ライフサイエンスコーパス: adrenocortical

1 Reduced adrenocortical ACTH signalling could explain reduced cor

2 of CRH neurons and the associated pituitary-adrenocortical activation may be accomplished by GLP-1's

3 like behavior, food intake, body weight, and adrenocortical activation were assessed in female rats d

4 et cycling, independently from the degree of adrenocortical activation.

5 istinguished by more protracted increases in adrenocortical activity compared with yoked-cocaine- and

6 Moreover, high adrenocortical activity in aging was associated with dow

7 These findings suggest that elevated adrenocortical activity is critical in mediating memory

8 tudies suggest a mechanism whereby increased adrenocortical activity resulting from chronic cocaine s

9 These studies suggest that increased adrenocortical activity resulting from cocaine self-admi

10 ively, dysregulated genes between ACC versus adrenocortical adenoma and ACC versus normal.

11 mutations are reported to be common in both adrenocortical adenoma and ACC, whereas elevated IGF2 ex

12 d abnormal beta-catenin accumulation in both adrenocortical adenoma and ACC.

13 vealed no major differences in normal versus adrenocortical adenoma whereas there are 808 and 1085, r

14 in ACC versus normal compared to ACC versus adrenocortical adenoma.

15 ent in only 3 of the 15 patients with single adrenocortical adenomas (20% [CI, 0% to 40.2%]).

16 ve plasma extracellular vesicle samples of 6 adrenocortical adenomas (ACA) and 6 histologically verif

17 es of 11 adrenocortical carcinomas (ACCs), 4 adrenocortical adenomas (ACAs), 3 normal adrenal cortice

18 A pairwise comparison of normal, adrenocortical adenomas and ACC gene expression profiles

19 ysis in human adrenocortical tissue (normal, adrenocortical adenomas and ACC) samples.

20 gene expression were also identified between adrenocortical adenomas and carcinomas.

21 Most of the adrenocortical adenomas were in asymptomatic women.

22 ased agonistic behavior and signs of chronic adrenocortical and gonadal activation, whereas the indiv

23 vivo data, Wnt4 repressed steroidogenesis in adrenocortical and Leydig cell lines, as evidenced by re

24 fadienolide inhibitor that is synthesized by adrenocortical and placental cells.

25 in kidney, thyroid, pituitary, leydig cell, adrenocortical and, more recently, in colorectal tumours

26 d skeletal muscle wasting and impose risk of adrenocortical atrophy.

27 ior but no changes in hypothalamus-pituitary-adrenocortical axis activity or in body weight growth, i

28 er anxiety, increased hypothalamus-pituitary-adrenocortical axis activity, and decreased body growth

29 ) are associated with hypothalamic-pituitary-adrenocortical axis dysregulation and prefrontal cortex

30 bit increases in depression-like behavior or adrenocortical axis hormones.

31 This review describes the function of the adrenocortical axis in this population and the effects o

32 elimbic PFC increased hypothalamic-pituitary-adrenocortical axis responses to acute stress and caused

33 the activation of the hypothalamic pituitary adrenocortical axis, and (b) these effects are more depe

34 ced activation of the hypothalamic-pituitary-adrenocortical axis.

35 and hyperactivity of hypothalamic-pituitary-adrenocortical axis.

36 tory influences on the hypothalamo-pituitary-adrenocortical axis.

37 Adrenocortical beta-arrestin-biased GPCR signaling is a

38 herwise normal animals, suggesting that this adrenocortical betaarr1-mediated signaling pathway is op

39 Further, the mechanism for adrenocortical blunting resides at the level of the adre

40 adenomas (ACA) and 6 histologically verified adrenocortical cancer (ACC) were first screened by Taqma

41 tical hyperplasias and tumors) and the H295R adrenocortical cancer cell line.

42 In human aldosterone-producing adrenocortical cancer cell lines, roxithromycin inhibite

43 F-1-mediated transcription by SUMOylation in adrenocortical cancer cells is mediated through reduced

44 pective analysis involving 177 patients with adrenocortical cancer who had undergone radical surgery

45 omy continues to be the most appropriate for adrenocortical cancer.

46 To gain insight into the pathogenesis of adrenocortical carcinoma (ACC) and whether there is prog

47 utant, R337H (p53tet-R337H), associated with adrenocortical carcinoma (ACC) in children, can be conve

48 Adrenocortical carcinoma (ACC) is a rare but aggressive

49 Adrenocortical carcinoma (ACC) is a rare malignancy with

50 Adrenocortical carcinoma (ACC) is a rare pediatric malig

51 Adrenocortical carcinoma (ACC) is an endocrine malignanc

52 pathway activity lead to poorer prognosis in adrenocortical carcinoma (ACC) patients.

53 ng could expose novel targets for therapy in adrenocortical carcinoma (ACC), a rare and lethal cancer

54 tudy, we investigated the role of RARRES2 in adrenocortical carcinoma (ACC), a rare lethal malignancy

55 mplicated in sporadic and syndromic forms of adrenocortical carcinoma (ACC).

56 ily member with a sarcoma, breast, brain, or adrenocortical carcinoma (ACC).

57 ts who underwent curative intent surgery for adrenocortical carcinoma (ACC).

58 a comprehensive genomic characterization of adrenocortical carcinoma (ACC).

59 relative to general population rates were in adrenocortical carcinoma and phyllodes tumour.

60 uence level, is required to fully understand adrenocortical carcinoma biology and apply that knowledg

61 ecent advances that promise to shed light on adrenocortical carcinoma biology.

62 Accordingly, treatment of adrenocortical carcinoma cells with exogenous HGF result

63 been the mainstay for primary and recurrent adrenocortical carcinoma due to the lack of effective ad

64 an important role for HGF/cMET signaling in adrenocortical carcinoma growth and resistance to common

65 ation of the involvement of BMP signaling in adrenocortical carcinoma growth regulation, and the disc

66 The molecular characterization of adrenocortical carcinoma has identified dysregulation of

67 esistance to chemotherapy, but their role in adrenocortical carcinoma has not been examined.

68 No significant advances in the treatment of adrenocortical carcinoma have been developed.

69 ent studies focusing on the tumorigenesis of adrenocortical carcinoma have focused on onco-developmen

70 Adrenocortical carcinoma is a rare cancer that has a poo

71 Paediatric adrenocortical carcinoma is a rare malignancy with poor

72 Adrenocortical carcinoma is a rare malignancy with poor

73 Adrenocortical carcinoma is a rare malignancy, accountin

74 Adrenocortical carcinoma is a rare neoplasm characterize

75 Adrenocortical carcinoma is a rare, aggressive cancer fo

76 Adrenocortical carcinoma is an aggressive, lethal malign

77 d nonfunctional tumors larger than 4 cm when adrenocortical carcinoma is not suspected.

78 rable progress has occurred in understanding adrenocortical carcinoma pathogenesis from the study of

79 A child with Down syndrome and a history of adrenocortical carcinoma resected at age 1 year presente

80 that increased HGF/cMET expression in human adrenocortical carcinoma samples was positively associat

81 randomly assigned 304 patients with advanced adrenocortical carcinoma to receive mitotane plus either

82 lly confirmed locally advanced or metastatic adrenocortical carcinoma were recruited at clinical site

83 nal tumors (16 adenomas, six metastases, one adrenocortical carcinoma) were reviewed.

84 previous systemic cytotoxic chemotherapy for adrenocortical carcinoma, Eastern Cooperative Oncology G

85 issue sarcomas, osteosarcoma, brain tumours, adrenocortical carcinoma, Wilms' tumour and phyllodes tu

86 gamut of clinical presentations, as well as adrenocortical carcinoma, with its advanced disease at p

87 survival in patients with radically resected adrenocortical carcinoma.

88 velop gonadal tumors and-when gonadectomized-adrenocortical carcinoma.

89 mg/m2 had improvement in liver metastases of adrenocortical carcinoma.

90 HGF/cMET expression and cancer hallmarks of adrenocortical carcinoma.

91 vestigate efficacy in patients with advanced adrenocortical carcinoma.

92 dualised and improved therapeutic options in adrenocortical carcinoma.

93 s pheochromocytomas, paragangliomas, and the adrenocortical carcinomas (ACC), adenomas (ACA), and hyp

94 spectrum was characterized by osteosarcomas, adrenocortical carcinomas (ACC), CNS tumors, and soft ti

95 we generated transcriptional profiles of 11 adrenocortical carcinomas (ACCs), 4 adrenocortical adeno

96 ly older (P=0.03) and had more stage I or II adrenocortical carcinomas (P=0.02) than did patients in

97 Images of 24 adrenocortical carcinomas were also reviewed to determin

98 In addition, pediatric adrenocortical carcinomas were found to share similar pa

99 noviral vectors suitable for gene therapy of adrenocortical carcinomas with poor prognosis.

100 eukemia, melanoma, duodenal adenocarninomas, adrenocortical carcinomas, and neuroblastomas.

101 's sarcomas, gliomas, rhabdomyosarcomas, and adrenocortical carcinomas.

102 There were no occult adrenocortical carcinomas.

103 characteristics of social rank have adverse adrenocortical, cardiovascular, reproductive, immunologi

104 In mice with Nnt loss, higher levels of adrenocortical cell apoptosis and impaired glucocorticoi

105 These fetal adrenocortical cell descendants within the adrenal capsu

106 is associated with a profound stimulation of adrenocortical cell function and glucocorticoid release.

107 NNT knockdown in a human adrenocortical cell line resulted in impaired redox pote

108 le of CaV1.3 on steroidogenesis in the human adrenocortical cell line, H295R, and in primary human ad

109 del of PPNAD (AdKO mice), in human and mouse adrenocortical cell lines in response to pharmacological

110 e infer that this increased lethality limits adrenocortical cell mass and the severity of aldosteroni

111 ulture conditions by encapsulation of bovine adrenocortical cells (BACs) in alginate (enBACs).

112 L168R, hereafter referred to as KCNJ5MUT) in adrenocortical cells account for half of APAs worldwide.

113 alian target of rapamycin (mTOR) pathways in adrenocortical cells and its possible involvement in apo

114 at ASAH1 is localized in the nuclei of H295R adrenocortical cells and that cyclic AMP (cAMP) signalin

115 ein kinase activity in both primary isolated adrenocortical cells and Y-1 cells.

116 Previously, we showed that bovine adrenocortical cells can be transplanted into severe com

117 tions and adrenocortical cells revealed that adrenocortical cells coexpress CYP11B2 and leptin recept

118 cing p54(nrb)/NONO expression in H295R human adrenocortical cells decreases the ability of the cells

119 Bovine adrenocortical cells express bTREK-1 K+ channels that se

120 Therefore, using bovine adrenocortical cells in primary culture, we analyzed the

121 ectly stimulated corticosterone secretion by adrenocortical cells in vitro.

122 Transient overexpression of HSL in Y1 adrenocortical cells increases mitochondrial cholesterol

123 ation of human CYP17 (hCYP17) in H295R human adrenocortical cells is established.

124 same time, the high level of transfection in adrenocortical cells might make appropriately modified a

125 We conclude that LDL CE selective uptake in adrenocortical cells occurs via SR-BI-independent and SR

126 evere depletion of cholesteryl ester (CE) in adrenocortical cells of apoA-I(-/-) mice suggests that a

127 he CYP27A1 gene in human trophoblast and rat adrenocortical cells reduced the expression of CYP27A1 m

128 staining of human adrenal cross-sections and adrenocortical cells revealed that adrenocortical cells

129 Analyses with subclones of Y1 adrenocortical cells showed that LDL-CE-selective uptake

130 On electron microscopy, adrenocortical cells showed ultrastructural signs of mar

131 s of capsular cells are descendants of fetal adrenocortical cells that once expressed Nr5a1.

132 Previous studies with Y1/E/tet/2/3 murine adrenocortical cells that were engineered to express apo

133 t through phospholipase C inhibit bTREK-1 in adrenocortical cells through simultaneous activation of

134 mTORC1 by rapamycin restored sensitivity of adrenocortical cells to apoptosis in AdKO but not in wil

135 mutations stimulate Wnt activation and cause adrenocortical cells to de-differentiate toward their co

136 hIP-on-chip was performed in NCI-H295R human adrenocortical cells using promoter tiling arrays, leadi

137 uration technique the Adx factor in mouse Y1 adrenocortical cells was found to be in the size range o

138 In TH-null mice, adrenocortical cells were characterized by an increase i

139 ivity in transiently transfected H295R human adrenocortical cells were stimulated by angiotensin II b

140 Primary human and bovine adrenocortical cells were transduced with retroviruses e

141 st cells and of corticosterone by 90% in rat adrenocortical cells when compared with cells transfecte

142 Treatment of Y-1 BS1 adrenocortical cells with either low density lipoprotein

143 We cotransfected primary bovine adrenocortical cells with plasmids encoding hTERT, SV40

144 s are present on pituitary corticotrophs and adrenocortical cells, consistent with the ability of IL-

145 I(-/-) HDL and its interaction with SR-BI on adrenocortical cells, hepatoma cells, and cells expressi

146 not detected in the Y1/E/tet/2/3 clone of Y1 adrenocortical cells, indicating the presence of a disti

147 ctivated by PKA signaling in human and mouse adrenocortical cells, leading to increased cell survival

148 catenin inactivation that did not affect all adrenocortical cells, permitting adrenal survival to rev

149 ss spectrometry, we show that in H295R human adrenocortical cells, SF1 is bound to phosphatidic acid

150 By use of nuclear extracts from adrenocortical cells, Sp1 and Sp3 are shown here to bind

151 In human and mouse adrenocortical cells, these mutations lead to increased

152 give rise only to non-steroidogenic stromal adrenocortical cells, which also express collagen 1a1, d

153 gnaling with [d-Ala(2)]GIP in mice and in Y1 adrenocortical cells.

154 renocorticotropic hormone-stimulated primary adrenocortical cells.

155 lling StAR expression and steroidogenesis in adrenocortical cells.

156 ered basal and stimulated steroidogenesis of adrenocortical cells.

157 of SR-BI blocked LDL-CE-selective uptake in adrenocortical cells.

158 ted leptin-mediated increases in CYP11B2, in adrenocortical cells.

159 Identical results were obtained in cultured adrenocortical cells.

160 inemia, and hyperglycemia include a critical adrenocortical component that is initiated by hypothalam

161 r plasma marinobufagenin levels doubled, and adrenocortical CYP27A1 mRNA and protein increased 1.6-fo

162 atogenic failure, ovarian insufficiency, and adrenocortical deficiency.

163 ing via beta-catenin, are also implicated in adrenocortical development.

164 nd associated with primary pigmented nodular adrenocortical disease (PPNAD) and increased steroid syn

165 ver, their role in primary pigmented nodular adrenocortical disease (PPNAD) has not been investigated

166 Primary pigmented nodular adrenocortical disease (PPNAD) is associated with inacti

167 1A mutations cause primary pigmented nodular adrenocortical disease (PPNAD) or Carney complex (CNC),

168 ease and 15 patients with primary unilateral adrenocortical disease (single adenomas).

169 ps consisted of 9 patients with macronodular adrenocortical disease and 15 patients with primary unil

170 Primary pigmented nodular adrenocortical disease causes the Cushing syndrome in ch

171 d kinase activity, primary pigmented nodular adrenocortical disease, and tumors of the thyroid and ot

172 ase, excluded all patients with macronodular adrenocortical disease, and was present in only 3 of the

173 6% to 91.8%]) with primary pigmented nodular adrenocortical disease, excluded all patients with macro

174 res reminiscent of primary pigmented nodular adrenocortical disease, histiocytic and epithelial hyper

175 Hypothalamo-pituitary-adrenocortical dysfunction contributes to morbidity and

176 Adrenocortical dysplasia (acd) is a spontaneous autosoma

177 Adrenocortical dysplasia (acd) is a spontaneous autosoma

178 In surviving adult mutants, adrenocortical dysplasia and hypofunction are predominan

179 exome sequencing, we identified mutations in Adrenocortical Dysplasia Homolog (ACD) (encoding TPP1),

180 TRF1-interacting nuclear factor 2 (TIN2) and adrenocortical dysplasia homolog (ACD) were identified i

181 y to impact the interaction between POT1 and adrenocortical dysplasia homolog (ACD), which is a part

182 activities, including roles in pigmentation, adrenocortical function and regulation of energy stores,

183 carboetomidate produces less suppression of adrenocortical function and smaller increases in proinfl

184 This study shows that basal adrenocortical function as well as adrenocortical respon

185 In sheep, it is known that basal adrenocortical function is delayed in twins relative to

186 lack of evidence delineating what the normal adrenocortical function is in this population, cortisol

187 ay contribute to the development of impaired adrenocortical function that is thought to contribute to

188 We sought to assess adrenocortical function using computer-assisted numerica

189 homeostatic regulation, including pituitary-adrenocortical function, cardiovascular tone, metabolic

190 important role in regulating and maintaining adrenocortical function, specifically steroidogenesis.

191 regulates genes that specify differentiated adrenocortical function.

192 important role in regulating and maintaining adrenocortical function.

193 ontrol of local blood flow and regulation of adrenocortical function.

194 e major effects being mediated by changes in adrenocortical function.

195 tudies suggest that prolonged disruptions in adrenocortical functioning may be sufficient to induce e

196 K+-stimulated aldosterone production in the adrenocortical glomerulosa cells requires induction of t

197 ut not 17alpha-hydroxylase activity in human adrenocortical HCI-H295A cells, suggesting an action on

198 Adrenocortical hormone excess, due to primary aldosteron

199 f dehydroepiandrosterone (DHEA), an abundant adrenocortical hormone in humans.

200 Initial activation of adrenocortical hormone production during early sepsis de

201 ension, dyslipidemia, hypothalamic pituitary adrenocortical (HPA) axis abnormalities and inflammation

202 ret or control odor on hypothalamo-pituitary-adrenocortical (HPA) axis activation.

203 rticosterone to assess hypothalamo-pituitary-adrenocortical (HPA) axis activation.

204 y exercise can reduce hypothalamic-pituitary-adrenocortical (HPA) axis activity in response to variou

205 uced activation of the hypothalamo-pituitary-adrenocortical (HPA) axis and high circulating glucocort

206 ting activation of the hypothalamo-pituitary-adrenocortical (HPA) axis and the release of adrenocorti

207 per-reactivity of the hypothalamic-pituitary-adrenocortical (HPA) axis and triggers symptoms associat

208 N), in the control of hypothalamic-pituitary-adrenocortical (HPA) axis function.

209 ary for activating the hypothalamo-pituitary-adrenocortical (HPA) axis in response to audiogenic stre

210 Development of the hypothalamo-pituitary-adrenocortical (HPA) axis is marked by a diminution in s

211 ress activation of the hypothalamo-pituitary-adrenocortical (HPA) axis is mediated in part by glutama

212 The hypothalamo-pituitary-adrenocortical (HPA) axis regulates stress physiology an

213 sis and indicate that hypothalamic-pituitary-adrenocortical (HPA) axis regulation is mediated by dail

214 reliably activates the hypothalamo-pituitary-adrenocortical (HPA) axis response in rodents, which is

215 d by sensitization of hypothalamic-pituitary-adrenocortical (HPA) axis responses and increased adreno

216 ced activation of the hypothalamic-pituitary-adrenocortical (HPA) axis.

217 ocorticoids within the hypothalamo-pituitary-adrenocortical (HPA) axis.

218 y influences upon the hypothalamic-pituitary-adrenocortical (HPA) axis.

219 c influences upon the hypothalamic-pituitary-adrenocortical (HPA) axis.

220 that can stimulate the hypothalamo-pituitary-adrenocortical (HPA) axis.

221 he discovery that the hypothalamic-pituitary-adrenocortical (HPA) endocrine stress axis controls an a

222 ids in the amygdala on hypothalamo-pituitary-adrenocortical (HPA) responses to the elevated plus maze

223 al damage disinhibits hypothalamic-pituitary-adrenocortical (HPA)-axis activity, thereby elevating pl

224 urce of Cushing syndrome in individuals with adrenocortical hyperplasia that was not caused by known

225 cently identified patients with micronodular adrenocortical hyperplasia who were carriers of inactiva

226 thyroid follicular hyperplasia and adenomas, adrenocortical hyperplasia, and other features reminisce

227 T-cell activation, testosterone production, adrenocortical hyperplasia, and thyroid function.

228 ormone expression, chronic hypercortisolism, adrenocortical hyperplasia, glucose intolerance and matu

229 its germline inactivation is associated with adrenocortical hyperplasia, suggesting another means by

230 xhibited a temporal progression of increased adrenocortical hyperplasia, with subsequent microscopic

231 umors, in addition to their association with adrenocortical hyperplasia.

232 n and transcription as possible mediators of adrenocortical hyperplasia.

233 ry increases in corticotropin secretion, and adrenocortical hyperplasia.

234 eight, six more cases of AIMAH, and 18 other adrenocortical hyperplasias and tumors) and the H295R ad

235 Relative adrenocortical immaturity in the twin fetus may reflect

236 may be a treatment option for patients with adrenocortical insufficiency and other stress-related di

237 ent of shock states possibly associated with adrenocortical insufficiency.

238 1 week, has been shown to negatively affect adrenocortical integrity and function.

239 xpression changes in ACCs compared to benign adrenocortical lesions.

240 ood marker for the preoperative diagnosis of adrenocortical malignancy.

241 lso found with the native receptor in bovine adrenocortical membrane preparations.

242 an important role of immune cell rather than adrenocortical MyD88 for adrenal inflammation and HPA-ax

243 hylation associated with gonadectomy-induced adrenocortical neoplasia in the mouse.

244 d neuroblastoma (2B and 4S), 2 had low-grade adrenocortical neoplasm, 2 had adrenal hemorrhage, and 2

245 a model for tissue-specific effects based on adrenocortical ontogeny.

246 undernutrition was associated with increased adrenocortical output in 2.5-year-old females only.

247 r, we verified previous reports showing that adrenocortical output is augmented by cocaine administra

248 howed decreased proliferation in presumptive adrenocortical precursor cells.

249 This study supports a role for adrenocortical PROG in the regulation of CA secretion du

250 idate, carboetomidate neither suppresses the adrenocortical response to endotoxemia nor enhances the

251 the sympathoadrenal and pressor but not the adrenocortical response to stress.

252 CRH neuroendocrine neurons that initiate the adrenocortical response to various glycemia-related chal

253 These adrenocortical responses ensure appropriate long-term gl

254 e the intracellular mechanisms that initiate adrenocortical responses to glycemia-related challenges

255 educed pituitary output (ACTH) but increased adrenocortical responsiveness (cortisol:ACTH area under

256 hat basal adrenocortical function as well as adrenocortical responsiveness is blunted in the twin rel

257 rial blood pressure, baroreflex threshold or adrenocortical responsiveness to ACTH, but had enhanced

258 study investigated the effect of twinning on adrenocortical responsiveness to either the physiologica

259 However, whether adrenocortical responsiveness to stress is also diminish

260 central noradrenergic, adrenomedullary, and adrenocortical secretion were also elevated.

261 The adrenocortical sensitivity to ACTH in the pm after CLP i

262 ver, corticosterone levels, ACTH levels, and adrenocortical size are markedly reduced, suggesting the

263 S were found in Mx1(Cre+)-MyD88(fl/fl) mice, adrenocortical-specific MyD88 deletion did not alter the

264 ting thereby in deletion of MyD88, which was adrenocortical-specific.

265 ns that define two separate origins of adult adrenocortical steroidogenic cells (fetal adrenal cortex

266 ton and six of the twin fetuses to determine adrenocortical steroidogenic sensitivity to exogenous AC

267 to physiological levels of anti-inflammatory adrenocortical steroids.

268 'stress steroids' to patients with presumed adrenocortical suppression.

269 In conclusion, both the adrenomedullary and adrenocortical systems demonstrate structural and functi

270 enomic hybridization (CGH) analysis in human adrenocortical tissue (normal, adrenocortical adenomas a

271 Adrenocortical tissue analysis from Armc5+/- mice at 18

272 protein level using immunohistochemistry and adrenocortical tissue microarrays.

273 Adrenocortical tissues carrying the R804H mutation showe

274 approach to a cohort of benign and malignant adrenocortical tissues would be potentially informative

275 ed in ACC as compared with normal and benign adrenocortical tissues, which is a result of CpG hyperme

276 ed genome-wide SNP genotyping, including the adrenocortical tumor DNA.

277 ts registered on the International Pediatric Adrenocortical Tumor Registry.

278 creased SF-1 dosage has been associated with adrenocortical tumorigenesis.

279 d outline a hypothetical model of paediatric adrenocortical tumorigenesis.

280 Pediatric adrenocortical tumors (ACT) are rare and often fatal mal

281 The incidence of pediatric adrenocortical tumors (ACTs) is remarkably high in south

282 pathogenesis, and outcomes in children with adrenocortical tumors (ACTs) without germline TP53 mutat

283 We created a registry for pediatric adrenocortical tumors (ACTs), which are rare and are not

284 with PRKAR1A or GNAS mutations and leads to adrenocortical tumors and Cushing syndrome.

285 Compared with adjacent normal tissue, the adrenocortical tumors showed reproducible gains and loss

286 Several types of adrenocortical tumors that lead to Cushing syndrome may

287 The 2 patients with adrenocortical tumors were resected because of a more th

288 genes were those known to be up-regulated in adrenocortical tumors, such as insulin-like growth facto

289 in plasma samples of patients suffering from adrenocortical tumors.

290 ate genes in an additional 171 patients with adrenocortical tumors.

291 and R867G were frequent among patients with adrenocortical tumors; although statistical significance

292 Here we analyse 37 adrenocortical tumours (ACTs) by whole-genome, whole-exo

293 Adrenocortical ultrastructure illustrated no morphologic

294 which express the endogenous IGRP gene, and adrenocortical Y1 cells, which do not.

295 y of SF-1 for Cyp11a1 transcription in mouse adrenocortical Y1 cells.

296 o its type 1 receptors (AT(1)Rs), present in adrenocortical zona glomerulosa (AZG) cell membranes.

297 It is produced and secreted by the adrenocortical zona glomerulosa (AZG) cells after angiot

298 Sgpl1-/- mice displayed disrupted adrenocortical zonation and defective expression of ster

299 These findings demonstrate that adrenocortical zonation and regeneration result from lin

300 are the APCC transcriptome with conventional adrenocortical zones [zona glomerulosa (ZG), zona fascic