58.33%).

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

25 dian age was 62 y (range, 31-90 y), most had ductal carcinoma (95%), and most were estrogen receptor-

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

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

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

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

30 new mechanistic insight into progression of ductal carcinoma and support clinical application of MNK

31 vation that most breast cancers are invasive ductal carcinomas and express E-cadherin in primary tumo

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

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

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

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

36 ditional patient was diagnosed with invasive ductal carcinoma at the time of 6-month follow-up.

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

38 sversion present in human genomic DNA from a ductal carcinoma cell line, a mutation commonly found in

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

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

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

42 dherin acts as a survival factor in invasive ductal carcinomas during the detachment, systemic dissem

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

44 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

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

46 ductal carcinoma in situ (DCIS) to invasive ductal carcinoma (IDC) are not well understood.

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

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

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

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

51 Invasive ductal carcinoma (IDC) often presents alone or with a co

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

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

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

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

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

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

58 atures from the more common subtype invasive ductal carcinoma (IDC).

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

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

61 common histologic subtypes were infiltrating ductal carcinoma (IDC, 84.9%) and luminal A (LA, 49.1%);

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

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

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

65 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

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

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

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

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

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

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

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

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

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

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

76 et their differentiation and perturbation in ductal carcinoma in situ (DCIS) are poorly understood.

77 Primary endocrine therapy for ductal carcinoma in situ (DCIS) as a potential alternati

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

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

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

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

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

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

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

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

86 Ductal carcinoma in situ (DCIS) encompasses a highly het

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

88 iR-223 expression was lost in microdissected ductal carcinoma in situ (DCIS) from patients with lumin

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

90 [64%] vs 349 of 845 [41%], P < .0001), have ductal carcinoma in situ (DCIS) in the index breast (31%

91 The recalls yielding ductal carcinoma in situ (DCIS) increased from 0.3 per 1

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

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

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

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

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

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

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

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

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

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

102 Background Most ductal carcinoma in situ (DCIS) lesions are first detect

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

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

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

106 A subset of patients with ductal carcinoma in situ (DCIS) of the breast develop ip

107 Historically, ductal carcinoma in situ (DCIS) of the breast has been m

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

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

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

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

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

113 Ductal Carcinoma In Situ (DCIS) represents a significant

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

115 e (PPV) of biopsy, using invasive cancer and ductal carcinoma in situ (DCIS) to define a positive ref

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

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

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

119 st cancers progress from relatively indolent ductal carcinoma in situ (DCIS) to invasive ductal carci

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

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

122 on on the re-intervention rate in women with ductal carcinoma in situ (DCIS) undergoing breast-conser

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

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

125 g surgery for node-negative breast cancer or ductal carcinoma in situ (DCIS) were randomly assigned t

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

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

128 804 study identified good-risk patients with ductal carcinoma in situ (DCIS), a breast cancer diagnos

129 Ductal carcinoma in situ (DCIS), although often diagnose

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

131 ied, including invasive breast cancer (IBC), ductal carcinoma in situ (DCIS), and adjacent benign tis

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

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

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

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

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

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

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

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

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

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

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

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

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

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

146 ncer is believed to evolve from non-invasive ductal carcinoma in situ (DCIS).

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

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

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

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

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

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

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

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

155 cer (HR, 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

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

157 51), invasive lobular carcinoma (n = 5), or ductal carcinoma in situ (n = 4).

158 1.3, 2.6]; P < .001), invasive cancer versus ductal carcinoma in situ (OR, 1.6 [95% CI: 1.0, 2.4]; P

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

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

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

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

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

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

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

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

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

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

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

170 ws intended to highlight the relationship of ductal carcinoma in situ as a precursor to breast cancer

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

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

173 Conclusion Ductal carcinoma in situ calcifications are more extensi

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

175 eased during the past 2 decades, whereas the ductal carcinoma in situ detection rate increased less r

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

177 ofractionation in patients with non-low-risk ductal carcinoma in situ following breast-conserving sur

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

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

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

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

182 Ductal carcinoma in situ is currently managed with excis

183 reast epithelial tissue and hormone-negative ductal carcinoma in situ lesions but were uncoupled in t

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

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

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

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

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

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

190 early breast cancer or extensive/high-grade ductal carcinoma in situ planned for standard radioactiv

191 damage repair pathway and provides a link in ductal carcinoma in situ progression to invasive ductal

192 , with co-expression of EGFR and MET marking ductal carcinoma in situ regions of normal-like tumors a

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

194 orial introduces this month's special Breast Ductal Carcinoma in Situ Theme Issue, a series of review

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

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

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

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

199 inhibitors to delay progression of indolent ductal carcinoma in situ to invasive ductal carcinoma.

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

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

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

203 1184 patients with low-risk invasive and ductal carcinoma in situ treated with breast-conserving

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

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

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

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

208 A 59% reduction in ductal carcinoma in situ was observed (0.41, 0.22-0.79,

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

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

211 r older with completely excised non-low-risk ductal carcinoma in situ were randomly assigned, by use

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

213 2963 were diagnosed with invasive cancer or ductal carcinoma in situ within 12 months of screening.

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

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

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

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

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

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

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

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

222 12% bilateral), with no dominant histology (ductal carcinoma in situ, 35%; infiltrating ductal carci

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

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

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

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

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

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

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

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

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

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

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

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

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

236 developed breast cancer (invasive, n = 129; ductal carcinoma in situ,n = 47) over a median follow-up

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

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

239 mphovascular invasion and intermediate grade ductal carcinoma in situ.

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

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

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

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

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

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

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

247 12 women: seven invasive carcinomas and five ductal carcinoma in situ.

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

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

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

251 ts with early stage breast cancer, including ductal carcinoma in situ.

252 nt or previous diagnosis of breast cancer or ductal carcinoma in situ.

253 s the incidence of invasive breast cancer or ductal carcinoma in situ.

254 n women without preexisting breast cancer or ductal carcinoma in situ.

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 The latter comprised eight ductal carcinomas in situ (88% intermediate or high grad

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

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 ected; 118 cancers were invasive and 21 were ductal carcinomas in situ.

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

267 Ductal carcinoma is one of the most common cancers among

268 39 phosphorylation of PIPKIgamma in invasive ductal carcinoma lesions and suggested a positive correl

269 the lesions to be benign (n = 55), invasive ductal carcinoma (n = 51), invasive lobular carcinoma (n

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

271 58 years; range, 32-83 years) with invasive ductal carcinoma of at least 10 mm were recruited to und

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

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

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

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 me (68 msec +/- 13) was observed in invasive ductal carcinoma (P < .001), whereas no statistical diff

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

279 nsmembrane protease, serine 13), in invasive ductal carcinoma patient tissue samples compared to norm

280 Pancreatic ductal carcinoma (PDAC) is a highly lethal cancer, and e

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

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

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

284 ositively correlated with Ki-67 for invasive ductal carcinoma (rho = 0.51, P = 0.02, n = 21).

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

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 riple-negative grade 3 cancers; two invasive ductal carcinomas that were estrogen and progesterone re

292 lecular level, the proliferation of invasive ductal carcinoma through breast tissue is beyond the ran

293 al carcinoma in situ progression to invasive ductal carcinoma through loss of SIM2s, increased genomi

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

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

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

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.