ライフサイエンスコーパス: ductal

1 type in our cohort and combined analyses was ductal (81%, 83%), grade 2; (40%, 44%), respectively.

2 y pathway, in beta cells by pancreatic intra-ductal AAV8-shAtg7 infusion in C57BL/6 mice, resulted in

3 ximately 50% of all patients with pancreatic ductal adenocarcinoma (PDA) develop diabetes mellitus be

4 Pancreatic ductal adenocarcinoma (PDA) is a deadly cancer that resi

5 Pancreatic ductal adenocarcinoma (PDA) is a highly lethal malignanc

6 e tumor microenvironment (TME) in pancreatic ductal adenocarcinoma (PDA) is characterized by immune t

7 in the treatment of patients with pancreatic ductal adenocarcinoma (PDA) is controversial.

8 Pancreatic ductal adenocarcinoma (PDA) is one of the most lethal hu

9 signaling pathways is frequent in pancreatic ductal adenocarcinoma (PDA), making developmental regula

10 is an established risk factor for pancreatic ductal adenocarcinoma (PDA).

11 ssion and therapeutic response in pancreatic ductal adenocarcinoma (PDA).

12 ighly expressed on macrophages in pancreatic ductal adenocarcinoma (PDA).

13 is an established risk factor for pancreatic ductal adenocarcinoma (PDA).

14 s may improve the poor outcome of pancreatic ductal adenocarcinoma (PDA).

15 somes at the distal tumor site of pancreatic ductal adenocarcinoma (PDAC) ablated the development of

16 Pancreatic ductal adenocarcinoma (PDAC) after complete surgical res

17 mucin, is aberrantly expressed in pancreatic ductal adenocarcinoma (PDAC) and generally correlates wi

18 2 is upregulated in patients with pancreatic ductal adenocarcinoma (PDAC) and in obese individuals, b

19 udy was to analyze the miRNome of pancreatic ductal adenocarcinoma (PDAC) and its preneoplastic lesio

20 astasis and prolonged survival in pancreatic ductal adenocarcinoma (PDAC) and our genomic analysis re

21 erexpressed in human specimens of pancreatic ductal adenocarcinoma (PDAC) and that the overall surviv

22 e hallmark genetic alterations in pancreatic ductal adenocarcinoma (PDAC) and the key drivers of its

23 elationships between diabetes and pancreatic ductal adenocarcinoma (PDAC) are complex.

24 Early-detection tests for pancreatic ductal adenocarcinoma (PDAC) are needed.

25 stress promote the development of pancreatic ductal adenocarcinoma (PDAC) are poorly defined.

26 The mechanisms of initiation of pancreatic ductal adenocarcinoma (PDAC) are still largely unknown.

27 Pancreatic ductal adenocarcinoma (PDAC) cells (PCC) have an excepti

28 oute for discharging lactate from pancreatic ductal adenocarcinoma (PDAC) cells.

29 ar stomatitis virus (VSV) against pancreatic ductal adenocarcinoma (PDAC) cells.

30 r metastasis, which in turn makes pancreatic ductal adenocarcinoma (PDAC) difficult to treat, especia

31 The genome of pancreatic ductal adenocarcinoma (PDAC) frequently contains deletio

32 Pancreatic ductal adenocarcinoma (PDAC) has generally a poor progno

33 rnative splicing (AS) analysis of pancreatic ductal adenocarcinoma (PDAC) has not been performed yet.

34 Pancreatic ductal adenocarcinoma (PDAC) has single-digit 5-year sur

35 The exact nature and dynamics of pancreatic ductal adenocarcinoma (PDAC) immune composition remains

36 oncogenic signaling to influence pancreatic ductal adenocarcinoma (PDAC) initiation, progression, an

37 taplasia (ADM) is a key event for pancreatic ductal adenocarcinoma (PDAC) initiation.

38 Pancreatic ductal adenocarcinoma (PDAC) is a deadly cancer in which

39 Pancreatic ductal adenocarcinoma (PDAC) is a devastating disease.

40 Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal and diss

41 Pancreatic ductal adenocarcinoma (PDAC) is almost uniformly fatal;

42 Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease th

43 Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy

44 Pancreatic Ductal Adenocarcinoma (PDAC) is an aggressive malignancy

45 Pancreatic ductal adenocarcinoma (PDAC) is characterized by a high

46 Pancreatic ductal adenocarcinoma (PDAC) is characterized by extensi

47 Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest mal

48 f systemic cancer therapeutics in pancreatic ductal adenocarcinoma (PDAC) is partly attributed to dep

49 of sympathetic nerve signaling in pancreatic ductal adenocarcinoma (PDAC) is poorly understood.

50 e in the malignant progression of pancreatic ductal adenocarcinoma (PDAC) is uncertain.

51 gnals regulate the development of pancreatic ductal adenocarcinoma (PDAC) may suggest novel therapeut

52 ed the ontogeny of TAMs in murine pancreatic ductal adenocarcinoma (PDAC) models.

53 f alcohol drinking and smoking on pancreatic ductal adenocarcinoma (PDAC) mortality are contradictory

54 d macrophages in a mouse model of pancreatic ductal adenocarcinoma (PDAC) originate from both the yol

55 that in cancer cells derived from pancreatic ductal adenocarcinoma (PDAC) PAR2 protein is necessary f

56 potassium" in chemotherapy-naive pancreatic ductal adenocarcinoma (PDAC) patients with peritoneal me

57 issue architecture contributes to pancreatic ductal adenocarcinoma (PDAC) phenotypes.

58 Outcomes for patients with pancreatic ductal adenocarcinoma (PDAC) remain poor.

59 Pancreatic ductal adenocarcinoma (PDAC) remains a highly lethal dis

60 To explore the role of pancreatic ductal adenocarcinoma (PDAC) size on surgical and surviv

61 pancreatic stellate cells within pancreatic ductal adenocarcinoma (PDAC) stroma secrete lumican and

62 ctral images of multiplex-labeled pancreatic ductal adenocarcinoma (PDAC) tissue samples.

63 t IL-35 is overexpressed in human pancreatic ductal adenocarcinoma (PDAC) tissues, and that IL-35 ove

64 nal oncogenic Kras mouse model of pancreatic ductal adenocarcinoma (PDAC), a malignancy that displays

65 mproved the survival prospects of pancreatic ductal adenocarcinoma (PDAC), additional engagement of t

66 o-oncogene KRAS are a hallmark of pancreatic ductal adenocarcinoma (PDAC), an aggressive malignancy w

67 itabine is commonly used to treat pancreatic ductal adenocarcinoma (PDAC), and we hypothesized that i

68 cancer (PC) including the most common type, ductal adenocarcinoma (PDAC), but its role and the mecha

69 nes for chemotherapy treatment in pancreatic ductal adenocarcinoma (PDAC), but patients often respond

70 e most frequently mutated gene in pancreatic ductal adenocarcinoma (PDAC), but the mechanisms underly

71 During the progression of pancreatic ductal adenocarcinoma (PDAC), heterogeneous subclonal po

72 In pancreatic ductal adenocarcinoma (PDAC), mutant KRAS stimulates the

73 at is critical for suppression of pancreatic ductal adenocarcinoma (PDAC), one of the most lethal mal

74 xpressed in many tumors including pancreatic ductal adenocarcinoma (PDAC).

75 a major susceptibility factor for pancreatic ductal adenocarcinoma (PDAC).

76 eoplasias (PanINs) and ultimately pancreatic ductal adenocarcinoma (PDAC).

77 robot-assisted approach, 24% for pancreatic ductal adenocarcinoma (PDAC).

78 PMN may include development of a new IPMN or ductal adenocarcinoma (PDAC).

79 ulated and leads to cell death in pancreatic ductal adenocarcinoma (PDAC).

80 , or distal CBD with those having pancreatic ductal adenocarcinoma (PDAC).

81 mmon in various cancers including pancreatic ductal adenocarcinoma (PDAC).

82 nd widely metastatic phenotype of pancreatic ductal adenocarcinoma (PDAC).

83 ion-based cohort of patients with pancreatic ductal adenocarcinoma (PDAC).

84 rsor lesion to the development of pancreatic ductal adenocarcinoma (PDAC).

85 benefit to date in patients with pancreatic ductal adenocarcinoma (PDAC).

86 s were shown to be deregulated in pancreatic ductal adenocarcinoma (PDAC).

87 ctivation are required to develop pancreatic ductal adenocarcinoma (PDAC).

88 adjuvant treatment of resectable pancreatic ductal adenocarcinoma (PDAC).

89 romote chemotherapy resistance in pancreatic ductal adenocarcinoma (PDAC).

90 ons rarely become fully malignant pancreatic ductal adenocarcinoma (PDAC).

91 (D-ECM), is a puzzling feature of pancreatic ductal adenocarcinoma (PDACs).

92 essential to tumorigenesis in the pancreatic ductal adenocarcinoma and lung adenocarcinoma patient co

93 We use pancreatic ductal adenocarcinoma as an in vitro and an in vivo canc

94 s effective against a majority of pancreatic ductal adenocarcinoma cell (PDAC) cell lines, some PDAC

95 Pancreatic ductal adenocarcinoma is a lethal cancer with fewer than

96 Pancreatic ductal adenocarcinoma is a notoriously difficult-to-trea

97 Purpose Metastatic pancreatic ductal adenocarcinoma is characterized by excessive hyal

98 Pancreatic ductal adenocarcinoma is on pace to become the second le

99 ast-conserving surgery for unifocal invasive ductal adenocarcinoma of grade 1-3, with a tumour size o

100 undergone complete macroscopic resection for ductal adenocarcinoma of the pancreas (R0 or R1 resectio

101 h previously untreated metastatic pancreatic ductal adenocarcinoma were randomly assigned to treatmen

102 ith histopathologically confirmed pancreatic ductal adenocarcinoma who received preoperative therapy

103 e obtained from 854 patients with pancreatic ductal adenocarcinoma, 288 patients with other pancreati

104 e models of renal cell carcinoma, pancreatic ductal adenocarcinoma, and melanoma triggered RagD-media

105 managing recalcitrant tumors like pancreatic ductal adenocarcinoma, cause off-target toxicities in no

106 roendocrine lineage plasticity in pancreatic ductal adenocarcinoma, contributing to poor survival and

107 plasia (PanINs), the precursor to pancreatic ductal adenocarcinoma, could generate new strategies for

108 Pancreatic ductal adenocarcinoma, even when diagnosed early, nearly

109 ollowing preoperative therapy for pancreatic ductal adenocarcinoma, it is associated with a significa

110 In contrast to pancreatic ductal adenocarcinoma, no recurrent point mutations are

111 tal and neuroendocrine markers in pancreatic ductal adenocarcinoma, revealing heterogeneous expressio

112 ypes of PC, including acinar cell carcinoma, ductal adenocarcinoma, sarcomatoid carcinoma and neuroen

113 opic mouse models of melanoma and pancreatic ductal adenocarcinoma, the compounds reduced tumor size

114 heterogeneity in mouse models of pancreatic ductal adenocarcinoma, where lineage tracing indicates t

115 f these patients (0.9%) developed a distinct ductal adenocarcinoma.

116 evaluable patients with resected pancreatic ductal adenocarcinoma.

117 d of care following resection for pancreatic ductal adenocarcinoma.

118 isk factor for the development of pancreatic ductal adenocarcinoma.

119 to image and quantify fibrosis in pancreatic ductal adenocarcinoma.

120 ue qualities as T-cell targets in pancreatic ductal adenocarcinoma.

121 ognostic factor for patients with pancreatic ductal adenocarcinoma.

122 survival after resection of pancreatic-head ductal adenocarcinoma.

123 ed survival compared with typical pancreatic ductal adenocarcinoma.

124 ve therapy and pancreatectomy for pancreatic ductal adenocarcinoma.

125 Pancreatic ductal adenocarcinomas (PDAC) harbor recurrent functiona

126 The majority of pancreatic ductal adenocarcinomas (PDAC) rely on the mRNA stability

127 the majority of the tumor bulk of pancreatic ductal adenocarcinomas (PDACs).

128 detected in a small proportion of pancreatic ductal adenocarcinomas (PDACs).

129 tic lesions that can develop into pancreatic ductal adenocarcinomas (PDACs).

130 ions in KRAS are detected in most pancreatic ductal adenocarcinomas (PDACs).

131 atic noncoding alterations in 308 pancreatic ductal adenocarcinomas (PDAs) and identify commonly muta

132 Human pancreatic ductal adenocarcinomas contain somatic mutations in the

133 D)-driven transformation and form pancreatic ductal adenocarcinomas in vivo after Cdkn2a inactivation

134 n/anastomosis is planned, because of varying ductal anatomy, risk of ductal injury and increased risk

135 ferate and differentiate into the endocrine, ductal and acinar lineages.

136 ng rise to three important lineages: acinar, ductal and endocrine.

137 e associated with age at diagnosis, sex, and ductal and IBD subtypes.

138 to become terminally differentiated acinar, ductal and myoepithelial cells.

139 We analyzed ductal and neuroendocrine markers in pancreatic ductal a

140 l);MMTV-Cre mice displayed severe defects in ductal branching and abnormal age-related involution com

141 AZD4547 significantly inhibited ductal branching and MEC proliferation in vivo, which co

142 Ductal branching followed the same pattern.

143 a new diagnosis of locally advanced invasive ductal breast cancer (n = 18) or invasive lobular breast

144 ignancy, including prostate cancer, invasive ductal breast cancer, and invasive lobular breast cancer

145 atients with lobular carcinoma vs those with ductal carcinoma (adjusted odds ratio, 1.44; 95% CI 1.06

146 sclosed a moderately differentiated invasive ductal carcinoma (diameter, 2.5 cm).

147 logical breast cancer subtype after invasive ductal carcinoma (IDC), accounting for around 10% of all

148 of 512 breast cancer patients with invasive ductal carcinoma (IDC).

149 DCIS is considered a precursor to invasive ductal carcinoma (IDC); however, approximately half of D

150 nohistochemical analysis of human pancreatic ductal carcinoma (PDAC) specimens, and in vitro validati

151 Fibrosis compromises pancreatic ductal carcinoma (PDAC) treatment and contributes to pat

152 ed a poorly differentiated, grade 3 invasive ductal carcinoma and ductal carcinoma in situ (largest f

153 ssible link between the presence of invasive ductal carcinoma and fatty acid fractions in breast adip

154 ith a stage II (T2N1), right-sided, invasive ductal carcinoma considered grade 2 of 3 on core biopsy,

155 Young age (P < .001) and presence of ductal carcinoma in situ (DCIS) (HR, 2.15; 95% CI, 1.36-

156 Ductal carcinoma in situ (DCIS) accounts for 20% of all

157 nonpalpable invasive breast cancer (IBC) or ductal carcinoma in situ (DCIS) and to examine whether t

158 st ultrasonography) in the identification of ductal carcinoma in situ (DCIS) components of biopsy-pro

159 on of the overdiagnosis and overtreatment of ductal carcinoma in situ (DCIS) detected by mammography

160 atient-derived epithelial cells derived from ductal carcinoma in situ (DCIS) increased secretion of t

161 Ductal carcinoma in situ (DCIS) is defined as a prolifer

162 e tumor bed after whole-breast RT (WBRT) for ductal carcinoma in situ (DCIS) is largely extrapolated

163 orrelates with HER2-positive status in human ductal carcinoma in situ (DCIS) lesions and invasive bre

164 at 271 invasive breast cancer tumors and 179 ductal carcinoma in situ (DCIS) lesions were overdiagnos

165 ic resonance (MR) images are associated with ductal carcinoma in situ (DCIS) recurrence risk after de

166 ilateral breast event (IBE) in patients with ductal carcinoma in situ (DCIS) treated with breast-cons

167 Purpose To compare detection rates of ductal carcinoma in situ (DCIS), classified according to

168 to clinical presentation of that cancer, for ductal carcinoma in situ (DCIS), invasive breast cancer,

169 cular alterations driving the progression of ductal carcinoma in situ (DCIS), we compared patients wi

170 usual ductal hyperplasia (UDH) or malignant ductal carcinoma in situ (DCIS).

171 py after breast-conserving surgery (BCS) for ductal carcinoma in situ (DCIS).

172 e absence of any residual invasive cancer or ductal carcinoma in situ (DCIS).

173 usual ductal hyperplasia and low/high grade ductal carcinoma in situ (DCIS).

174 of early-stage breast lesions, most commonly ductal carcinoma in situ (DCIS).

175 ssociation between risk factors and incident ductal carcinoma in situ (DCIS; n = 1,453) with that of

176 iated, grade 3 invasive ductal carcinoma and ductal carcinoma in situ (largest focus, 3.5 cm).

177 size T3/T4), inflammatory breast cancer, or ductal carcinoma in situ (when breast-conserving surgery

178 but is significantly reduced in precancerous ductal carcinoma in situ and all breast cancer subtypes.

179 ubsequent breast cancers in each subset were ductal carcinoma in situ or stage I.

180 ersus tamoxifen in postmenopausal women with ductal carcinoma in situ undergoing lumpectomy plus radi

181 f 18437 women with invasive breast cancer or ductal carcinoma in situ were enrolled as cases and matc

182 e, missing stage or treatment data, and with ductal carcinoma in situ were excluded, leaving 3729 pat

183 2963 were diagnosed with invasive cancer or ductal carcinoma in situ within 12 months of screening.

184 aging depicted 60 additional breast cancers (ductal carcinoma in situ, n = 20; invasive carcinoma, n

185 II invasive ductal or lobular breast cancer, ductal carcinoma in situ, or prophylaxis.

186 In cellular models of breast ductal carcinoma in situ, we reveal a link between filop

187 breast cancer and multicentric tumors, with ductal carcinoma in situ, who will undergo mastectomy, w

188 rom surgery for invasive breast carcinoma or ductal carcinoma in situ.

189 ncers detected at screening mammography were ductal carcinoma in situ.

190 mphovascular invasion and intermediate grade ductal carcinoma in situ.

191 de glioma, and 2 preinvasive breast cancers [ductal carcinoma in situ]); all but 1 required only rese

192 criptional events among subtypes of invasive ductal carcinoma in The Cancer Genome Atlas (TCGA) Breas

193 r in vivo and to human specimens of invasive ductal carcinoma that express ErbB2 ex vivo.

194 0.6 x 0.5 cm Nottingham grade 1 infiltrating ductal carcinoma was removed from the right upper outer

195 years) with a diagnosis of primary invasive ductal carcinoma were included.

196 A core biopsy confirmed invasive ductal carcinoma, grade 2 of 3, that was estrogen recept

197 ed to manually annotated regions of invasive ductal carcinoma.

198 Outcomes included invasive lobular or ductal carcinoma.

199 ,453) with that of risk factors and invasive ductal carcinomas (n = 7,525); in addition, we compared

200 of DCIS but lower risks of LCIS and invasive ductal carcinomas (P for heterogeneity < 0.01).

201 invasive breast cancer, which revealed that ductal carcinomas in situ show intratumor genetic hetero

202 ts A total of 45 cancers (33 invasive and 12 ductal carcinomas in situ) were diagnosed, 43 were seen

203 uencing data from 680 cases of TCGA invasive ductal carcinomas of the breast and correlated them to c

204 xpress aquaporin-1 (AQP1), presumably in the ductal cell layer and/or in surviving acinar cells, to d

205 ng the native gene locus in a human salivary ductal cell line and primary salivary human stem/progeni

206 hout activated Kras, we found evidence for a ductal cell origin of IPMNs.

207 Mice with ductal cell-specific disruption of Pten but not control

208 In analyses of mice with ductal cell-specific disruption of Pten, with or without

209 uctal progenitor cells (HPNE) and pancreatic ductal cells (HPDE).

210 mice with disruption of Pten specifically in ductal cells (Sox9CreER(T2);Pten(flox/flox);R26R(YFP) or

211 T cells, apoptosis of Kras mutant neoplastic ductal cells and pancreatic regeneration after acute pan

212 Biliary ductal cells proliferate from the portal areas of chroni

213 y inducing AQP1 expression in human salivary ductal cells through epigenetic editing of the native pr

214 ative ability of adult pancreatic acinar and ductal cells to respond to oncogenic Kras and mutant Tp5

215 Within Kras:p53 mutant pancreatic ductal cells, Yap drives the expression and secretion of

216 essential for the survival of acinar but not ductal cells.

217 hepatocytes formed hepatic, endothelial, and ductal colonies within 1 month.

218 tions indicated that exocrine, endocrine and ductal compartments retained the normal proportions and

219 th decreases in hepatic fibrosis and biliary ductal damage relative to the control animals, although

220 tive PDA stent and BT shunt for infants with ductal-dependent pulmonary blood flow adjusted for diffe

221 Infants with ductal-dependent pulmonary blood flow may undergo pallia

222 Infants with ductal-dependent pulmonary blood flow palliated with eit

223 receptors have a recognized role in mammary ductal development and stem cell maintenance, but the li

224 poptosis, which aided lumen formation during ductal development.

225 t(+) progenitor cells and suppress premature ductal differentiation in early developing embryonic sub

226 ific PTEN deletion greatly restricts mammary ductal elongation and induces aberrant alveolar side-bra

227 We present a model of ductal elongation that exploits the geometrically-constr

228 ue remodeling in the mammary gland involving ductal elongation, resolution into the mature epithelial

229 gically, MG acinar atrophy was observed with ductal enlargement and ductal epithelial hyperstratifica

230 ased angiogenesis, desmoplasia, and abnormal ductal epithelial cell growth.

231 investigate whether cigarette smoke promotes ductal epithelial cell hyperplasia by stimulating stroma

232 act the stemness and proliferation of normal ductal epithelial cells and early-stage breast cancer in

233 phy was observed with ductal enlargement and ductal epithelial hyperstratification.

234 eveloping gland and increased density of the ductal epithelial network.

235 1b leads to a Cdkn2a-dependent exhaustion of ductal epithelium and loss of epithelial cell regenerati

236 s activation of Kras and mutant p53 in adult ductal epithelium generated invasive PDAC in 75% of mice

237 ssion profile and short-term contribution to ductal extension.

238 he principle phenotype of MBC was luminal A, ductal, grade 2.

239 The second phase of ductal growth and branching is driven by the highly inva

240 nt doses (1 nM), BPA significantly increased ductal growth, as previously observed in vivo, while 1 m

241 lted in monotonic inhibition of mammary buds ductal growth.

242 ivo, while 1 muM BPA significantly inhibited ductal growth.

243 Atypical ductal hyperplasia (ADH) is a known risk factor for brea

244 Usual ductal hyperplasia (UDH) of the breast is generally rega

245 ion of breast lesions as either benign usual ductal hyperplasia (UDH) or malignant ductal carcinoma i

246 four histological types: normal cases, usual ductal hyperplasia and low/high grade ductal carcinoma i

247 Atypical ductal hyperplasia diagnosed via excisional biopsy was a

248 ased cell division and a distinctive form of ductal hyperplasia with 'squamoid' ghost cell nodules in

249 age and HRL histologic results (eg, atypical ductal hyperplasia).

250 , because of varying ductal anatomy, risk of ductal injury and increased risk of postoperative pancre

251 e neuroendocrine marker Synaptophysin within ductal lesions.

252 creas that accumulates within the pancreatic ductal lumen.

253 ive for the proliferation marker Ki67 or the ductal marker CK19 vs. control subjects, and islet infla

254 ructures and TGF-alpha-induced expression of ductal markers in ex vivo acinar explant cultures.

255 ith control cells, had reduced expression of ductal markers, and formed smaller tumors (71.61 +/- 30.

256 a third of LAP+ fetal hepatocytes expressed ductal markers.

257 /2-mediated signaling is critical for proper ductal maturation.

258 Acinar-to-ductal metaplasia (ADM) has been identified as a key tum

259 suggest that pancreatitis-induced acinar-to-ductal metaplasia (ADM) is a key event for pancreatic du

260 atic acinar cell state can lead to acinar-to-ductal metaplasia (ADM), a precursor lesion to the devel

261 quired for oncogenic Kras-mediated acinar-to-ductal metaplasia (ADM), pancreatic intraepithelial neop

262 that express KrasG12D by promoting acinar-to-ductal metaplasia (ADM).

263 Using the acini-ductal network of the developing human and murine saliva

264 c1, residual milk and cell corpses flood the ductal network, causing gross dilation, chronic inflamma

265 (SMGs), are composed of branched epithelial ductal networks that terminate in acini that together pr

266 in mouse tumor cells and loss of MYC reduces ductal-neuroendocrine lineage heterogeneity, while dereg

267 ogether, we demonstrate that MYC facilitates ductal-neuroendocrine lineage plasticity in pancreatic d

268 such as severe oligozoospermia, non-remedial ductal obstruction, and absence of sperm fertilising abi

269 Ductal occlusion has been postulated to precipitate foca

270 ion that will differentiate into the acinar, ductal or endocrine lineages.

271 dergo mastectomy for stage I to III invasive ductal or lobular breast cancer, ductal carcinoma in sit

272 ammary bud growth, as well as TEB formation, ductal outgrowth and branching during puberty.

273 ulated during puberty, a period of extensive ductal outgrowth and branching.

274 cal stroma, with systemic Ptch1 required for ductal outgrowth and proper hormone receptor expression

275 e mammary gland fat pad, undergo unperturbed ductal outgrowth and terminal differentiation.

276 e) deletion of Sharpin, have reduced mammary ductal outgrowth during puberty.

277 Further, a phenotypically normal ductal outgrowth resulted from a single inoculation of E

278 evidence of the feasibility of treatment of ductal pancreatic adenocarcinoma using (177)Lu-3BP-227.

279 Six patients with confirmed ductal pancreatic adenocarcinoma who had exhausted all o

280 tensin receptor 1 (NTR1) is overexpressed in ductal pancreatic adenocarcinoma, which is still one of

281 s, and suggests a genetic mechanism for ALGS ductal paucity.The hepatopancreatic duct cells connect l

282 holangiocyte populations that constitute the ductal plate.

283 orylated SOX9 expression in human pancreatic ductal progenitor cells (HPNE) and pancreatic ductal cel

284 gulin signaling promotes the identity of SMG ductal progenitors and that removal of nuclear Yap by La

285 red for the expansion of Krt5/Krt14-positive ductal progenitors.

286 differentiated acinar cells to proliferative ductal progenitors.

287 an aberrant increase in cells expressing the ductal proteins K19 and K7, with a reduction in Kit(+) p

288 ted using phase contrast angiography and pre-ductal pulse oximetry, while regional cerebral oxygen sa

289 and enhances endocrine specification during ductal reprogramming.

290 ogenous expression of IRF6 in the developing ductal, serous, and mucous acinar cells of salivary glan

291 Patients undergoing surgical shunt or ductal stent were less likely to have virtual atresia (H

292 TGF-alpha-induced acinar cell metaplasia to ductal structures and TGF-alpha-induced expression of du

293 ap in developing SMGs results in the loss of ductal structures, arising from reduced expression of th

294 ry epithelial cells that can form functional ductal structures.

295 KEY POINTS: The ductal system of the pancreas secretes large volumes of

296 een the exocrine lobules and adjacent to the ductal system of the pancreas.

297 read to the genital tract via the continuous ductal system, eliciting bacterial prostatitis and/or ep

298 the oral cavity by a complex multifunctional ductal system.

299 luding the kidneys, gonads, and reproductive ductal systems: the intermediate mesoderm.

300 called terminal end buds (TEBs) that form at ductal tips at the onset of puberty.