ライフサイエンスコーパス: DCIS

1 DCIS is considered a precursor to invasive ductal carcin

2 DCIS-like lesions developed throughout the mammary ducts

3 in 66 of the 72 ADH cases and in 117 of 118 DCIS cases.

4 Similarly, of 14 DCISs, all were detected by MRI, whereas mammography and

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

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

7 noma in situ [DCIS] with microinvasion and a DCIS with < 10-mm invasive areas).

8 7 patients died of breast cancer following a DCIS diagnosis (mean follow-up, 7.5 [range, 0-23.9] year

9 ors for death from breast cancer following a DCIS diagnosis include age at diagnosis and black ethnic

10 90% of units had a DCIS detection frequency within the range of 1.00 to 2.2

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 The more aggressive DCIS-C1 (highly proliferative, basal-like, or ERBB2(+))

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

16 Although DCIS has minimal mortality, recurrence rates after breas

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

18 (95% CI, 3%-6%) were underinterpreted; among DCIS cases (2097 interpretations), 84% (95% CI, 82%-86%)

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

20 compared with nonunderestimation, in ADH and DCIS respectively.

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

22 to identify two DCIS subgroups (DCIS-C1 and DCIS-C2) based on their tumor-intrinsic subtypes, prolif

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

24 veloped ductal intraepithelial neoplasia and DCIS, and progressed to invasive carcinoma, suggesting t

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

26 ection rates of invasive cancers, as well as DCIS.

27 n experience a second primary breast cancer (DCIS or invasive), and some ultimately die of breast can

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

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

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

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

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

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

34 48.3% [including DCIS] and 38.6% [excluding DCIS]).

35 24.4% [including DCIS] and 14.7% [excluding DCIS]).

36 7% (11 of 37); the sensitivity for extensive DCIS components was 91.7% (55 of 60) versus 41.7% (25 of

37 , HER2 and HER3 signaling pathways and fewer DCIS myoepithelial progenitor cells in vivo.

38 ammography and ultrasound each detected five DCISs (35.7%).

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

40 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

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

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

43 detection rate for invasive cancers and for DCIS was assessed.

44 arcinoma and lower levels of concordance for DCIS and atypia.

45 Data for DCIS diagnoses were obtained for women aged 50-64 years

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

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

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

49 2009 who had not undergone radiotherapy for DCIS and experienced a subsequent breast cancer or DCIS

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

51 had not previously received radiotherapy for DCIS.

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

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

54 ficance of early detection and treatment for DCIS remains unclear.

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

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

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

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

59 y stem cells and cancer stem-like cells from DCIS tumors revealed that miR-140 is significantly downr

60 stimate the hazard ratio (HR) for death from DCIS by age at diagnosis, clinical features, ethnicity,

61 5 per thousand): 419 diagnoses of high-grade DCIS (detection rate, 0.57 per thousand), 388 diagnoses

62 and methylome analysis of 30 pure high-grade DCIS (HG-DCIS) and 10 normal breast epithelial samples.

63 -0.12; r = 0.89; P < .001) and of high-grade DCIS (range, 0.03-0.11; r = 0.88; P < .001).

64 0 women screened) and highest for high-grade DCIS (range, 0.53[271 of 508 817 patients] to 0.59 [237

65 % (22 of 63); the sensitivity for high-grade DCIS components was 91.8% (45 of 49) versus 36.7% (18 of

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

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

68 Of note, the detection rate for high-grade DCIS showed a significant increase with age (odds ratio,

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

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

71 azard ratios of intermediate- and high-grade DCIS were significantly different (low grade: hazard rat

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

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

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

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

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

77 r smaller (n = 561); or cohort 2: high-grade DCIS, tumor size 1 cm or smaller (n = 104).

78 er than that for intermediate- or high-grade DCIS.

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

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

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

82 cancer detection rate of intermediate-grade DCIS (range, 0.02-0.12; r = 0.89; P < .001) and of high-

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

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

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

86 5194 study (cohort 1: low/intermediate-grade DCIS, </= 2.5 cm; cohort 2: high-grade DCIS, </= 1 cm) w

87 igned): cohort 1: low- or intermediate-grade DCIS, tumor size 2.5 cm or smaller (n = 561); or cohort

88 an increase in high- and intermediate-grade DCIS, which are precursor lesions that carry a higher ri

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

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

91 with the cancer detection rate of low-grade DCIS (range, 0.004-0.05; r = 0.49; P = .052), and it sho

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

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

94 ses) because of three nonenhancing low-grade DCIS cases; in turn, MR imaging depicted additional inva

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

96 t of performing breast surgery for low-grade DCIS was lower than that for intermediate- or high-grade

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

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

99 For low-grade DCIS, the weighted 10-year breast cancer-specific surviv

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

101 essive invasive breast cancer than low-grade DCIS.

102 surgery and nonsurgery groups for low-grade DCIS.

103 surveillance for the management of low-grade DCIS.

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

105 lome analysis of 30 pure high-grade DCIS (HG-DCIS) and 10 normal breast epithelial samples.

106 We conclude that most HG-DCIS lesions, in spite of representing a preinvasive sta

107 Sixty-two percent of HG-DCIS cases displayed mutations affecting cancer driver g

108 mary ducts with full representation of human DCIS histologic patterns.

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

110 ceptor 2 (ErbB2) overexpression is common in DCIS, as is disruption of the retinoblastoma tumor suppr

111 in normal breast but is highly expressed in DCIS lesions.

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

113 we observed upregulation of lncRNA HOTAIR in DCIS-C1 lesions and hypermethylation of HOXA5 and SOX ge

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

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

116 HER2/neu is frequently overexpressed in DCIS but is less common in IBC, thereby suggesting addit

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

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

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

120 2010 (overdiagnosis rate of 48.3% [including DCIS] and 38.6% [excluding DCIS]).

121 2010 (overdiagnosis rate of 24.4% [including DCIS] and 14.7% [excluding DCIS]).

122 like subpopulations in a model of basal-like DCIS and identify subpopulations of CD49f+/CD24- stem-li

123 ative strategies in patients with basal-like DCIS.

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

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

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

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

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

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

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

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

132 clinical indicator of the aggressiveness of DCIS.

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

134 Of 57,222 cases of DCIS identified in this study, 1169 cases (2.0%) were ma

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

136 ween 1988 and 2011, 57,222 eligible cases of DCIS with known nuclear grade and surgery status were id

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

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

139 pectively reviewed a prospective database of DCIS patients undergoing breast-conserving surgery from

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

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

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

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

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

145 l study of women who received a diagnosis of DCIS from 1988 to 2011 in the Surveillance, Epidemiology

146 h DCIS, the mean (range) age at diagnosis of DCIS was 53.8 (15-69) years and the mean (range) duratio

147 after biopsy in 72 cases, and a diagnosis of DCIS was obtained in 118 cases.

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

149 aintenance of BCIC, facilitates formation of DCIS, a necessary step before development of invasive di

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

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

152 %; 51 of 139) (P < .0001); more than half of DCIS components (51.1%; 71 of 139) were detected only wi

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

154 of similar age without a personal history of DCIS.

155 al role in the initiation and maintenance of DCIS and that reduction of AIB1 causes loss of BCIC, los

156 e conservative approach to the management of DCIS without surgical intervention or radiation therapy

157 care treatment options in the management of DCIS.

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

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

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

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

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

163 cular events that promote the progression of DCIS to invasive disease.

164 roles for semaphorin 7a in the promotion of DCIS growth, motility and invasion as well as lymphangio

165 An IBE was defined as local recurrence of DCIS or invasive carcinoma in the treated breast.

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

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

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

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

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

171 identification of alphavbeta6 in a subset of DCIS presents a unique way to stratify patients with DCI

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

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

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

175 tandard of care for the initial treatment of DCIS.

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

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

178 ithelial cell p63 and calponin expression on DCIS progression to invasive disease.

179 ared with positive margins defined as ink on DCIS.

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

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

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

183 nd experienced a subsequent breast cancer or DCIS diagnosis.

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

185 s absence of any residual invasive cancer or DCIS.

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

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

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

189 opausal women with hormone-receptor-positive DCIS.

190 h locally excised, hormone-receptor-positive DCIS.

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

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

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

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

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

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

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

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

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

200 s obtained from 16 women diagnosed with pure DCIS, a similar loss in myoepithelial cell markers was o

201 oint was all recurrence, including recurrent DCIS and new contralateral tumours.

202 We found that SFN treatment could reprogram DCIS stem-like cells as evidenced by significant changes

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

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

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

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

207 r the formation of ductal carcinoma in situ (DCIS) and its progression to invasive breast carcinoma h

208 tion of women with ductal carcinoma in situ (DCIS) and long follow-up, the relationship between margi

209 ion of early-stage ductal carcinoma in situ (DCIS) and report that compromised myoepithelial cell dif

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

211 erplasia (ADH) and ductal carcinoma in situ (DCIS) at magnetic resonance (MR) imaging-guided vacuum-a

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

213 nd that basal-like ductal carcinoma in situ (DCIS) contains cancer stem-like cells.

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

215 , P < .0001), have ductal carcinoma in situ (DCIS) in the index breast (31% [27 of 86] vs 19% [164 of

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

217 Ductal carcinoma in situ (DCIS) is a heterogeneous group of non-invasive lesions o

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

219 Ductal carcinoma in situ (DCIS) is a noninvasive precursor lesion to invasive brea

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

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

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

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

224 the prevalence of ductal carcinoma in situ (DCIS) of the breast has increased substantially followin

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

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

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

228 he transition from ductal carcinoma in situ (DCIS) to invasive breast cancer (IBC) is a crucial step

229 the progression of ductal carcinoma in situ (DCIS) to invasive breast cancer remain poorly understood

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 breast cancer, 73 ductal carcinoma in situ (DCIS), 72 with atypical hyperplasia (atypia), and 72 ben

233 risk patients with ductal carcinoma in situ (DCIS), a breast cancer diagnosis found frequently in mam

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

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

236 Women with ductal carcinoma in situ (DCIS), or stage 0 breast cancer, often experience a seco

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

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

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

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

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

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

243 -receptor-positive ductal carcinoma in situ (DCIS).

244 en demonstrated in ductal carcinoma in situ (DCIS).

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

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

247 surgery (BCS) for 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 mmography alone (a ductal carcinoma in situ [DCIS] with microinvasion and a DCIS with < 10-mm invasiv

250 itive (23 cases of ductal carcinoma in situ [DCIS], 43 invasive cancers) and 287 (81.3%) were false-p

251 still have no understanding on why only some DCIS lesions evolve to invasive cancer whereas others ap

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

253 a allowed us to identify two DCIS subgroups (DCIS-C1 and DCIS-C2) based on their tumor-intrinsic subt

254 Matching included age and surrogate DCIS subtypes.

255 erved in the mouse myoepithelium surrounding DCIS-involved ducts.

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 The DCIS subsequent screening rate was higher for DR photon

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 However, no strategy incorporating the DCIS Score was cost effective.

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

263 ocol specifications included excision of the DCIS tumor with a minimum negative margin width of at le

264 Conclusion Strategies using the DCIS Score lowered the proportion of women undergoing RT

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

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

267 Total DCIS detection rates increase with age, mostly because o

268 The cancer detection rate of total DCIS with grading varied among screening units (range, 0

269 Likewise, the total DCIS cancer detection rate was separated into rates for

270 s of RNA-seq data allowed us to identify two DCIS subgroups (DCIS-C1 and DCIS-C2) based on their tumo

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

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

273 n orthotopic xenograft assays, compared with DCIS-like lesions developing from RB-proficient cells.

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

275 Of women identified with DCIS, 26,580 (74.7%) underwent BCS while 9011 (25.3%) un

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 of health-related QoL in 1,604 patients with DCIS diagnosed in 1997 to 2006 with up to four follow-up

283 sents a unique way to stratify patients with DCIS into those who may or may not progress to more seri

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

285 For patients with DCIS selected for favorable clinical and pathologic char

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

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

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

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

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

291 In this good-risk subset of patients with DCIS, with a median follow-up of 7 years, the LF rate wa

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

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

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

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

296 benefit of axillary evaluation in women with DCIS is needed.

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

298 axillary lymph node evaluation in women with DCIS undergoing BCS and uncertainty regarding its use wi

299 d in the Perspective database for women with DCIS who underwent breast-conserving surgery (BCS) or ma

300 clinical trial was performed for women with DCIS who were selected for low-risk clinical and patholo

301 Among the 108 196 women with DCIS, the mean (range) age at diagnosis of DCIS was 53.8

302 evaluation is often performed in women with DCIS.

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