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

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

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

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

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

20 onstrate that Gq signaling is sufficient for adrenocortical aldosterone production and implicate this

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

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

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

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

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

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

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

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

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

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

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

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

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

34 and hyperactivity of hypothalamic-pituitary-adrenocortical axis.

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

36 Adrenocortical beta-arrestin-biased GPCR signaling is a

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

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

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

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

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

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

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

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

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

46 nalyze the incidence of and risk factors for adrenocortical carcinoma (ACC) in adrenal incidentaloma

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

48 Adrenocortical carcinoma (ACC) is a rare and aggressive

49 Adrenocortical carcinoma (ACC) is a rare but aggressive

50 Adrenocortical carcinoma (ACC) is a rare malignancy with

51 Adrenocortical carcinoma (ACC) is a rare pediatric malig

52 Adrenocortical carcinoma (ACC) is an endocrine malignanc

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

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

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

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

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

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

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

60 Pediatric adrenocortical carcinoma (pACC) is a rare and aggressive

61 ad partial responses (two patients each with adrenocortical carcinoma and mesothelioma, and one patie

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

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

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

65 Finally, our data from NCI-H295R adrenocortical carcinoma cells suggest that adrenocortic

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

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

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

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

70 The molecular characterization of adrenocortical carcinoma has identified dysregulation of

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

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

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

74 Adrenocortical carcinoma is a rare cancer that has a poo

75 Paediatric adrenocortical carcinoma is a rare malignancy with poor

76 Adrenocortical carcinoma is a rare malignancy with poor

77 Adrenocortical carcinoma is a rare malignancy, accountin

78 Adrenocortical carcinoma is a rare neoplasm characterize

79 Adrenocortical carcinoma is a rare, aggressive cancer fo

80 Adrenocortical carcinoma is an aggressive, lethal malign

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

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

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

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

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

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

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

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

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

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

91 survival in patients with radically resected adrenocortical carcinoma.

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

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

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

95 vestigate efficacy in patients with advanced adrenocortical carcinoma.

96 dualised and improved therapeutic options in adrenocortical carcinoma.

97 Adrenocortical carcinomas (ACC) are rare and aggressive

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

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

100 Adrenocortical carcinomas (ACCs) are rare and highly mal

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

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

103 at instead of treatment with mitotane, human adrenocortical carcinomas may be much more sensitive to

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

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

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

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

108 There were no occult adrenocortical carcinomas.

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

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

111 These fetal adrenocortical cell descendants within the adrenal capsu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 ectly stimulated corticosterone secretion by adrenocortical cells in vitro.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

152 renocorticotropic hormone-stimulated primary adrenocortical cells.

153 and reduced steroid production in intact Y1 adrenocortical cells.

154 lling StAR expression and steroidogenesis in adrenocortical cells.

155 ered basal and stimulated steroidogenesis of adrenocortical cells.

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

157 Identical results were obtained in cultured adrenocortical cells.

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

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

160 atogenic failure, ovarian insufficiency, and adrenocortical deficiency.

161 at kisspeptin may be involved in human fetal adrenocortical development and function.

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

163 d its recently described role in human fetal 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 d kinase activity, primary pigmented nodular adrenocortical disease, and tumors of the thyroid and ot

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

170 Hypothalamo-pituitary-adrenocortical dysfunction contributes to morbidity and

171 Adrenocortical dysplasia (acd) is a spontaneous autosoma

172 Adrenocortical dysplasia (acd) is a spontaneous autosoma

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

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

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

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

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

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

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

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

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

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

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

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

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

186 alivary cortisol cut-off value for screening adrenocortical function.

187 regulates genes that specify differentiated adrenocortical function.

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

189 important role in regulating and maintaining adrenocortical function.

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

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

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

193 Adrenocortical hormone excess, due to primary aldosteron

194 Initial activation of adrenocortical hormone production during early sepsis de

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

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

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

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

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

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

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

202 odels reveal that the hypothalamic-pituitary-adrenocortical (HPA) axis calibrates to the harshness of

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

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

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

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

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

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

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

210 ely activation of the hypothalamic-pituitary-adrenocortical (HPA) axis.

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

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

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

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

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

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

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

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

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

220 proximal tubular injury, focal pancreatitis, adrenocortical hyperplasia, and lymphocyte depletion of

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

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

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

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

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

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

227 n and transcription as possible mediators of adrenocortical hyperplasia.

228 ry increases in corticotropin secretion, and adrenocortical hyperplasia.

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

230 Relative adrenocortical immaturity in the twin fetus may reflect

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

232 ent of shock states possibly associated with adrenocortical insufficiency.

233 1 week, has been shown to negatively affect adrenocortical integrity and function.

234 xpression changes in ACCs compared to benign adrenocortical lesions.

235 ood marker for the preoperative diagnosis of adrenocortical malignancy.

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

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

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

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

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

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

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

243 howed decreased proliferation in presumptive adrenocortical precursor cells.

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

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

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

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

248 These adrenocortical responses ensure appropriate long-term gl

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

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

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

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

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

254 However, whether adrenocortical responsiveness to stress is also diminish

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

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

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

258 C, including urothelial, prostate, pancreas, adrenocortical, small bowel, sarcoma, mesothelioma, mela

259 Here, we demonstrate that adrenocortical-specific loss of ZNRF3, but not RNF43, re

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

261 b2(AS)(Cre) mouse line to generate mice with adrenocortical-specific Wnt/beta-catenin activation, Trp

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

263 ole in adrenal function in mice and possibly adrenocortical steroid hormone secretion in humans, beyo

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

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

266 to physiological levels of anti-inflammatory adrenocortical steroids.

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

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

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

270 protein level using immunohistochemistry and adrenocortical tissue microarrays.

271 Adrenocortical tissues carrying the R804H mutation showe

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

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

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

275 ts registered on the International Pediatric Adrenocortical Tumor Registry.

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

277 d outline a hypothetical model of paediatric adrenocortical tumorigenesis.

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

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

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

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

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

283 orts demonstrated similar rates of pediatric adrenocortical tumors and other LFS component cancers, b

284 adrenocortical carcinoma cells suggest that adrenocortical tumors may evade these regulatory control

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 ate genes in an additional 171 patients with adrenocortical tumors.

290 in plasma samples of patients suffering from 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