ライフサイエンスコーパス: DCIS

1 DCIS and IBC were distinguished on the basis of cell sig

2 DCIS is a nonobligatory precursor for invasive carcinoma

3 DCIS is considered a precursor to invasive ductal carcin

4 from 1952 invasive breast cancer samples, 10 DCIS, 9 benign samples and 144 tumour adjacent normal br

5 OS was observed for tumors containing >=25% DCIS component.

6 Results A total of 74 DCIS calcifications and 148 benign calcifications were i

7 QoL after a DCIS diagnosis was generally comparable to that of women

8 In the first 5 years after a DCIS diagnosis, mental QoL was significantly higher amon

9 90% of units had a DCIS detection frequency within the range of 1.00 to 2.2

10 Thus, the presence of a DCIS component in patients with IDC is associated with f

11 These findings suggest that a DCIS RT boost to the tumor bed could be considered to pr

12 11 and for 757 women in SEER-Medicare with a DCIS diagnosis between 1991 and 2009 who had not undergo

13 ially in the first 5 years, while additional DCIS is an indication for longer follow-up, emphasizing

14 t tissue, atypical ductal hyperplasia (ADH), DCIS and invasive breast cancer.

15 issue persistence, improves efficacy against DCIS lesions in vivo, and requires 5-fold less CPX to ac

16 that it could be used to identify aggressive DCIS and predict the response to targeted therapy.

17 ficant benefit in decreasing IBTR across all DCIS age groups, similar to that seen in patients with i

18 More than half of all DCIS lesions were high grade (52.6%; 393 of 747).

19 th physical and mental measures of QoL among DCIS survivors at fewer than 2 years after diagnosis wer

20 sion The rates of underestimation in ADH and DCIS diagnosed at MR imaging-guided vacuum-assisted biop

21 compared with nonunderestimation, in ADH and DCIS respectively.

22 The ADH and DCIS underestimation rates were 25.8% (17 of 66) and 23.

23 clustering accounted for matching benign and DCIS groups.

24 e related to both invasive breast cancer and DCIS within certain geographic regions and PM component

25 For detection of invasive cancer and DCIS, sensitivity was 95.7% (95% CI, 79.0%-99.2%) with a

26 In clinical samples, IDC and DCIS with microinvasion expressed higher levels of phosp

27 ials to reduce the risk of both invasive and DCIS recurrence, but neither affects survival.

28 Importantly, we identify invasive-only and DCIS-specific DNA methylation alterations that could pot

29 y vs BCS at a second breast event defined as DCIS recurrence or new invasive cancer.

30 dentified distinct lipid composition between DCIS and IBC and across molecular subtypes of breast can

31 The MNK1/2 inhibitor SEL201 blocked DCIS progression to invasive disease in vivo.

32 ment of tools such as the Oncotype DX Breast DCIS Score, a gene expression-based assay with the poten

33 he four molecular subtypes of breast cancer, DCIS, and normal tissue, and add to the understanding of

34 asive breast cancer, and all breast cancers (DCIS plus invasive) for U.S. women undergoing screening

35 Surgical-pathologic assessment demonstrated DCIS components in 139 of the 593 women (23.4%).

36 K1 (caMNK1)-expressing human MCF-10A-derived DCIS cell lines, which were orthotopically injected into

37 The association between screen-detected DCIS and subsequent invasive interval cancers suggests t

38 cant negative association of screen-detected DCIS cases with the rate of invasive interval cancers (P

39 ive MR imaging in women with newly diagnosed DCIS show promise for association with breast cancer rec

40 Purpose The Oncotype DX DCIS Score short form (DCIS Score) estimates the risk of

41 48.3% [including DCIS] and 38.6% [excluding DCIS]).

42 24.4% [including DCIS] and 14.7% [excluding DCIS]).

43 7% (11 of 37); the sensitivity for extensive DCIS components was 91.7% (55 of 60) versus 41.7% (25 of

44 Additionally, extracellular DCIS miRNAs, such as those found in exosomes, may promot

45 e to obligate overdiagnosis rates (0.15% for DCIS and less than 0.1% for invasive breast cancer and a

46 ikely in mass (n = 20 for ADH and n = 20 for DCIS) than in non-mass (n = 46 for ADH and n = 97 for DC

47 the United States are estimated to be 9% for DCIS and approximately 7% for both invasive breast cance

48 n in non-mass (n = 46 for ADH and n = 97 for DCIS), compared with nonunderestimation, in ADH and DCIS

49 cer with or without DCIS in 17 women and for DCIS alone in another 6.

50 the purpose of miRNA therapy development for DCIS.

51 cific morphologic and kinetic parameters for DCIS were identified.

52 -guided lesion bracketing were performed for DCIS components visible at MR imaging alone.

53 of DCIS, and discuss future perspectives for DCIS biomarker discovery.

54 gional practice patterns of radiotherapy for DCIS affect the use of mastectomy in these patients.

55 2009 who had not undergone radiotherapy for DCIS and experienced a subsequent breast cancer or DCIS

56 who do not receive initial radiotherapy for DCIS are candidates for subsequent BCS if they experienc

57 had not previously received radiotherapy for DCIS.

58 obligate (or type 1) overdiagnosis rates for DCIS, invasive breast cancer, and all breast cancers (DC

59 ased study, the patient prognostic score for DCIS is associated with the magnitude of improvement in

60 Areas with more radiotherapy use for DCIS had increased use of mastectomy at the time of a se

61 haracterized by greater radiotherapy use for DCIS increased the likelihood of receiving mastectomy vs

62 s to 30%, 21%, and 22.5% at age 80 years for DCIS, invasive breast cancer, and all breast cancers, re

63 rpose The Oncotype DX DCIS Score short form (DCIS Score) estimates the risk of an ipsilateral breast

64 1 and NODAL versus low-grade (invasion-free) DCIS.

65 5 per thousand): 419 diagnoses of high-grade DCIS (detection rate, 0.57 per thousand), 388 diagnoses

66 0 women screened) and highest for high-grade DCIS (range, 0.53[271 of 508 817 patients] to 0.59 [237

67 % (22 of 63); the sensitivity for high-grade DCIS components was 91.8% (45 of 49) versus 36.7% (18 of

68 he molecular level, low-grade and high-grade DCIS have different molecular alterations, and the intri

69 sistently high detection rates of high-grade DCIS in two consecutive subsequent screening rounds comp

70 Conversely, the detection rate of high-grade DCIS remained at the high level found in the prevalence

71 with a clinical diagnosis of non-high-grade DCIS that would preclude active surveillance.

72 trials randomizing women with non-high-grade DCIS to active surveillance, defined as imaging surveill

73 with a clinical diagnosis of non-high-grade DCIS who underwent definitive surgical treatment.

74 t proportion of patients with non-high-grade DCIS will harbor invasive carcinoma.

75 grade DCIS, </= 2.5 cm; cohort 2: high-grade DCIS, </= 1 cm) with each of five strategies: (1) no tes

76 with a clinical diagnosis of non-high-grade DCIS, 8320 (22.2%) had invasive carcinoma based on final

77 DCIS, test for intermediate- and high-grade DCIS, RT for intermediate- or high-risk scores; (4) test

78 erentiating between low-grade and high-grade DCIS.

79 ousand), 388 diagnoses of intermediate-grade DCIS (detection rate, 0.53 per thousand), and 182 diagno

80 he increase was lower for intermediate-grade DCIS (odds ratio, 1.11; P = .016) and not significant fo

81 27); the sensitivity for intermediate-grade DCIS components was 84.1% (53 of 63) versus 34.9% (22 of

82 DCIS and, less markedly, intermediate-grade DCIS decreased in subsequent rounds.

83 ion of detection rates of intermediate-grade DCIS was less pronounced (OR = 0.79, P = .006 and OR = 0

84 5194 study (cohort 1: low/intermediate-grade DCIS, </= 2.5 cm; cohort 2: high-grade DCIS, </= 1 cm) w

85 er thousand), and 182 diagnoses of low-grade DCIS (detection rate, 0.25 per thousand).

86 P = .016) and not significant for low-grade DCIS (P = .10).

87 er detection rates were lowest for low-grade DCIS (range, 0.11 [58 of 508 817 patients] to 0.25 [178

88 alence round; conversely, rates of low-grade DCIS and, less markedly, intermediate-grade DCIS decreas

89 ng versus conventional imaging for low-grade DCIS components was 74.0% (20 of 27) versus 40.7% (11 of

90 Detection rates for low-grade DCIS were significantly lower in the first (odds ratio [

91 T only for cohort 2; (3) no RT for low-grade DCIS, test for intermediate- and high-grade DCIS, RT for

92 tinguish high-, intermediate-, and low-grade DCIS.

93 There were 989 graded DCIS diagnoses among 733 905 women (detection rate, 1.35

94 IDC + DCIS could be a useful prognostic factor for patients wi

95 ng ductal carcinoma in situ component (IDC + DCIS).

96 significantly superior OS observed for IDC + DCIS was limited to patients with invasive tumor size <

97 We also found IDC + DCIS to be associated with lower T/N stage, low/intermed

98 nts diagnosed with either IDC alone or IDC + DCIS.

99 bit different biological behavior than IDC + DCIS, but whether this translates to a difference in out

100 We found that IDC + DCIS was associated with significantly better overall su

101 DK4/6 inhibitors and its loss could identify DCIS lesions that are likely to progress into invasive b

102 e activity of typical myoepithelial cells in DCIS was lowered.

103 ial cells is also significantly decreased in DCIS, which may be associated with invasive progression.

104 at exist in invasive carcinoma also exist in DCIS with prognostic implications.

105 Most of these genes were highly expressed in DCIS samples with IBC, including PLAU (P = 0.002), COL1A

106 view the miRNAs that have been identified in DCIS and how they may contribute to the progression to i

107 we review the miRNA signatures identified in DCIS, describe how these signatures may be used to predi

108 in as the standard for an adequate margin in DCIS treated with WBRT is associated with low rates of I

109 miRNAs in DCIS have been shown to influence hormone signaling, cel

110 ic and transcriptomic changes are present in DCIS before the emergence of invasive disease, indicatin

111 of this study was to assess long-term QoL in DCIS survivors in relation to age at diagnosis, time sin

112 reoperative MRI to be clinically relevant in DCIS staging.

113 er pathway(s) that play an important role in DCIS progression.

114 2010 (overdiagnosis rate of 48.3% [including DCIS] and 38.6% [excluding DCIS]).

115 2010 (overdiagnosis rate of 24.4% [including DCIS] and 14.7% [excluding DCIS]).

116 f MNK1 repressed NODAL expression, inhibited DCIS to IDC conversion, and decreased tumor relapse and

117 ancer and which could remain as pre-invasive DCIS.

118 were matched with 12 patients with a limited DCIS component and IBC, representing lesions with a high

119 ns were performed with digital mammography), DCIS detection rates were determined for 5-year age grou

120 sus conventional imaging for small, marginal DCIS components was 56.8% (21 of 37) versus 29.7% (11 of

121 X11 confers distinct features to ER-negative DCIS.com breast cancer cells, leading to populations enr

122 Detection of triple-negative DCIS (TN-DCIS) is challenging, therefore strategies to s

123 making a precise localization of nonpalpable DCIS lesions even more important.

124 More than 50% of DCIS lesions are benign and will remain indolent, never

125 Obligate overdiagnosis occurs in 9% of DCIS and approximately 7% of both invasive breast cancer

126 w irrespective of the presence or absence of DCIS components.

127 may be used to predict the aggressiveness of DCIS, and discuss future perspectives for DCIS biomarker

128 clinical indicator of the aggressiveness of DCIS.

129 Mammograms from all cases of DCIS (n = 404) were reviewed for calcifications that wer

130 at 1 in every 3 invasive tumors and cases of DCIS diagnosed in women offered screening represent over

131 nd that 711 invasive tumors and 180 cases of DCIS were overdiagnosed in 2010 (overdiagnosis rate of 4

132 ts, for every three screen-detected cases of DCIS, there was one fewer invasive interval cancer in th

133 Grade-related changes of DCIS detection are suggestive of distinct dynamics of le

134 sion Breast MR imaging improves depiction of DCIS components of invasive breast cancers before surger

135 stimate the association between detection of DCIS at screening and invasive interval cancers subseque

136 asive carcinoma vs those with a diagnosis of DCIS based on final surgical pathologic findings.

137 d for 2679 women in SEER with a diagnosis of DCIS between 1990 and 2011 and for 757 women in SEER-Med

138 nsitivity of MR imaging for the diagnosis of DCIS components pre-operatively (84.9%; 118 of 139) was

139 The distribution of DCIS grades was stable during the 20-year screening peri

140 nished during follow-up, while the effect of DCIS adjacent to invasive tumor seemed to remain stable.

141 nostic biomarkers, and molecular features of DCIS.

142 The average frequency of DCIS detected at screening was 1.60 per 1000 women scree

143 g increased with increasing nuclear grade of DCIS components, as follows: The sensitivity of MR imagi

144 %; 51 of 139) (P < .0001); more than half of DCIS components (51.1%; 71 of 139) were detected only wi

145 cinoma (IDC); however, approximately half of DCIS may progress to IDC, if left untreated.

146 of similar age without a personal history of DCIS.

147 t of screening mammography, the incidence of DCIS has significantly increased.

148 e annual increase in the long-axis length of DCIS calcifications was greater than that of benign brea

149 care treatment options in the management of DCIS.

150 dth of 2 mm or greater for the management of DCIS; however, controversy regarding re-excision remains

151 ine cross-talk-based biological mechanism of DCIS progressing to invasive cancer.

152 In two mouse xenograft models of DCIS, we found that RNAi-mediated silencing of NEMO incr

153 bution of 0.15% to obligate overdiagnosis of DCIS and a contribution of less than 0.1% to the obligat

154 t the relative effect of age and presence of DCIS seemed stable over time.

155 is required for the invasive progression of DCIS and other early-stage tumors.

156 nts required for the invasive progression of DCIS occur at the preinvasive stage, and these events in

157 Purpose To quantify the growth rates of DCIS and benign breast disease that manifest as mammogra

158 iated with the risk of LCIS than the risk of DCIS (P for heterogeneity = 0.04).

159 nopause was associated with a higher risk of DCIS but lower risks of LCIS and invasive ductal carcino

160 g increased with increasing relative size of DCIS components, as follows: The sensitivity of MR imagi

161 BRIM identified subpopulations of DCIS lesions with ratiometric properties resembling eith

162 the existence of distinct subpopulations of DCIS lesions, which will likely have utility in breast c

163 electing patients for active surveillance of DCIS, factors other than tumor biology associated with i

164 tent to which the diagnosis and treatment of DCIS could prevent the occurrence of invasive breast can

165 ers suggests that detection and treatment of DCIS is worthwhile in prevention of future invasive dise

166 once the gold standard for the treatment of DCIS; however, breast-conserving surgery (BCS) has been

167 Detection rate for types of DCIS combined increased significantly across age groups

168 ared with positive margins defined as ink on DCIS.

169 Gene expression profiling was performed on DCIS cells to identify transcriptional differences betwe

170 evidence regarding the role of the Oncotype DCIS Score in estimating the risk of ipsilateral local r

171 The Oncotype DCIS Score is a commercially available multigene assay t

172 er parameters were associated with of ADH or DCIS upgrade at surgery.

173 low likelihood that a diagnosis of atypia or DCIS would be verified by a reference consensus diagnosi

174 nd experienced a subsequent breast cancer or DCIS diagnosis.

175 rradiation of node-negative breast cancer or DCIS did not result in more breast induration compared w

176 s with nonpalpable invasive breast cancer or DCIS visible on ultrasound were enrolled in this randomi

177 s absence of any residual invasive cancer or DCIS.

178 ng women with histologically verified IBC or DCIS having wire-guided BCS performed between January 1,

179 fter wire-guided BCS in patients with IBC or DCIS.

180 (DCIS and invasive), invasive stage only or DCIS stage only of TN-DCIS progression.

181 Our established orthotopic DCIS rat model was used to evaluate efficacy.

182 rwent surgery per study protocol, persistent DCIS remained in 50 patients (85%), invasive cancer was

183 c changes in estrogen receptor (ER)-positive DCIS.

184 nopausal patients diagnosed with ER-positive DCIS without invasion.

185 ort of postmenopausal women with ER-positive DCIS, preoperative letrozole resulted in significant ima

186 opausal women with hormone-receptor-positive DCIS, which may be be more appropriate for some women wi

187 opausal women with hormone-receptor-positive DCIS.

188 60); the sensitivity for large, predominant DCIS components was 100.0% (42 of 42) versus 35.7% (15 o

189 Treatment intensity for primary DCIS (high, medium, low), as defined by separating healt

190 However, the factors that promote DCIS invasion remain poorly understood.

191 be a MNK1/NODAL signaling axis that promotes DCIS progression to IDC.

192 Women with biopsy-proven DCIS corresponding to a unifocal microcalcification clus

193 All patients had newly diagnosed pure DCIS (no microinvasion), underwent breast-conserving sur

194 Twelve patients with extensive pure DCIS were included as a representation of indolent lesio

195 registry provided data for 1970 graded pure DCIS cases from 16 screening regions of the prevalence r

196 howed a higher expression in cases with pure DCIS (P = 0.015 and P = 0.028, respectively).

197 situ (DCIS), we compared patients with pure DCIS and patients with DCIS and synchronous invasive bre

198 Patients with pure DCIS have a different gene expression pattern as compare

199 Of these 37 women, 12 (32.4%) had residual DCIS only, 20 (54.1%) had minimal residual tumor (<5 mm)

200 ected in six patients (10%), and no residual DCIS or invasive cancer was seen in nine patients (15%).

201 Prospective studies of women with "low-risk" DCIS treated with BCS alone have successfully identified

202 erinterpreted) and ductal carcinoma in situ (DCIS) (18.5% overinterpreted and 11.8% underinterpreted)

203 1) and presence of ductal carcinoma in situ (DCIS) (HR, 2.15; 95% CI, 1.36-3.38; P = .001) were assoc

204 Ductal carcinoma in situ (DCIS) accounts for 20% of all newly diagnosed breast can

205 st cancer (IBC) or ductal carcinoma in situ (DCIS) and to examine whether the risk of reoperation is

206 nd perturbation in ductal carcinoma in situ (DCIS) are poorly understood.

207 ocrine therapy for ductal carcinoma in situ (DCIS) as a potential alternative to surgery has been und

208 5 invasive and 623 ductal carcinoma in situ (DCIS) cases were identified.

209 identification of ductal carcinoma in situ (DCIS) components of biopsy-proven invasive breast cancer

210 d overtreatment of ductal carcinoma in situ (DCIS) detected by mammography has led to the development

211 Ductal carcinoma in situ (DCIS) encompasses a highly heterogeneous group of lesion

212 Testing of ductal carcinoma in situ (DCIS) for ER is recommended to determine potential benef

213 in microdissected ductal carcinoma in situ (DCIS) from patients with luminal and HER2-positive breas

214 e recalls yielding ductal carcinoma in situ (DCIS) increased from 0.3 per 1000 screening examinations

215 cells derived from ductal carcinoma in situ (DCIS) increased secretion of the proinflammatory cytokin

216 n and treatment of ductal carcinoma in situ (DCIS) is a matter of controversy.

217 Ductal carcinoma in situ (DCIS) is defined as a proliferation of neoplastic cells

218 east RT (WBRT) for ductal carcinoma in situ (DCIS) is largely extrapolated from invasive cancer data,

219 ve status in human ductal carcinoma in situ (DCIS) lesions and invasive breast cancers as well as wit

220 Background Most ductal carcinoma in situ (DCIS) lesions are first detected on screening mammograms

221 cer tumors and 179 ductal carcinoma in situ (DCIS) lesions were overdiagnosed in 2010 (overdiagnosis

222 t of patients with ductal carcinoma in situ (DCIS) of the breast develop ipsilateral invasive breast

223 Historically, ductal carcinoma in situ (DCIS) of the breast has been managed aggressively with s

224 Ductal carcinoma in situ (DCIS) of the breast represents a disease process that co

225 a potent driver of ductal carcinoma in situ (DCIS) progression.

226 re associated with ductal carcinoma in situ (DCIS) recurrence risk after definitive treatment.

227 Ductal Carcinoma In Situ (DCIS) represents a significant fraction (~20-25%) of all

228 nvasive cancer and ductal carcinoma in situ (DCIS) to define a positive reference standard.

229 elatively indolent ductal carcinoma in situ (DCIS) to invasive ductal carcinoma (IDC) are not well un

230 e margin width for ductal carcinoma in situ (DCIS) treated with breast-conserving surgery and whole-b

231 ) in patients with ductal carcinoma in situ (DCIS) treated with breast-conserving surgery without adj

232 rate in women with ductal carcinoma in situ (DCIS) undergoing breast-conserving surgery.

233 e breast cancer or ductal carcinoma in situ (DCIS) were randomly assigned to radiotherapy at a dose o

234 Ductal carcinoma in situ (DCIS), although often diagnosed as breast cancer, is a p

235 east cancer (IBC), ductal carcinoma in situ (DCIS), and adjacent benign tissue (ABT), and metabolomic

236 detection rates of ductal carcinoma in situ (DCIS), classified according to nuclear grade, between th

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

238 ggressive forms of ductal carcinoma in situ (DCIS), they cannot be identified with conventional histo

239 the progression of ductal carcinoma in situ (DCIS), we compared patients with pure DCIS and patients

240 invasive cancer or ductal carcinoma in situ (DCIS).

241 (UDH) or malignant ductal carcinoma in situ (DCIS).

242 surgery (BCS) for ductal carcinoma in situ (DCIS).

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

244 ons, most commonly ductal carcinoma in situ (DCIS).

245 among survivors of ductal carcinoma in situ (DCIS).

246 the management of ductal carcinoma in situ (DCIS).

247 from non-invasive ductal carcinoma in situ (DCIS).

248 ctors and incident ductal carcinoma in situ (DCIS; n = 1,453) with that of risk factors and invasive

249 py as primary nonoperative treatment of some DCIS.

250 We found that SOX11+DCIS tumour cells metastasize to brain and bone at great

251 and in non-carrier controls, and in sporadic DCIS.

252 tus of gene candidates to define late-stage (DCIS and invasive), invasive stage only or DCIS stage on

253 adherin/E-cadherin, and CD74/CD59 stratified DCIS samples.

254 Matching included age and surrogate DCIS subtypes.

255 risk of future breast cancer, while testing DCIS for PgR is considered optional.

256 hormone therapy were stronger for LCIS than DCIS (P for heterogeneity = 0.03) and invasive lobular c

257 Our findings suggest that DCIS survivors, and particularly those diagnosed at a yo

258 ent concerns and evidence that suggests that DCIS can be stratified according to risk of recurrence o

259 hat these changes are already present at the DCIS stage.

260 power analysis was conducted to estimate the DCIS sample size needed to detect the anticipated benefi

261 indicating that the malignant nature of the DCIS is defined before invasion.

262 Results No strategy using the DCIS Score was cost effective.

263 Here, we study a canine TN-DCIS progression and investigate the DNA methylation lan

264 Detection of triple-negative DCIS (TN-DCIS) is challenging, therefore strategies to study mole

265 Changes in DNA methylation during TN-DCIS progression in this canine model correspond with ge

266 nts governing progression of pre-invasive TN-DCIS to invasive TNBC are needed.

267 invasive stage only or DCIS stage only of TN-DCIS progression.

268 cancer data, but robust evidence specific to DCIS is lacking.

269 ministered drug delivery system for treating DCIS, for which no primary chemotherapy option is availa

270 reen detection rate as the outcome variable; DCIS detection frequencies were fitted first as a contin

271 enabled an era of precision medicine, where DCIS can be molecularly analyzed by tools, such as next-

272 (95% CI:1.02, 1.11), respectively] and with DCIS but not with invasive cancer.

273 r the risk of reoperation is associated with DCIS or histologic type of the IBC.

274 Calcifications associated with DCIS were larger than those associated with benign breas

275 crease the number of patients diagnosed with DCIS, making a precise localization of nonpalpable DCIS

276 Significantly more patients with DCIS (271 of 727 [37.3%]) than with IBC (454 of 3391 [13

277 ression pattern as compared to patients with DCIS and synchronous IBC.

278 ed patients with pure DCIS and patients with DCIS and synchronous invasive breast cancer (IBC).

279 he type of reoperation between patients with DCIS and those with IBC.

280 Mental measures of QoL among patients with DCIS declined at >/= 10 years after diagnosis and were s

281 tudy was performed to identify patients with DCIS diagnosed between 1988 and 2007 and treated with BC

282 r biomarkers that can stratify patients with DCIS into different prognostic groups based on the biolo

283 with matched control subjects, patients with DCIS recurrence exhibited significantly greater FTV (med

284 ns was significantly higher in patients with DCIS vs those with IBC (unadjusted odds ratio, 2.21; 95%

285 er, the risk of reoperation in patients with DCIS was 3 times higher than in those with IBC.

286 ousand four hundred ninety-one patients with DCIS who underwent breast-conserving surgery from 1996 t

287 Materials and Methods Patients with DCIS who underwent preoperative dynamic contrast materia

288 We identified 32,144 eligible patients with DCIS, 20,329 (63%) in the RT group and 11,815 (37%) in t

289 Among patients with DCIS, we examined trends in QoL over time since diagnosi

290 ts with adenocarcinoma and 246 patients with DCIS.

291 For each patient, a control subject with DCIS that did not recur was identified and matched on th

292 Results Of 415 subjects with DCIS who underwent preoperative MR imaging, 14 experienc

293 e goal of identifying a subset of women with DCIS at minimal risk of recurrence after surgical excisi

294 fer significantly between the 139 women with DCIS components (5.0% [95% CI: 2.0%, 10.1%]) compared wi

295 breast tumor recurrence (IBTR) in women with DCIS treated with vs without the RT boost after breast-c

296 n with invasive cancer and 5 of 6 women with DCIS.

297 n with invasive cancer and 2 of 6 women with DCIS.

298 ies have found enormous heterogeneity within DCIS.

299 positive for invasive cancer with or without DCIS in 17 women and for DCIS alone in another 6.

300 seline QoL to 1,055 control patients without DCIS.