ライフサイエンスコーパス: lobular

1 e risk 2.25, 95% CI 2.00-2.52), mixed ductal-lobular (2.13, 1.68-2.70), and tubular cancers (2.66, 2.

2 5,334 ductal, 836 lobular, 639 mixed ductal-lobular, 216 mucinous, and 132 tubular breast cancers we

3 ) were invasive, including 8007 ductal, 1526 lobular, 365 mixed ductal-lobular, 492 tubular, 71 medul

4 8007 ductal, 1526 lobular, 365 mixed ductal-lobular, 492 tubular, 71 medullary, and 148 mucinous can

5 During that time period, 5,334 ductal, 836 lobular, 639 mixed ductal-lobular, 216 mucinous, and 132

6 oscopy of rtn1Delta yop1Delta cells revealed lobular abnormalities in SPB structure.

7 The differential diagnosis of lobular abnormalities is based on comparisons between lo

8 y and tertiary branching, along with reduced lobular-alveolar development during pregnancy and lactat

9 Tgfbr2 in the mammary epithelium results in lobular-alveolar hyperplasia in the developing mammary g

10 SnoN elevation increased side-branching and lobular-alveolar proliferation in virgin glands, while a

11 Upon compound exposure, lobular analogues developed a variety of clearance and h

12 bnormalities is based on comparisons between lobular anatomy and lung pathology.

13 Pathologic alterations in secondary lobular anatomy visible on thin-section CT scans include

14 st cancer from a Japanese study; and (ii) 20 lobular and 24 ductal cancers from the Imperial College.

15 a clear difference in ER expression between lobular and ductal breast cancer and suggest (i) that ta

16 Invasive lobular and ductal breast tumors have distinct histologi

17 ntify genes differentially expressed between lobular and ductal tumors.

18 In women age 50 to 69 years, invasive lobular and ER-positive cancer rates declined steadily i

19 These associations were stronger for lobular and hormone-receptor-positive tumors but were ab

20 ant fibrosis were more likely to have higher lobular and portal inflammation scores (P < 0.01), peris

21 In both groups, lobular and portal inflammation scores had no associatio

22 ohepatitis (NASH), histologically defined by lobular and portal inflammation, and accompanied by mark

23 between stainable iron in portal triads and lobular and total Ishak inflammatory and fibrosis scores

24 ng 7 of 13 invasive ductal, 5 of 13 invasive lobular, and 1 of 13 metaplastic carcinomas.

25 nced MR imaging of nine tumors showed large, lobular, and intensely and heterogeneously enhancing mas

26 fects of hormone therapy on invasive ductal, lobular, and tubular cancer were generally greater for o

27 ancers included 74 (88%) ductal, eight (10%) lobular, and two (2%) mixed cancers.

28 ing of L-type Ca(2+) channels located on the lobular appendages.

29 arge glycinergic synapses at their dendritic lobular appendages.

30 capillary vessel segments that comprise each lobular area of the choriocapillaris vascular plexus.

31 Lobular area was similarly associated with risk.

32 Combining acinar count and lobular area, the c statistic was 0.68 (95% CI, 0.58 to

33 y determining number of acini per lobule and lobular area.

34 all fraction of the cancer cells invaded the lobular area.

35 (MS), testing the contribution of cerebellar lobular atrophy to both motor and cognitive performances

36 of connections between the bile duct and the lobular bile canalicular network by the canals of Hering

37 Invasive lobular breast cancer (ILBC) is the second most common h

38 ve ductal breast cancer (n = 18) or invasive lobular breast cancer (n = 6) underwent (18)F-fluciclovi

39 ve ductal breast cancer (n = 18) or invasive lobular breast cancer (n = 6) underwent (18)F-fluciclovi

40 ry effects of TAM in SUM44 and MDA-MB-134 VI lobular breast cancer cells.

41 ectomy for stage I to III invasive ductal or lobular breast cancer, ductal carcinoma in situ, or prop

42 ore accurate preclinical model of metastatic lobular breast cancer, our work offers advances supporti

43 Next, in a mouse model for invasive lobular breast cancer, the effects of TRC105 and SU5416

44 f 40; and families with a history of DGC and lobular breast cancer, with 1 diagnosis before the age o

45 icantly increased risk of gastric cancer and lobular breast cancer.

46 2002 for stage I to IIIA invasive ductal and lobular breast cancer.

47 in the 22 families whose families developed lobular breast cancer.

48 invasive ductal breast cancer, and invasive lobular breast cancer.

49 entify new markers distinguishing ductal and lobular breast cancers.

50 model of Tamoxifen (TAM)-resistant invasive lobular breast carcinoma cells that provides novel insig

51 trongly associated with the risk of invasive lobular breast carcinoma than that of invasive ductal ca

52 an female with recently diagnosed metastatic lobular breast carcinoma to skin was referred to gastroe

53 tation carrier status and a prior history of lobular breast carcinoma underwent prophylactic total ga

54 c outlet obstruction secondary to metastatic lobular breast carcinoma.

55 use (signet ring cell) gastric carcinoma and lobular breast carcinoma.

56 rom comparable areas of normal terminal duct lobular breast tissue (n = 10) were determined.

57 In 766 patients with invasive lobular cancer (ILC), outcomes were as follows: initial

58 r and 17% (eight of 47 axillae) for invasive lobular cancer (P < .01).

59 may be more effective in late than in early lobular cancer and (ii) a potential role for ERbeta agon

60 ERbeta was expressed, but in the high-grade lobular cancer ERbeta was lost and ERalpha and Ki67 expr

61 , ERalpha-positive, ERbeta-negative disease, lobular cancer expresses both ERalpha and ERbeta but wit

62 entinel lymph nodes (SLNs) from a woman with lobular cancer of the breast is frequently challenging.

63 e false-negative rate for N2 and N3 invasive lobular cancer was significantly higher than that for in

64 3 (95% CI: 1.30, 2.05); and for mixed ductal/lobular cancer, 2.51 (95% CI: 1.20, 5.24).

65 egional and distant spread including that of lobular cancer, though identification of hepatic metasta

66 About 80% of ductal cancers (IDCs) and all lobular cancers (ILCs) lost at least part of 16q.

67 ients or for those with unfavorable biology, lobular cancers, or cancers with an extensive intraducta

68 ) were in situ, including 1443 ductal and 86 lobular cancers.

69 male patients were diagnosed with periocular lobular capillary hemangioma at a median age of 39 years

70 hemangioendotheliomas (KHEs), and childhood lobular capillary hemangiomas (LCHs).

71 ary hemangiomas are more common in children, lobular capillary hemangiomas can also arise in the peri

72 tal carcinoma (IDC) (0.2-8.9 cm), 3.5 cm for lobular carcinoma (1.6-8.0 cm), and 5.7 cm for phyllodes

73 ases versus 10 of 29 (34%) cases of invasive lobular carcinoma (ILC) (P < .001) and 21 of 38 (55%) ca

74 Invasive lobular carcinoma (ILC) accounts for approximately 10% t

75 Invasive ductal carcinoma (IDC) and invasive lobular carcinoma (ILC) are the two major histological t

76 Invasive lobular carcinoma (ILC) is a histologic subtype of breas

77 Because invasive lobular carcinoma (ILC) is less conspicuous than invasiv

78 Invasive lobular carcinoma (ILC) is the second most common breast

79 Invasive lobular carcinoma (ILC) is the second most frequently oc

80 Invasive lobular carcinoma (ILC) is the second most prevalent his

81 e ductal carcinoma (IDC) or classic invasive lobular carcinoma (ILC) who were randomly assigned onto

82 invasive ductal carcinoma (IDC) and invasive lobular carcinoma (ILC).

83 ion, we orthotopically transplanted invasive lobular carcinoma (mILC) fragments into mammary glands o

84 ER-positive infiltrating lobular carcinoma differed from ER-positive infiltrating

85 east cancer risk conferred by a diagnosis of lobular carcinoma in situ (LCIS) is poorly understood.

86 red the association between risk factors and lobular carcinoma in situ (LCIS; n = 186) with that of r

87 in the atypical lobular hyperplasia (n = 2), lobular carcinoma in situ (n = 5), or radial scar (n = 3

88 Excisional findings included lobular carcinoma in situ (n=2), ductal carcinoma in sit

89 oman was found to have ductal cancer and one lobular carcinoma in situ at time of CDR.

90 two, atypical lobular hyperplasia and focal lobular carcinoma in situ in one, and ductal hyperplasia

91 ical type (p=0.03), with a relative risk for lobular carcinoma in situ of 2.82 (1.72-4.63) and 1.56 (

92 ecent year of diagnosis, and the presence of lobular carcinoma in situ were significantly associated

93 ar invasion (LVI), and 8% lobular neoplasia (lobular carcinoma in situ).

94 ts (one atypical lobular hyperplasia and one lobular carcinoma in situ).

95 diotherapy, ductal carcinoma with concurrent lobular carcinoma in situ, and DCIS in elderly people an

96 h-risk lesions (atypical ductal hyperplasia, lobular carcinoma in situ, atypical lobular hyperplasia)

97 l hyperplasia, atypical lobular hyperplasia, lobular carcinoma in situ, or radial scar) was identifie

98 ost in the vast majority (13/17) of cases of lobular carcinoma in situ, which is defined by cellular

99 perplasia, atypical lobular hyperplasia, and lobular carcinoma in situ.

100 gn, 47 showed atypical histology, and 4 were lobular carcinoma in situ.

101 equivalent measure) or women diagnosed with lobular carcinoma in situ.

102 f breast cancer,ductal carcinoma in situ, or lobular carcinoma in situ.

103 or atypical ductal or lobular hyperplasia or lobular carcinoma in situ; or ductal carcinoma in situ w

104 nfiltrating ductal carcinoma or infiltrating lobular carcinoma in the breast or axillary lymph nodes)

105 Metastatic lobular carcinoma is difficult to identify in SLN becaus

106 Lobular carcinoma is less common than ductal carcinoma b

107 ase presents a clinical challenge given that lobular carcinoma is more difficult to detect than ducta

108 Agreement on lobular carcinoma metastasis classification improved fro

109 ed essentially constant from 1987-1999 while lobular carcinoma rates increased steadily.

110 entified for the intraoperative detection of lobular carcinoma versus ductal carcinoma.

111 ozole is greater for patients diagnosed with lobular carcinoma versus ductal carcinoma.

112 was significantly increased in patients with lobular carcinoma vs those with ductal carcinoma (adjust

113 Sixty-one cases of pure invasive lobular carcinoma were identified.

114 erative discovery of predefined factors (eg, lobular carcinoma) could trigger addition of external be

115 carcinoma, 1 high-grade mammary carcinoma, 3 lobular carcinoma, 1 invasive papilloma, and 4 sentinel

116 ltrating ductal carcinoma, 29%; infiltrating lobular carcinoma, 27%; other, 9%).

117 (95% CI, 1.7-4.3) increased risk of invasive lobular carcinoma, a 1.5-fold (95% CI, 1.1-2.0) increase

118 tients yielded 3 carcinomas: an infiltrating lobular carcinoma, a ductal carcinoma in situ, and an in

119 Twist expression is correlated with invasive lobular carcinoma, a highly infiltrating tumor type asso

120 invasive ductal carcinoma, two had invasive lobular carcinoma, and one had mixed invasive ductal and

121 % CI, 1.3-5.3] increases in risk of invasive lobular carcinoma, respectively.

122 oplasms may be broadly divided into invasive lobular carcinoma, well-differentiated subtypes of invas

123 ptions are becoming widely used for invasive lobular carcinoma, yielding outcomes equivalent to those

124 ive breast cancer (IBC) after a diagnosis of lobular carcinoma-in-situ (LCIS) by using Surveillance,

125 at 30, 48, and 60 months-including two with lobular carcinoma.

126 The technique is not recommended for lobular carcinoma.

127 ctal carcinoma, and ER-positive infiltrating lobular carcinoma.

128 inoma, and one had mixed invasive ductal and lobular carcinoma.

129 om this cohort, we studied SLN from cases of lobular carcinoma.

130 es, using any technique, to evaluate SLN for lobular carcinoma.

131 However, invasive lobular carcinomas (ILC) comprise up to 15% of newly dia

132 186) with that of risk factors and invasive lobular carcinomas (n = 1,191).

133 IS (P for heterogeneity = 0.03) and invasive lobular carcinomas (P for heterogeneity < 0.01).

134 ations generally were similar for ductal and lobular carcinomas (P-heterogeneity=0.43) and by tumor s

135 frequently amplified and highly expressed in lobular carcinomas of the breast.

136 d in cell lines derived from mouse and human lobular carcinomas that possess high FGFR1 activity.

137 s a critical component of FGFR1 signaling in lobular carcinomas, thus implicating RSK as a candidate

138 , 1997, through May 31, 1999 (histology: 196 lobular cases, 656 ductal cases, 114 cases with other hi

139 Lobular CD4 staining, absent in healthy controls, was no

140 To investigate global and lobular cerebellar volumetries in patients with progress

141 Subcortical (chi(2) (1)=4.65, P=0.031) and lobular (chi(2) (1)=5.17, P=0.023) GluCEST contrast leve

142 The proportion of breast cancers with a lobular component increased from 9.5% in 1987 to 15.6% i

143 es the first quantitative examination of the lobular correlates of a broad range of cognitive and mot

144 plasmic inclusions in ALS and frontotemporal lobular degeneration (FTLD) patients' brains and spinal

145 in neurons of patients with fronto-temporal lobular dementia and amyotrophic lateral sclerosis (ALS)

146 100% penetrance: arrest of mammary alveolar/lobular development and mammary tumorigenesis.

147 e two phenotypes: arrest of mammary alveolar/lobular development and mammary tumorigenesis.

148 An acute hepatitic pattern with lobular disarray is seen in acute infection, during acut

149 d apoptosis and more frequently demonstrated lobular disarray, rosette formation, and hemorrhage than

150 ptal thickening and diseases with peripheral lobular distribution, centrilobular abnormalities, and p

151 an BRCA1(mut/+) mammary glands showed marked lobular expression of nuclear NF-kappaB.

152 s conventionally assessed histologically for lobular features of inflammation, development of portal

153 evolving AIH, finally leading to portal and lobular fibrosis.

154 ith mild, as well as established, portal and lobular fibrosis.

155 Initially, nuclear lobular formation is lost and some granules are released

156 cific changes in gene expression distinguish lobular from ductal breast carcinomas.

157 h higher grades of steatosis (taurocholate), lobular (glycocholate) and portal inflammation (taurolit

158 On CT, neovascularity, lobular ground-glass opacification, and hilar and interc

159 apulmonary vessels, termed "neovascularity," lobular ground-glass opacification, and systemic perihil

160 iver histology showed granulomata in 75% and lobular hepatitis in 90% of specimens.

161 th stage N2 or N3 disease, eight (57.1%) had lobular histologic characteristics and six (42.9%) had d

162 g after LCIS more often represented invasive lobular histology (23.1%) compared with primary IBCs (6.

163 lower grade (case-only P= 6.7 x 10(-3)) and lobular histology (case-only P= 0.01).

164 The tumor had lobular histology and was considered grade 2 of 3.

165 Young patient age, non-Hispanic white race, lobular histology, and previous cancer diagnosis were as

166 tumors, with a predominant association with lobular histology.

167 8.8 [95% CI: 4.7, 16.7]; P < .001), invasive lobular histopathologic results versus invasive ductal p

168 contrast to clear positive associations with lobular (HR = 1.82, 95% CI: 1.39, 2.37) and mixed ductal

169 = 1.82, 95% CI: 1.39, 2.37) and mixed ductal-lobular (HR = 1.87, 95% CI: 1.39, 2.51) tumors.

170 was the same breast diagnosed with atypical lobular hyperplasia (ipsilateral) in 34 (68%) and the co

171 No malignancy was found in the atypical lobular hyperplasia (n = 2), lobular carcinoma in situ (

172 atypical ductal hyperplasia in two, atypical lobular hyperplasia and focal lobular carcinoma in situ

173 ed atypical histologic results (one atypical lobular hyperplasia and one lobular carcinoma in situ).

174 Clinical decisions about atypical lobular hyperplasia are based on the belief that later i

175 enign surgical biopsies that showed atypical lobular hyperplasia from 1950 to 1985, as part of the Na

176 uggest a model of premalignancy for atypical lobular hyperplasia intermediate between a local precurs

177 ng within 5 years); prior atypical ductal or lobular hyperplasia or lobular carcinoma in situ; or duc

178 For six women with atypical lobular hyperplasia plus atypical ductal hyperplasia, th

179 risk of breast cancer in women with atypical lobular hyperplasia was 3.1 (95% CI 2.3-4.3, p<0.0001).

180 ilateral/ contralateral cancers for atypical lobular hyperplasia without other atypical lesions was 1

181 rplasia, lobular carcinoma in situ, atypical lobular hyperplasia).

182 he rate-limiting factor in initiation of DH, lobular hyperplasia, and DCIS.

183 ial cells developed ductal hyperplasia (DH), lobular hyperplasia, and ductal carcinoma in situ (DCIS)

184 was similar for atypical ductal and atypical lobular hyperplasia, and family history added no signifi

185 ns are atypical ductal hyperplasia, atypical lobular hyperplasia, and lobular carcinoma in situ.

186 n (ie, atypical ductal hyperplasia, atypical lobular hyperplasia, lobular carcinoma in situ, or radia

187 nvasive breast cancer in women with atypical lobular hyperplasia.

188 l ductal hyperplasia (ADH), and one atypical lobular hyperplasia.

189 ity of lobuloalveolar impairment ranged from lobular hypoplasia to aplasia in some cases and was asso

190 ver, incidence rates of tumors classified as lobular increased 1.52-fold (95% CI, 1.42-1.63), and tho

191 -1.63), and those classified as mixed ductal-lobular increased 1.96-fold (95% CI, 1.80-2.14); rates o

192 n steatosis (-1.36 versus -0.41, P < 0.001), lobular inflammation (-0.82 versus -0.24, P = 0.03), bal

193 luated semi-quantitatively: steatosis (0-3), lobular inflammation (0-2), hepatocellular ballooning (0

194 allooning (r = 0.65; P < 0.001), followed by lobular inflammation (0.48; P < 0.001), steatosis (0.46;

195 = .008), and a larger proportion had reduced lobular inflammation (36% in the CBDR group vs 21% in th

196 .9 versus -0.04 with placebo, P < 0.001) and lobular inflammation (median change -1 versus 0 with pla

197 ncreasing severity of steatosis (P < 0.001), lobular inflammation (P < 0.001), ballooning (P = 0.002)

198 rrelated with steatosis severity (P < 0.02), lobular inflammation (P < 0.01), and nonalcoholic fatty

199 009), hepatocellular ballooning (P = .0001), lobular inflammation (P = .0001), fibrosis (P = .0001),

200 03), portal inflammation (P = 2.5 x 10(-4)), lobular inflammation (P = 0.005), Mallory-Denk bodies (P

201 vitamin E and P<0.001 for pioglitazone) and lobular inflammation (P=0.02 for vitamin E and P=0.004 f

202 ent negatively correlated with the degree of lobular inflammation (r = -0.59, P < .0001), ballooning

203 h NASH grade (r = 0.51, P = 8.11 x 10(-7) ), lobular inflammation (r = 0.49, P = 2.35 x 10(-6) ), and

204 element-binding protein and featured portal/lobular inflammation along with total, whole-body insuli

205 In contrast, HFD-fed KO mice had increased lobular inflammation and hepatocyte apoptosis.

206 Lobular inflammation as well as NAFLD Activity Score (NA

207 ssessment of steatosis, cellular injury, and lobular inflammation did not detect any effect of treatm

208 % of samples (n = 69; 95% CI: 74.4-91.3) and lobular inflammation in 67.1% (n = 55; 95% CI: 55.8-77.1

209 SNPs associated with lobular inflammation included SNP rs1227756 on chromosom

210 resonance elastography, collagen content and lobular inflammation on liver biopsy, as well as improve

211 26 and disease severity (P = 0.027), but not lobular inflammation or fibrosis; rs58542926 was not ass

212 utants exhibited no histological evidence of lobular inflammation or necrosis.

213 e MCD diet the extension of liver injury and lobular inflammation paralleled the development of immun

214 AnxA1 KO mice was characterized by enhanced lobular inflammation resulting from increased macrophage

215 lyophilized probiotic mixtures, reduction of lobular inflammation was observed.

216 The activity score (ballooning + lobular inflammation) enabled discriminating NASH becaus

217 osed NAS is the unweighted sum of steatosis, lobular inflammation, and hepatocellular ballooning scor

218 were improvement in ballooning degeneration, lobular inflammation, and steatosis.

219 but further stimulated transaminase release, lobular inflammation, and the hepatic expression of proi

220 ures of NASH through reduction in steatosis, lobular inflammation, and/or hepatocellular ballooning a

221 posite of standardized scores for steatosis, lobular inflammation, hepatocellular ballooning, and fib

222 correlation was not confounded by age, sex, lobular inflammation, hepatocellular ballooning, NASH di

223 d elevated in PN28d/DSS mice associated with lobular inflammation, hepatocyte apoptosis, peliosis, an

224 Ds over vitamin E on improving steatosis and lobular inflammation, which had moderate-quality evidenc

225 range of chronic active portal/interface and lobular inflammation, with significant portal hepatitis

226 o alcohol, with elevated ALT, steatosis, and lobular inflammation.

227 of steatosis, hepatocellular ballooning, and lobular inflammation.

228 d between the decrease in HETEs and improved lobular inflammation.

229 s, hepatic inflammatory gene expression, and lobular inflammation.

230 ildren, but not with ALT, autoantibodies, or lobular inflammation.

231 y increased its contribution to the range of lobular inflammation.

232 ntraobserver agreement was only moderate for lobular inflammation.

233 for steatosis, 0.56 for injury, and 0.45 for lobular inflammation.

234 nt significantly reduced liver steatosis and lobular inflammation.

235 uctions in serum aminotransferase levels and lobular inflammation.

236 entoxifylline, and obeticholic acid decrease lobular inflammation.

237 Although there was no difference in lobular insulin and glucagon expression between genotype

238 he majority of Thy-1(+) cells located at the lobular interface and in the parenchyma coexpress desmin

239 Mammographic density and lobular involution are both significant risk factors for

240 ough a delocalization process of BSEP at the lobular level.

241 tial intracellular measurements at different lobular locations within the same mouse.

242 inoculated with wild type exhibited moderate lobular lymphoplasmacytic hepatitis with hepatocytic coa

243 mode and cells adopt a highly Rho-dependent, lobular mode of motility.

244 yer (ML) were arrested, disrupting layer and lobular morphology.

245 rade, node status, tumor size, and ductal or lobular morphology.

246 2.31; P = 0.005) and with severe (grade 2-3) lobular necroinflammation (odds ratio, 1.47; 95% confide

247 Although periportal and lobular necroinflammation vanished, portal inflammation

248 arkers of lipid peroxidation/oxidant stress, lobular necroinflammation, and fibrosis.

249 on levels were significantly associated with lobular necroinflammatory grade and HCV genotype 1.

250 C), or lymphovascular invasion (LVI), and 8% lobular neoplasia (lobular carcinoma in situ).

251 a (n = 7), ductal carcinoma in situ (n = 1), lobular neoplasia (n = 1), or atypical ductal hyperplasi

252 isk lesions (atypical ductal hyperplasia and lobular neoplasia) showed significantly lower ADCs than

253 age, presence of palpable mass, presence of lobular neoplasia, nuclear grade, and necrosis were test

254 Outcomes included invasive lobular or ductal carcinoma.

255 f "Indian files," described for infiltrating lobular or metaplastic breast carcinomas.

256 whereas stage 3 metastases exhibited either lobular or portal growth patterns.

257 The later stage exhibits a lobular or portal pattern of growth.

258 clusters, representing an alternative to the lobular organization observed in several macroscopic ann

259 ow-grade luminal breast cancers, tubular and lobular (p=0.02).

260 ith increased dermal mucin and a superficial lobular panniculitis.

261 Likewise, CB, lobular plug, and mushroom body neurons do not require A

262 ritic plexus in the OFF-layer and only a few lobular processes extending into the ON-layer of the inn

263 cells in mouse retina are bistratified with lobular processes in the ON sublamina and arboreal dendr

264 tem cell as well as lineage-limited duct and lobular progenitor cell functions.

265 Furthermore, lobular progenitor function is ultimately controlled by

266 ed all of the properties of fully functional lobular progenitors including giving rise to ERalpha+, P

267 PI-MECs and that the expansion of functional lobular progenitors is required for secretory alveolar d

268 study of 3 tumor specimens revealed similar lobular proliferations of bland endothelial cells.

269 uct concentration and a hepatic cellular and lobular redistribution of ERK-1/2 that correlated with 4

270 In the lobular region, CXCL10-expressing and CXCL9-expressing h

271 yers of dilated ducts and hyperproliferative lobular regions in the mammary glands of Brca1(FL/FL) mi

272 never users of hormone therapy were seen for lobular (relative risk 2.25, 95% CI 2.00-2.52), mixed du

273 classified according to pattern and extent (lobular, segmental, lobar, or whole lung).

274 Therefore, they can easily remodel into the lobular structure.

275 LMP2A-infected cells formed large, lobular structures rather than hollow acini.

276 As women age, these lobular structures should regress, which results in redu

277 found in both normal and abnormal ductal and lobular structures.

278 5 [1.11-1.20]; interaction P = .008) and for lobular than ductal tumors (1.35 [1.23-1.49] vs 1.10 [1.

279 All three associations were stronger for lobular than for ductal tumours (p<0.006 for each compar

280 oestrogen receptor-negative disease and for lobular than for ductal tumours.

281 locked their differentiation into ductal and lobular tissue rudiments.

282 The RR(Q5vsQ1) of lobular tumors was 0.66 (95% CI: 0.44, 0.97; P for trend

283 risk of breast cancer, particularly invasive lobular tumors, whether the progestin component was take

284 al tumors, and 1.52 (95% CI: 0.95, 2.44) for lobular tumors.

285 were significant for ductal and mixed ductal/lobular types.

286 for each lesion relative to terminal ductal-lobular unit baseline, and group comparisons revealed th

287 Each large duct or terminal duct-lobular unit containing ADH was considered a focus and c

288 s previously observed in the terminal ductal lobular unit-like structures of the parous gland.

289 A expressed in the regressed terminal ductal lobular unit-like structures of the parous mammary gland

290 y 50% of histologically-normal terminal duct lobular units (from which most breast cancer is thought

291 These hyperplastic enlarged lobular units (HELUs) are important clinically as the ea

292 Enlargement of normal terminal duct lobular units (TDLUs) by hyperplastic columnar epithelia

293 ed to stoma surrounding normal terminal duct lobular units (TDLUs), and overexpression of miR-132 in

294 nsists of collecting ducts and terminal duct lobular units (TDLUs).

295 sia lesions compared to normal terminal duct lobular units by using microdissection and miRNA microar

296 numerous and more developed terminal ductal lobular units than in controls.

297 of staining predominates in terminal ductal lobular units, rather than in interlobular ducts.

298 d that they were differentially expressed in lobular versus ductal tumors.

299 -ligand production, portal/periportal versus lobular, were observed.

300 Despite ductular proliferation vanishing and lobular zonation restoration, portal inflammation and si