ライフサイエンスコーパス: invasive breast cancer

1 or frequently altered in the patients having invasive breast cancer.

2 CIS lesions that are likely to progress into invasive breast cancer.

3 sociated with opposite histologic changes in invasive breast cancer.

4 nd metastasis formation in the PyMT model of invasive breast cancer.

5 opausal women with hormone-receptor-positive invasive breast cancer.

6 molog 1 (DACH1), whose expression is lost in invasive breast cancer.

7 6.9 years, 17,908 women were diagnosed with invasive breast cancer.

8 p, 865 daughters developed incident cases of invasive breast cancer.

9 follow-up of 15 years, 4,484 women developed invasive breast cancer.

10 second most prevalent histologic subtype of invasive breast cancer.

11 itional four independent genetic datasets in invasive breast cancer.

12 ed molecular profiles indistinguishable from invasive breast cancer.

13 ion to offer to BRCA1 mutation carriers with invasive breast cancer.

14 were classified as being at elevated risk of invasive breast cancer.

15 from noninvasive ductal carcinoma in situ to invasive breast cancer.

16 argin width in breast-conserving surgery for invasive breast cancer.

17 imaging increases detection of node-negative invasive breast cancer.

18 cases was associated with increased risk for invasive breast cancer.

19 ]) were associated with a lower incidence of invasive breast cancer.

20 ductal carcinoma in situ or stages I to III invasive breast cancer.

21 artum are associated with protection against invasive breast cancer.

22 a novel therapeutic target for treatment of invasive breast cancer.

23 ulates the worst prognosis for patients with invasive breast cancer.

24 We documented 4,734 cases of incident invasive breast cancer.

25 aluation of axillary status in patients with invasive breast cancer.

26 betes was associated with lower incidence of invasive breast cancer.

27 tion-based dietary index scores and incident invasive breast cancer.

28 e observe that loss of Sfrp3 predisposes for invasive breast cancer.

29 c chemotherapy is an effective treatment for invasive breast cancer.

30 aggressiveness in subsets of preinvasive and invasive breast cancer.

31 roups, similar to that seen in patients with invasive breast cancer.

32 atypical ductal hyperplasia (ADH), DCIS and invasive breast cancer.

33 observed in approximately 40% of women with invasive breast cancer.

34 ccording to their risk of developing primary invasive breast cancer.

35 Ten-year cumulative risk of invasive breast cancer.

36 eatment for women diagnosed with early stage invasive breast cancer.

37 stromal and immune microenvironment in HER2+ invasive breast cancer.

38 tologic sections of 10 patients with stage 2 invasive breast cancers.

39 N-myc and STAT interactor) is compromised in invasive breast cancers.

40 e peripheral blood of patients with advanced invasive breast cancers.

41 eters squared, >35.0) (hazard ratio [HR] for invasive breast cancer, 1.58; 95% CI, 1.40-1.79).

42 Over an average of 10.5 years, 6,658 invasive breast cancers, 1,198 endometrial cancers, and

43 the 66 AA patients who developed subsequent invasive breast cancer, 16 (24.2%) developed TNBC compar

44 Of 373,563 women with invasive breast cancer, 268,675 (71.9%) were non-Hispani

45 f PSPHL using genomic DNA from AAW (199 with invasive breast cancer, 360 controls) and CW (invasive b

46 nvasive breast cancer, 360 controls) and CW (invasive breast cancer =589, 364 controls).

47 Of 496,488 women diagnosed with unilateral invasive breast cancer, 59.6% underwent breast-conservin

48 es, 1 slide per case), including 23 cases of invasive breast cancer, 73 ductal carcinoma in situ (DCI

49 fewer per 10 000 woman-years) and increased invasive breast cancer (8 more per 10 000 woman-years),

50 rson-years, were significantly increased for invasive breast cancer (9 more cases [95% CI, 1 to 19]),

51 better 5-year disease-specific survival for invasive breast cancer (97% vs 87% for patient- and phys

52 andard of care in the surgical management of invasive breast cancer, a benefit has not been demonstra

53 lts of this study suggest that in women with invasive breast cancer, a miRNA score that incorporates

54 Current 10-year risks of invasive breast cancer after a diagnosis of ADH may be l

55 itu (DCIS) of the breast develop ipsilateral invasive breast cancer after breast-conserving surgery w

56 ormalized urinary cadmium concentration, and invasive breast cancer among 12,701 postmenopausal women

57 cancer, but we did see a 19% excess risk of invasive breast cancer among those with AF (adjusted haz

58 PM2.5 was associated with a higher risk of invasive breast cancer among two of seven identified com

59 years of follow-up (1993-2010), 508 cases of invasive breast cancer and 1,050 comparison women were i

60 ean number of IVF cycles, 3.6), 839 cases of invasive breast cancer and 109 cases of in situ breast c

61 board-approved study included 125 women with invasive breast cancer and 274 age- and race-matched con

62 ntify methylation from 640 incident cases of invasive breast cancer and 741 controls.

63 Multivariable HRs for primary invasive breast cancer and 95% CIs were estimated by usi

64 s in 9% of DCIS and approximately 7% of both invasive breast cancer and all breast cancers in the U.S

65 rates (0.15% for DCIS and less than 0.1% for invasive breast cancer and all breast cancers).

66 0.1% to the obligate overdiagnosis rates of invasive breast cancer and all breast cancers.

67 be 9% for DCIS and approximately 7% for both invasive breast cancer and all breast cancers.

68 Verification of invasive breast cancer and benign without atypia diagnos

69 ogenous hormones improve risk prediction for invasive breast cancer and could help identify women who

70 Air pollution measures were related to both invasive breast cancer and DCIS within certain geographi

71 ndpoint was the occurrence of breast cancer (invasive breast cancer and ductal carcinoma in situ), an

72 Medications reduced the incidence of invasive breast cancer and fractures and increased the i

73 ic features used to predict the prognosis of invasive breast cancer and may serve as a marker for stu

74 which postmenopausal women with HR-positive invasive breast cancer and no prior therapy for advanced

75 NAC use in patients with initially operable invasive breast cancer and potential impact on breast co

76 e change for >35% of patients diagnosed with invasive breast cancer and refined OS estimates.

77 receptor (ER)-positive, lymph node-negative invasive breast cancer and to determine the relationship

78 agnosed with noninflammatory, nonmetastatic, invasive breast cancer and underwent surgery as initial

79 romotes constitutive NF-kappaB activation in invasive breast cancers and activation of this pathway i

80 the 94 WA patients who developed subsequent invasive breast cancers and had complete biomarker data

81 Comparing risk factor associations between invasive breast cancers and possible precursors may furt

82 A-to-I RNA-edited form of Gabra3 only in non-invasive breast cancers and show that edited Gabra3 supp

83 ine whether WISP1 expression is increased in invasive breast cancer, and 3) to determine whether a ge

84 te (or type 1) overdiagnosis rates for DCIS, invasive breast cancer, and all breast cancers (DCIS plu

85 0%, 21%, and 22.5% at age 80 years for DCIS, invasive breast cancer, and all breast cancers, respecti

86 cancer, for ductal carcinoma in situ (DCIS), invasive breast cancer, and all breast cancers.

87 e surgeons' approach to surgical margins for invasive breast cancer, and changes in postlumpectomy su

88 n-progestin (stroke, coronary heart disease, invasive breast cancer, and pulmonary embolism), and ral

89 ptor-positive and estrogen receptor-negative invasive breast cancer, and the emergence of distinct pa

90 ressed and amplified in approximately 15% of invasive breast cancers, and is the molecular target and

91 Kinetic data in invasive breast cancer are associated with the patient's

92 h anti-tumor immunity were obtained from the invasive breast cancer arm of the Cancer Genome Atlas st

93 ductal carcinoma in situ (DCIS) lesions and invasive breast cancers as well as with increased mortal

94 h increased DCIS incidence, the diagnosis of invasive breast cancer at earlier stages, and increased

95 ts diagnosed with a first primary unilateral invasive breast cancer at Kaiser Permanente Institute fo

96 ts diagnosed with a first primary unilateral invasive breast cancer at Kaiser Permanente Institute fo

97 a in situ (DCIS) components of biopsy-proven invasive breast cancer before surgery and (b) investigat

98 ing improves depiction of DCIS components of invasive breast cancers before surgery and is associated

99 iagnosed with incident localized or regional invasive breast cancer between 1988 and 2008; a subset o

100 We documented 2,866 incident cases of invasive breast cancer between 1991 and 2011.

101 who underwent surgery for primary unilateral invasive breast cancer between 2003 and 2008 were select

102 pliant protocol, 408 patients diagnosed with invasive breast cancer between 2004 and 2013 who underwe

103 o were 18 to 64 years old and diagnosed with invasive breast cancer between 2007 and 2009, linking ca

104 of 238726 adult patients diagnosed as having invasive breast cancer between 2010 and 2013 for whom th

105 premenopausal women who were diagnosed with invasive breast cancer between 26 and 47 years of age.

106 tified 247 719 women who were diagnosed with invasive breast cancer between Jan 1, 2001, and Dec 31,

107 Among a convenience cohort of patients with invasive breast cancer, breast tumor and matched normal

108 ncreases in the detection of early-stage non-invasive breast cancer but no noteworthy change in the i

109 a diagnosis of an ipsilateral second primary invasive breast cancer, but prevention of these recurren

110 tyrosine kinase Pyk2 is highly expressed in invasive breast cancer, but the mechanism by which it po

111 gnalling cross talk has been demonstrated in invasive breast cancer, but their role in DCIS stem and

112 rea under the curve (AUC) for 5-year risk of invasive breast cancer by adding each hormone to the Gai

113 white woman in the United States developing invasive breast cancer by age 80 years is 11.3%.

114 We investigated risk factor associations for invasive breast cancer by method of detection within a s

115 sed imaging or targeted therapy, we screened invasive breast cancers by immunohistochemistry for the

116 t Panel continues to recommend ER testing of invasive breast cancers by validated immunohistochemistr

117 ty (Body Image Scale); and perceived risk of invasive breast cancer (Cancer Worry Scale and a study-s

118 ted case-control study in 621 postmenopausal invasive breast cancer cases and 621 matched controls in

119 tudy in the Nurses' Health Study, with 1,506 invasive breast cancer cases diagnosed after blood donat

120 We documented 1,700 invasive breast cancer cases through 2015 (mean follow-u

121 Incident invasive breast cancer cases were confirmed by medical r

122 Between 1995 and 2008, 2482 invasive breast cancer cases were diagnosed among 57,403

123 During follow-up, a total of 5,483 invasive breast cancer cases were diagnosed.

124 rs of follow-up through June 30, 2007, 4,084 invasive breast cancer cases were diagnosed.

125 and 2001; median follow-up, 8.9 years; 1,905 invasive breast cancer cases).

126 e absence of both Nischarin and LKB1 from an invasive breast cancer cell line (MDA-MB-231) enhances m

127 Actopaxin phosphorylation is elevated in the invasive breast cancer cell line MDA-MB-231 compared wit

128 atic breast-231 cells, a prototypical highly invasive breast cancer cell line, to degrade the extrace

129 n factor 1 (ARF1) is overexpressed in highly invasive breast cancer cell lines and that epidermal gro

130 The highly invasive breast cancer cell lines, MDA-MB-231 and 4T1, e

131 Second, we stably overexpressed PLD2 in low-invasive breast cancer cells (MCF-7) with a biscistronic

132 Attachment of invasive breast cancer cells (MDA-MB-231) to human umbil

133 By contrast, primary cultures of invasive breast cancer cells convert glutamine to glutam

134 and cell migration assays were performed for invasive breast cancer cells cultured in mechanically pl

135 It was found that highly-invasive breast cancer cells exhibited greater deformabi

136 e show that depletion of ezrin expression in invasive breast cancer cells impairs both FA and invadop

137 optimized compounds reduced extravasation of invasive breast cancer cells in a zebrafish model.

138 ified stromal fibroblast-induced gene in non-invasive breast cancer cells is highly overexpressed in

139 own of plakoglobin in these low motility non-invasive breast cancer cells rearranged the actin filame

140 Reduction of DP103 expression in invasive breast cancer cells reduced phosphorylation of

141 Here, using invasive breast cancer cells we show that the Ca(2+) - a

142 , either recombinant or secreted from highly invasive breast cancer cells, down-regulates the tumor s

143 Moreover, when NAT1 was deleted in highly invasive breast cancer cells, MMP9 mRNA and protein sign

144 colocalizes with cortactin to invadopodia of invasive breast cancer cells, where it mediates epiderma

145 down of ERK3 reduces metastatic potential of invasive breast cancer cells.

146 the tumorigenic and metastatic potential of invasive breast cancer cells.

147 exhibited greater deformability than weakly-invasive breast cancer cells.

148 to force-dependent directional migration of invasive breast cancer cells.

149 o determine how MSCs affect the migration of invasive breast cancer cells.

150 he regulation of ARF1 and ARF6 activation in invasive breast cancer cells.

151 hondrial movement toward the leading edge in invasive breast cancer cells.

152 Rac3 and promote invadopodial maturation in invasive breast cancer cells.

153 volumetric imaging of fluorescent beads and invasive breast cancer cells.

154 a is needed in patients with newly diagnosed invasive breast cancer, CNB is more sensitive than FNAB.

155 trials) were associated with lower risks of invasive breast cancer compared with placebo; results we

156 quartile of DASH scores had a lower risk of invasive breast cancer compared with those in the lowest

157 increased risk of estrogen receptor-positive invasive breast cancer compared with women who never wor

158 protein array data show that PEA15 levels in invasive breast cancers correlate with patient survival,

159 sociated with a significantly higher rate of invasive breast cancer detection.

160 A total of 8,421 cases of invasive breast cancer developed in postmenopausal women

161 The study comprised a cohort of women with invasive breast cancer diagnosed <50 years and treated b

162 total of 24 843 patients with stage I to III invasive breast cancer diagnosed between January 1, 2005

163 A cohort of 6,294 patients with invasive breast cancer diagnosed under 50 years of age a

164 emerging medical applications including non-invasive breast cancer diagnosis, cancer margin evaluati

165 ted with increased survival in patients with invasive breast cancer, especially in patients with inva

166 en of European ancestry diagnosed with first invasive breast cancer from 1990 onward with follow-up f

167 102 women ages 20 to 49 years diagnosed with invasive breast cancer from 1990 to 2009.

168 with early-stage, hormone receptor-positive invasive breast cancer from 1998 to 2003.

169 Women diagnosed with invasive breast cancer from 2001 to 2008 in Stockholm, S

170 Observational study of women diagnosed with invasive breast cancer from 2004 to 2011 who were identi

171 y confirmed triple-negative operable primary invasive breast cancer from 360 sites in 37 countries.

172 Patients with a diagnosis of invasive breast cancer from January 2005 through Decembe

173 Main analyses included patients with invasive breast cancer from population- and hospital-bas

174 ages 18-years and older diagnosed with 2907 invasive breast cancers from January 2003 to December 20

175 20 to 45 years at the time of diagnosis with invasive breast cancer, from January 1, 2003, to Decembe

176 nd particularly as the surgical treatment of invasive breast cancer has changed.

177 es attenuated the association between AF and invasive breast cancer (HR = 1.01, 95% CI: 0.85, 1.20).

178 de use was strongly associated with incident invasive breast cancer (HR = 1.68, 95% CI: 1.33, 2.12) i

179 0.78-1.14) and 104 vs 135, respectively, for invasive breast cancer (HR, 0.79; 95% CI, 0.61-1.02); cu

180 0.95-1.45) and 206 vs 155, respectively, for invasive breast cancer (HR, 1.24; 95% CI, 1.01-1.53).

181 increased after experience of an ipsilateral invasive breast cancer (HR, 18.1 [95% CI, 14.0-23.6]; P

182 mal growth factor receptor 2 (HER2)-positive invasive breast cancer (IBC) at risk for treatment failu

183 tion from ductal carcinoma in situ (DCIS) to invasive breast cancer (IBC) is a crucial step in breast

184 nts with histologically verified nonpalpable invasive breast cancer (IBC) or ductal carcinoma in situ

185 gions of interest were identified, including invasive breast cancer (IBC), ductal carcinoma in situ (

186 DCIS and patients with DCIS and synchronous invasive breast cancer (IBC).

187 ta set consisting of tumor/TIL maps for 1090 invasive breast cancer images from The Cancer Genome Atl

188 case-control Carolina Breast Cancer Study of invasive breast cancer in 1,391 black (725 cases, 666 co

189 ted comparing the 10-year cumulative risk of invasive breast cancer in 955331 women undergoing mammog

190 se of hormonal contraception and the risk of invasive breast cancer in a nationwide prospective cohor

191 d 18-89 years who had been diagnosed with an invasive breast cancer in Brazil during 2001-14.

192 ith early-stage, estrogen receptor-positive, invasive breast cancer in the absence of additional prog

193 ment of DCIS could prevent the occurrence of invasive breast cancer in the future is not clear.

194 s were associated with lower risk of primary invasive breast cancer in women but also were associated

195 Analyzed were 117 invasive breast cancers in 117 patients.

196 fier is associated with indolent behavior of invasive breast cancers in women followed for 2 decades.

197 [95% CI, 1.11 to 1.23]) but no difference in invasive breast cancer incidence (adjusted OR, 1.00 [CI,

198 ne, a steroidal aromatase inhibitor, reduced invasive breast cancer incidence by 65% among 4,560 post

199 Time-specific invasive breast cancer incidence rates and exploratory a

200 The data set of biopsy-proven invasive breast cancers included 74 (88%) ductal, eight

201 ears of follow-up, there were 1,851 incident invasive breast cancers, including 914 ER+ and 468 ER- c

202 The 10-y absolute risk of invasive breast cancer increased from 3,749 per 100,000

203 ent dietary risk factor for premalignant and invasive breast cancer is alcohol, whether consumed duri

204 Invasive breast cancer is believed to evolve from non-in

205 An important clinical biomarker for invasive breast cancer is human epidermal growth factor

206 ing data from 4140 women with a diagnosis of invasive breast cancer made between 1995 and 2009.

207 Results: Among 7541 women with invasive breast cancer, median age at initial breast can

208 Among 7541 women with invasive breast cancer, median age at initial breast can

209 elial-stromal co-expression relationships in invasive breast cancer mostly represent self-loops, in w

210 improved risk prediction for postmenopausal invasive breast cancer (n = 437 patient cases and n = 77

211 We evaluated all invasive breast cancers (N = 641) that were systematical

212 We included 3,012 patients with invasive breast cancer newly diagnosed between 2001 and

213 e patients were women with clinical T1 or T2 invasive breast cancer, no palpable axillary adenopathy,

214 from 1980-2006, during which 3,398 incident invasive breast cancers occurred over 1.4 million person

215 February 4, 2016, patients with nonpalpable invasive breast cancer or DCIS visible on ultrasound wer

216 A total of 18437 women with invasive breast cancer or ductal carcinoma in situ were

217 The primary end point was the incidence of invasive breast cancer or ductal carcinoma in situ.

218 9, 95% CI 0.29-0.81, p for trend = 0.01) and invasive breast cancer (OR = 0.63; 95% CI: 0.42, 0.93, P

219 cted in 61% of CW compared to 6% of AAW with invasive breast cancer (P < 0.0001); genotype frequencie

220 ative (P<0.05) and with triple negative (TN) invasive breast cancer (P<0.05).

221 l-stromal crosstalk plays a critical role in invasive breast cancer pathogenesis; however, little is

222 ry in two independent cohorts of early stage invasive breast cancer patients (discovery n = 1352; val

223 , Massachusetts, and New Hampshire (n=15,648 invasive breast cancer patients and 17,602 controls aged

224 cer Association Consortium containing 68,521 invasive breast cancer patients and 54,865 controls.

225 and determine whether survival differed for invasive breast cancer patients based on hormone recepto

226 ome in a retrospective cohort of 146 primary invasive breast cancer patients.

227 1999 to 2002, women with completely excised invasive breast cancer (pT1-3a, pN0-1, M0) were enrolled

228 rs) with newly diagnosed HER2-negative early invasive breast cancer (radiological tumour size >20 mm,

229 Methods: Twenty-two patients with invasive breast cancer received (18)F-FDG (5 MBq/kg) 45-

230 Twenty-two patients with invasive breast cancer received (18)F-FDG (5 MBq/kg) 45-

231 Clinical outcomes were invasive breast cancer recurrence and new primary breast

232 ipsilateral local recurrence and ipsilateral invasive breast cancer recurrence.

233 ession of ductal carcinoma in situ (DCIS) to invasive breast cancer remain largely unknown.

234 ession of ductal carcinoma in situ (DCIS) to invasive breast cancer remain poorly understood.

235 tcomes were coronary heart disease (CHD) and invasive breast cancer, respectively.

236 ivariable-adjusted HRs and 95% CIs for total invasive breast cancer risk and by estrogen receptor (ER

237 Obesity is associated with increased invasive breast cancer risk in postmenopausal women.

238 BPE is associated with future invasive breast cancer risk independent of breast densit

239 o were overweight and obese had an increased invasive breast cancer risk vs women of normal weight.

240 In the estrogen alone trial, the HR for invasive breast cancer risk was lower than 1 throughout

241 ial outdoor light at night may contribute to invasive breast cancer risk.

242 monstrated on gene expression data from 1952 invasive breast cancer samples, 10 DCIS, 9 benign sample

243 In invasive breast cancer specimens, Rictor expression was

244 how that S100A14 and HER2 are coexpressed in invasive breast cancer specimens,andthere is a significa

245 ncer-related genes become more pronounced at invasive breast cancer stage.

246 the deletion allele in AAW with and without invasive breast cancer suggests that this difference rep

247 from Medicare claims as having had incident invasive breast cancer surgery in 2003.

248 ive oestrogen alone had a lower incidence of invasive breast cancer than did those who received place

249 igher risk for transition to more aggressive invasive breast cancer than low-grade DCIS.

250 Incidence of coronary heart disease and invasive breast cancer (the trial's 2 primary end points

251 Among US women diagnosed with invasive breast cancer, the likelihood of diagnosis at a

252 nosis and that these lesions may progress to invasive breast cancer through a variety of evolutionary

253 al breast tissue among LCIS patients without invasive breast cancer to determine whether expression d

254 Women who have large or locally advanced invasive breast cancer (tumor size T3/T4), inflammatory

255 Women who have large or locally advanced invasive breast cancer (tumor size T3/T4), inflammatory

256 The first estimation approach found that 271 invasive breast cancer tumors and 179 ductal carcinoma i

257 006-2012) were used to identify females with invasive breast cancer undergoing planned mastectomy.

258 informed consent, 531 women with unilateral invasive breast cancer underwent dynamic contrast-enhanc

259 The estimated OR for invasive breast cancer was 2.26 (95%CI, 1.90 to 2.69; P

260 g a diagnosis of ADH, the cumulative risk of invasive breast cancer was 2.6 (95% CI, 2.0-3.4) times h

261 tely 15 years of follow-up, the incidence of invasive breast cancer was 5.7%, and the incidence of co

262 Oncogenic transformation in invasive breast cancer was associated with an increase i

263 Invasive breast cancer was associated with PM2.5 only in

264 elevated risk for estrogen receptor-positive invasive breast cancer was associated with solvent expos

265 h whole-breast irradiation in stage I and II invasive breast cancer was considered for endorsement.

266 The gene expression signature in invasive breast cancer was consistent with WISP1 as a pa

267 Risk for invasive breast cancer was higher for raloxifene than ta

268 situ was higher (P = .019) while the rate of invasive breast cancer was lower (P < .001) for FFDM com

269 Overall the risk of invasive breast cancer was not associated with lifetime

270 ctors (and controlled for age), the PAR% for invasive breast cancers was 70.0% (95% confidence interv

271 >/=20 ng/mL), the adjusted ORs (95% CIs) for invasive breast cancer were 6.1 (2.4, 15.1) for women wi

272 From 2005 to 2018, 1,815 patients with invasive breast cancer were enrolled in a lymphedema scr

273 Multivariable HRs (95% CIs) for primary invasive breast cancer were estimated with the use of Co

274 A total of 39,888 patients with invasive breast cancer were included, 7793 of whom were

275 Patients with mammography-detected invasive breast cancer were more often treated with lump

276 Women with operable HER2-positive invasive breast cancer were randomly assigned (1:1) with

277 stage hormone (oestrogen) receptor-positive invasive breast cancer were randomly assigned to exemest

278 rs; median age, 59 years) with nonmetastatic invasive breast cancer were recruited and followed for u

279 men younger than 70 years with nonmetastatic invasive breast cancer were recruited from Columbia Univ

280 Women with a diagnosis of incident invasive breast cancer were typically consented and enro

281 f 11.5 y (IQR: 10.1-12.3 y), 10,197 incident invasive breast cancers were diagnosed [3479 estrogen an

282 During follow-up (mean = 6.4 years), 1,843 invasive breast cancers were diagnosed.

283 mean follow-up of 6.3 y, 20 incident primary invasive breast cancers were observed.

284 of 13 years of follow-up through 2010; 3388 invasive breast cancers were observed.

285 Methods: Twenty-eight women with 29 primary invasive breast cancers were prospectively enrolled in a

286 Cyclin E is altered in nearly a third of invasive breast cancers where it is a powerful independe

287 ed and overexpressed in approximately 20% of invasive breast cancers where it is associated with meta

288 ere to study the progression from in situ to invasive breast cancer, which revealed that ductal carci

289 jor cancer centers with a first diagnosis of invasive breast cancer who identified themselves and all

290 593 consecutive patients with biopsy-proven invasive breast cancer who underwent breast MR imaging i

291 nts ages 29 to 85 years with stages I to III invasive breast cancer who underwent breast-conserving t

292 tients with ER-positive, lymph node-negative invasive breast cancer who underwent genomic testing fro

293 oved study was performed in 62 patients with invasive breast cancer who underwent multiagent NACT wit

294 ke in a cohort of 22,890 women with incident invasive breast cancer who were residents of Wisconsin,

295 patients with histopathologically confirmed invasive breast cancer who were undergoing NST were incl

296 mean age, 55 years; range, 23-83 years) with invasive breast cancers who had undergone MR imaging wer

297 We identified 509 patients with invasive breast cancer with a positive SLN who underwent

298 ic breast carcinoma is an aggressive form of invasive breast cancer with histological evidence of epi

299 Incident DCIS and invasive breast cancer within 1 year after mammography,

300 Similar to women with invasive breast cancer, women with CIS who are naturally