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

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

18 t common breast cancer histologies, invasive lobular and invasive ductal carcinoma.

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

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

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

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

23 of breast cancer: group A (classic invasive lobular and tubular carcinomas); group B (IBC-NST, metap

24 ighest values were found in classic invasive lobular and tubular carcinomas.

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

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

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

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

29 Lobular appendages are present in mutant mice lacking BC

30 elaborate their presynaptic structures, the lobular appendages, until BCs differentiate about a week

31 ion: (1) a loss of mitochondria inside their lobular appendages, which may indicate an energetic fail

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

33 arge glycinergic synapses at their dendritic lobular appendages.

34 etochores in aged women and mice, making the lobular architecture a prominent feature of the female m

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

36 Lobular area was similarly associated with risk.

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

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

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

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

41 collagen IV, a main component of the breast lobular basement membrane.

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

43 Lobular boundaries, commonly used to summarize functiona

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

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

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

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

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

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

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

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

52 igh prevalence of diffuse gastric cancer and lobular breast cancer.

53 th risk for diffuse gastric cancer (DGC) and lobular breast cancer.

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

55 2002 for stage I to IIIA invasive ductal and lobular breast cancer.

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

57 as novel drivers and therapeutic targets for lobular breast cancer.

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

59 entify new markers distinguishing ductal and lobular breast cancers.

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

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

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

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

64 c outlet obstruction secondary to metastatic lobular breast carcinoma.

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

66 de 1 and 2 invasive cancers (both ductal and lobular), but no change in the detection of grade 3 inva

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

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

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

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

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

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

73 3 (95% CI: 1.30, 2.05); and for mixed ductal/lobular cancer, 2.51 (95% CI: 1.20, 5.24).

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

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

76 invasive cancers, including both ductal and lobular cancers, but no change in the detection of grade

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

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

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

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

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

82 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

83 Invasive lobular carcinoma (ILC) accounts for 8%-14% of all breas

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

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

86 Invasive lobular carcinoma (ILC) demonstrates lower conspicuity o

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

88 Invasive lobular carcinoma (ILC) is a histological subtype of bre

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

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

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

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

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

94 ade 3; and one grade 2 ER/PR+ HER2- invasive lobular carcinoma (ILC).

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

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

97 invasive ductal carcinoma (n = 51), invasive lobular carcinoma (n = 5), or ductal carcinoma in situ (

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

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

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

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

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

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

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

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

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

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

108 s atypical ductal or lobular hyperplasia and lobular carcinoma in situ).

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

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

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

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

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

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

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

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

117 Agreement on lobular carcinoma metastasis classification improved fro

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

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

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

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

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

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

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

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

126 Invasive lobular carcinoma, postsurgical size>20mm, and p53<15% w

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

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

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

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

131 The technique is not recommended for lobular carcinoma.

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

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

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

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

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

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

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

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

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

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

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

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

144 ytic infiltrates and ductular proliferation, lobular cholestasis, and acute liver cell necrosis, toge

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

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

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

148 CD4(+) T cells, Tbet(+) /CD8(+) T cells, and lobular dendritic cells in the non-TOL group.

149 Foxp3+CD4+ T cells, T-bet+CD8+ T cells, and lobular dendritic cells in the non-TOL group.

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

151 100% penetrance: arrest of mammary alveolar/lobular development and mammary tumorigenesis.

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

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

154 rchitectural distortion, intralobular lines, lobular distortion, and traction bronchiectasis may occu

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

156 g the detection and quantification of occult lobular enlargement in the liver secondary to hilar obst

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

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

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

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

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

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

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

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

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

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

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

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

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

170 s or less; patients with de-novo metastases, lobular histology, and bone-only disease; patients with

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

172 tumors, with a predominant association with lobular histology.

173 8.8 [95% CI: 4.7, 16.7]; P < .001), invasive lobular histopathologic results versus invasive ductal p

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

175 = 1.82, 95% CI: 1.39, 2.37) and mixed ductal-lobular (HR = 1.87, 95% CI: 1.39, 2.51) tumors.

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

177 esions on biopsy (such as atypical ductal or lobular hyperplasia and lobular carcinoma in situ).

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

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

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

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

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

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

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

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

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

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

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

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

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

191 .9 versus -0.04 with placebo, P < 0.001) and lobular inflammation (median change -1 versus 0 with pla

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

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

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

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

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

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

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

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

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

201 Lobular inflammation as well as NAFLD Activity Score (NA

202 gliosis, renal parenchymal damage and liver lobular inflammation dependent on the dose and time of e

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

204 % of samples (n = 69; 95% CI: 74.4-91.3) and lobular inflammation in 67.1% (n = 55; 95% CI: 55.8-77.1

205 SNPs associated with lobular inflammation included SNP rs1227756 on chromosom

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

207 26 and disease severity (P = 0.027), but not lobular inflammation or fibrosis; rs58542926 was not ass

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

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

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

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

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

213 ern on liver histology, including steatosis, lobular inflammation, and ballooning with or without per

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

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

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

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

218 Saroglitazar improved steatosis, lobular inflammation, hepatocellular ballooning and fibr

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

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

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

222 nt validation set, including macrosteatosis, lobular inflammation, hepatocyte ballooning degeneration

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

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

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

226 of steatosis, hepatocellular ballooning, and lobular inflammation.

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

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

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

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

231 ntraobserver agreement was only moderate for lobular inflammation.

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

233 nt significantly reduced liver steatosis and lobular inflammation.

234 uctions in serum aminotransferase levels and lobular inflammation.

235 entoxifylline, and obeticholic acid decrease lobular inflammation.

236 ng, Mallory-Denk bodies, and portal, but not 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 al of all hepatocytes, irrespective of their lobular location or ploidy status.

242 ternalization is the combined consequence of lobular-location-dependent drug-induced cellular damage

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

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

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

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

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

248 2.31; P = 0.005) and with severe (grade 2-3) lobular necroinflammation (odds ratio, 1.47; 95% confide

249 Although periportal and lobular necroinflammation vanished, portal inflammation

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

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

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

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

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

255 Outcomes included invasive lobular or ductal carcinoma.

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

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

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

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

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

261 ith increased dermal mucin and a superficial lobular panniculitis.

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

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

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

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

266 Furthermore, lobular progenitor function is ultimately controlled by

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

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

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

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

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

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

273 ortal triads that are situated in periportal lobular regions to the central vein via a polarized sinu

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

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

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

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

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

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

280 5 [1.11-1.20]; interaction P = .008) and for lobular than ductal tumors (1.35 [1.23-1.49] vs 1.10 [1.

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

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

283 locked their differentiation into ductal and lobular tissue rudiments.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

299 modal motor training, we compared cerebellar lobular volume and white matter microstructure, as well

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

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