Database : MEDLINE
Search on : adrenocortical and carcinoma [Words]
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[PMID]: 29524503
[Au] Autor:Huang H; Liu L; Li J; Zhu C; Xie X; Ao Y; Wang H
[Ad] Address:Department of Pharmacology, School of Basic Medical Sciences, Wuhan University, Wuhan 430071, China; Department of Pharmacy, Wuhan No. 1 Hospital, Wuhan 430022, China.
[Ti] Title:Autophagy as a compensation mechanism participates in ethanol-induced fetal adrenal dysfunction in female rats.
[So] Source:Toxicol Appl Pharmacol;, 2018 Mar 07.
[Is] ISSN:1096-0333
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Autophagy plays a vital role in embryonic development and cell differentiation. Our previous study demonstrated that prenatal ethanol exposure (PEE) resulted in intrauterine growth retardation (IUGR) and adrenal developmental toxicities in rat offspring. The present study focused on PEE-induced autophagy as an underlying mechanism and its biological significance in female fetal rats. Female fetuses in the PEE group exhibited lower body weights and suffered adrenal structural abnormalities compared to the controls. Cell proliferation was inhibited, the insulin-like growth factor 1 (IGF1) pathway was reduced, and autophagy was activated in the glands of female fetal rats. Ethanol increased the ratio of microtubule-associated protein light chain 3 beta-II (LC3ß-II) to LC3ß-I in vitro, and it reduced cortisol levels in time- and concentration-dependent manners in human adrenocortical carcinoma cells (NCI-H295A). Bafilomycin A1 inhibited autophagy, steroidogenic factor 1 (SF1) protein and steroidogenesis in the present study. Rapamycin with ethanol up-regulated autophagy and SF1 expression and activated steroidogenesis when compared with ethanol alone. In addition, ethanol inhibited IGF1 receptor (IGF1R) and phospho-mTOR (Ser2448) expression in a concentration-dependent manner. These results demonstrate that PEE activated autophagy in fetal adrenal glands, and the underlying mechanism may be associated with inhibition of the IGF1R/phospho-mTOR (Ser2448) pathway. Autophagy may be a compensatory mechanism for the PEE-induced inhibition of fetal adrenal steroidogenesis to maintain fetal adrenal development.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 4176 MEDLINE  
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[PMID]: 29523633
[Au] Autor:Brue T; Amodru V; Castinetti F
[Ad] Address:T Brue, Endocrinology, Assistance Publique - Hôpitaux de Marseille (AP-HM) La Timone and Aix-Marseille University, Marseille, France thierry.brue@ap-hm.fr.
[Ti] Title:MANAGEMENT OF ENDOCRINE DISEASE: Management of Cushing's syndrome during Pregnancy: solved and unsolved questions.
[So] Source:Eur J Endocrinol;, 2018 Mar 09.
[Is] ISSN:1479-683X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:With fewer than 200 reported cases, Cushing's syndrome (CS) in pregnancy remains a diagnostic and therapeutic challenge. In normal pregnancies, misleading signs may be observed such as striae or hypokalemia, while plasma cortisol and urinary free cortisol may rise up to 2-3-fold. While the dexamethasone suppression test is difficult to use, reference values for salivary cortisol appear valid. The predominant cause is adrenal adenoma (sometimes without decreased ACTH), rather than Cushing's disease. There are considerable imaging pitfalls in Cushing's disease. Aberrant receptors may, in rare cases, lead to increased cortisol production during pregnancy in response to HCG, LHRH, glucagon, vasopressin or after a meal. Adrenocortical carcinoma (ACC) is rare and has poor prognosis. Active CS during pregnancy is associated with a high rate of maternal complications: hypertension or preeclampsia, diabetes, fractures; more rarely, cardiac failure, psychiatric disorders, infection and maternal death. Increased fetal morbidity includes prematurity, intrauterine growth retardation, and less prevalently stillbirth, spontaneous abortion, intrauterine death, and hypoadrenalism. Therapy is also challenging. Milder cases can be managed conservatively by controlling comorbidities. Pituitary or adrenal surgery should ideally be performed during the second trimester and patients should then be treated for adrenal insufficiency. Experience with anticortisolic drugs is limited. Metyrapone was found to allow control of hypercortisolism, with a risk of worsening hypertension. Cabergoline may be an alternative option. The use of other drugs is not advised because of potential teratogenicity and/or lack of information. Non-hormonal (mechanical) contraception is recommended until sustained biological remission is obtained.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 4176 MEDLINE  
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[PMID]: 29377868
[Au] Autor:Shiroky JS; Lerner-Ellis JP; Govindarajan A; Urbach DR; Devon KM
[Ad] Address:Department of Surgery, University of Toronto, Toronto, Canada.
[Ti] Title:Characteristics of Adrenal Masses in Familial Adenomatous Polyposis.
[So] Source:Dis Colon Rectum;, 2018 Jan 24.
[Is] ISSN:1530-0358
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Adrenal masses are a known extraintestinal manifestation of familial adenomatous polyposis. However, the literature on this association is largely confined to case reports. OBJECTIVE: This study aimed to determine the characteristics of adrenal masses in familial adenomatous polyposis and their clinical significance, as well as to estimate their prevalence. Mutational analysis was conducted to determine if any potential genotype-phenotype correlations exist. DESIGN: This is a retrospective cohort study. SETTING: Analysis included all patients meeting the criteria of classic familial adenomatous polyposis who were registered with the Familial Gastrointestinal Cancer Registry, a national Canadian database. PATIENTS: Appropriate imaging or autopsy reports were available in 311 registry patients. Patients with adrenal metastases were excluded. OUTCOME MEASURES: Data collection included demographic data, mutation genotype, adrenal mass characteristics, surgical interventions and mortality. RESULTS: The prevalence of adrenal masses was 16% (n = 48/311). The median age at diagnosis of adrenal mass was 45 years. The median diameter of adrenal mass at diagnosis was 1.7 cm (interquartile range, 1.4-3.0) with a median maximal diameter of 2.5 cm (interquartile range, 1.7-4.1) with median imaging follow-up of 48 months. The majority of adrenal masses were benign (97%, n = 61/63). Surgery was performed on 7 patients because of concerns for size, malignancy, or hormonal secretion. One adrenal-related death was due to an adrenocortical carcinoma. Mutation analysis did not identify any specific genotype-phenotype correlations. LIMITATIONS: There were incomplete or insufficient endocrinology data available in the registry to allow for the analysis of hormone secretion patterns. CONCLUSIONS: Adrenal masses are approximately twice as prevalent in the familial adenomatous polyposis population as in previous studies of the general population. Nearly all mutations led to truncation of the APC gene; however, there was no genetic signature to help predict those at increased risk. The majority of adrenal lesions identified were of benign etiology; thus, an intensive management or surveillance strategy with imaging screening is likely unwarranted. See Video Abstract at http://links.lww.com/DCR/A507.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1097/DCR.0000000000001008

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[PMID]: 29192018
[Au] Autor:Pape E; Feliu C; Yéléhé-Okouma M; Colling N; Djerada Z; Gambier N; Weryha G; Scala-Bertola J
[Ad] Address:Department of Clinical Pharmacology and Toxicology, University Hospital of Nancy, Nancy, France.
[Ti] Title:High-Dose Mitotane-Induced Encephalopathy in the Treatment of Adrenocortical Carcinoma.
[So] Source:Oncologist;23(3):389-390, 2018 Mar.
[Is] ISSN:1549-490X
[Cp] Country of publication:United States
[La] Language:eng
[Pt] Publication type:LETTER
[Em] Entry month:1712
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review
[do] DOI:10.1634/theoncologist.2017-0426

  5 / 4176 MEDLINE  
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[PMID]: 29506536
[Au] Autor:Kou K; Zhang H; Zhang C; Xie E; Chen Y; Wang G; Lv G
[Ad] Address:Department of Hepatobiliary and Pancreatic Surgery, Bethune Hospital 1, Changchun, Jilin, 130021, China.
[Ti] Title:A case of adrenocortical carcinoma accompanying secondary acute adrenal hypofunction postoperation.
[So] Source:World J Surg Oncol;16(1):43, 2018 Mar 05.
[Is] ISSN:1477-7819
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Adrenocortical carcinoma (ACC) is a rare, heterogeneous malignancy with a poor prognosis. ACCs are classified as functioning and non-functioning. The pathogenesis of ACC remains elusive, and diagnosis of ACC is currently based on pathology. In the absence of other effective approaches, surgical resection is the preferred treatment option. CASE PRESENTATION: Here, we report a case of ACC in the retroperitoneum. The patient underwent radical adrenalectomy and remained disease-free throughout a 6-month follow-up. CONCLUSIONS: Radical surgical resection is an efficient therapy for ACC, and hydrocortisone can be used to alleviate symptoms of secondary acute adrenal hypofunction.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.1186/s12957-018-1326-5

  6 / 4176 MEDLINE  
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[PMID]: 29342266
[Au] Autor:Elhassan YS; Idkowiak J; Smith K; Asia M; Gleeson H; Webster R; Arlt W; O'Reilly MW
[Ad] Address:Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, United Kingdom.
[Ti] Title:Causes, Patterns, and Severity of Androgen Excess in 1205 Consecutively Recruited Women.
[So] Source:J Clin Endocrinol Metab;103(3):1214-1223, 2018 Mar 01.
[Is] ISSN:1945-7197
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Context: Androgen excess in women is predominantly due to underlying polycystic ovary syndrome (PCOS). However, there is a lack of clarity regarding patterns and severity of androgen excess that should be considered predictive of non-PCOS pathology. Objective: We examined the diagnostic utility of simultaneous measurement of serum dehydroepiandrosterone sulfate (DHEAS), androstenedione (A4), and testosterone (T) to delineate biochemical signatures and cutoffs predictive of non-PCOS disorders in women with androgen excess. Design: Retrospective review of all women undergoing serum androgen measurement at a large tertiary referral center between 2012 and 2016. Serum A4 and T were measured by tandem mass spectrometry and DHEAS by immunoassay. Patients with at least one increased serum androgen underwent phenotyping by clinical notes review. Results: In 1205 women, DHEAS, A4, and T were measured simultaneously. PCOS was the most common diagnosis in premenopausal (89%) and postmenopausal women (29%). A4 was increased in all adrenocortical carcinoma (ACC) cases (n = 15) and T in all ovarian hyperthecosis (OHT) cases (n = 7); all but one case of congenital adrenal hyperplasia (CAH; n = 18) were identified by increased levels of A4 and/or T. In premenopausal women, CAH was a prevalent cause of severe A4 (59%) and T (43%) excess; severe DHEAS excess was predominantly due to PCOS (80%). In postmenopausal women, all cases of severe DHEAS and A4 excess were caused by ACC and severe T excess equally by ACC and OHT. Conclusions: Pattern and severity of androgen excess are important predictors of non-PCOS pathology and may be used to guide further investigations as appropriate.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review
[do] DOI:10.1210/jc.2017-02426

  7 / 4176 MEDLINE  
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[PMID]: 29516499
[Au] Autor:Agosta C; Laugier J; Guyon L; Denis J; Bertherat J; Libé R; Boisson B; Sturm N; Feige JJ; Chabre O; Cherradi N
[Ad] Address:Centre Hospitalier Universitaire Grenoble Alpes, Service d'Endocrinologie, F-38000 Grenoble, France.
[Ti] Title:MiR-483-5p and miR-139-5p promote aggressiveness by targeting N-Myc Downstream-Regulated Gene family members in adrenocortical cancer.
[So] Source:Int J Cancer;, 2018 Mar 08.
[Is] ISSN:1097-0215
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Adrenocortical carcinoma (ACC) is a tumor with poor prognosis in which overexpression of a panel of microRNAs has been associated with malignancy but a very limited number of investigations on their role in ACC pathogenesis have been conducted. We examined the involvement of miR-483-5p and miR-139-5p in adrenocortical cancer aggressiveness. Using bioinformatics predictions and mRNA/miRNA expression profiles, we performed an integrated analysis to identify inversely correlated miRNA-mRNA pairs in ACC. We identified N-Myc Downstream-Regulated Gene family members 2 and 4 (NDRG2 and NDRG4) as targets of miR-483-5p and miR-139-5p, respectively. NDRG2 and NDRG4 expressions were inversely correlated respectively with miR-483-5p and miR-139-5p levels in aggressive ACC samples from two independent cohorts of 20 and 44 ACC. Moreover, upregulation of miR-139-5p and downregulation of NDRG4 demonstrated a striking prognostic value. A direct interaction between miR-483-5p or miR-139-5p and their targets was demonstrated in reporter assays. Downregulation of miR-483-5p or miR-139-5p in the ACC cell lines NCI-H295R and SW13 increased NDRG2 or NDRG4 mRNA and protein expression, compromised adrenocortical cancer cell invasiveness and anchorage-independent growth. MiR-483-5p or miR-139-5p overexpression and NDRG2 or NDRG4 inhibition produce similar changes, which are rescued by NDRG2 or NDRG4 ectopic expression. We established that key factors mediating epithelial-to-mesenchymal transition are downstream effectors of miR-483-5p/NDRG2 and miR-139-5p/NDRG4 pathways. Collectively, our data show for the first time that miR-483-5p/NDRG2 and miR-139-5p/NDRG4 axes promote ACC aggressiveness, with potential implications for prognosis and therapeutic interventions in adrenocortical malignancies. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1002/ijc.31363

  8 / 4176 MEDLINE  
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[PMID]: 29452402
[Au] Autor:Megerle F; Herrmann W; Schloetelburg W; Ronchi CL; Pulzer A; Quinkler M; Beuschlein F; Hahner S; Kroiss M; Fassnacht M; German ACC Study Group
[Ad] Address:Dept. of Internal Medicine I, Division of Endocrinology and Diabetes, University Hospital Würzburg, University of Würzburg, Germany.
[Ti] Title:Mitotane monotherapy in patients with advanced adrenocortical carcinoma.
[So] Source:J Clin Endocrinol Metab;, 2018 Feb 14.
[Is] ISSN:1945-7197
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Context: While mitotane is the only approved drug for the treatment of adrenocortical carcinoma (ACC), data on monotherapy in advanced disease is still scarce. Objective: To assess the efficacy of mitotane in advanced ACC in a contemporary setting and to identify predictive factors. Design/Setting: Multicenter cohort study of three German referral centers. Patients: 127 patients with advanced ACC treated with mitotane monotherapy. Outcome measures: RECIST evaluation. Progression-free and overall survival (PFS, OS) by Kaplan-Meier method. Predictive factors by Cox-regression. Results: Twenty-six patients (20.5%) experienced objective response including three with complete remission. Overall, median PFS was 4.1 months (range 1.0-73) and median OS 18.5 months (range 1.3-220). Multivariate analysis indicated two main predictive factors: low tumor burden (<10 tumoral lesions): hazard ratio (HR) for progression of 0.51(p=0.002) and for death of 0.59(p=0.017), and initiation of mitotane at delayed advanced recurrence: HR 0.35(p<0.001) and 0.34(p<0.001), respectively. Accordingly, 67% of patients with low tumor burden and mitotane initiation ≥360 days after primary diagnosis experienced a clinical benefit (stable disease >180 days). Patients who achieved mitotane levels >14 mg/l had significantly better OS (HR 0.42; p=0.003). Conclusions: With 20.5% the objective response rate was slightly lower than previously reported. However, more than 20% of patients experienced a long-term disease control >1 year. In general, patients with late diagnosis of advanced disease and low tumor burden might especially benefit from mitotane monotherapy, whereas patients with early advanced disease and high tumor burden are probably better candidates for combined therapy of mitotane and cytotoxic drugs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1210/jc.2017-02591

  9 / 4176 MEDLINE  
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[PMID]: 29500765
[Au] Autor:Anderson KL; Adam MA; Thomas SM; Youngwirth L; Stang MT; Scheri RP; Roman SA; Sosa JA
[Ad] Address:Duke University School of Medicine, Durham, NC, USA.
[Ti] Title:Impact of Micro- and Macroscopically Positive Surgical Margins on Survival after Resection of Adrenocortical Carcinoma.
[So] Source:Ann Surg Oncol;, 2018 Mar 02.
[Is] ISSN:1534-4681
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE: Adrenocortical carcinoma (ACC) is a rare, aggressive cancer; complete surgical resection offers the best chance for long-term survival. The impact of surgical margin status on survival is poorly understood. Our objective was to determine the association of margin status with survival. METHODS: Patients with ACC were identified from the National Cancer Data Base, 1998-2012, and stratified based on surgical margin status (negative vs. microscopically positive [+] vs. macroscopically [+]). Univariate/multivariate regression/survival analyses were utilized to determine factors associated with margin status and overall survival (OS). RESULTS: A total of 1553 patients underwent surgery at 589 institutions: 86% had negative, 12% microscopically (+), and 2% macroscopically (+) margins. Those with microscopically (+) and macroscopically (+) margins more often received adjuvant chemotherapy (39.4% macroscopically (+) vs. 38.5% microscopically (+) vs. 25.2% negative margins, p < 0.001). For unadjusted analysis, there was a significant difference in OS between the groups (log-rank p < 0.001), with median survival times of 58 months (95% confidence interval [CI] 49-66) for those with negative margins, 22 months (95% CI 18-34) microscopically (+), and 14 months (95% CI 6-27) macroscopically (+) margins. After adjustment, both microscopically (+) (HR 1.76, p < 0.001) and macroscopically (+) (HR 2.10, p = 0.0019) margin status were associated with compromised survival. CONCLUSIONS: Having micro- or macroscopically (+) margin status after ACC resection is associated with dose-dependent compromised survival. These results underscore the importance of achieving negative surgical margins for optimizing long-term patient outcomes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180303
[Lr] Last revision date:180303
[St] Status:Publisher
[do] DOI:10.1245/s10434-018-6398-5

  10 / 4176 MEDLINE  
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[PMID]: 29371329
[Au] Autor:Kiseljak-Vassiliades K; Zhang Y; Bagby SM; Kar A; Pozdeyev N; Xu M; Gowan K; Sharma V; Raeburn CD; Albuja-Cruz M; Jones KL; Fishbein L; Schweppe RE; Somerset H; Pitts TM; Leong S; Wierman ME
[Ad] Address:Division of EndocrinologyMetabolism and Diabetes, University of Colorado School of Medicine, Aurora, Colorado, USA margaret.wierman@ucdenver.edu katja.kiseljak-vassiliades@ucdenver.edu.
[Ti] Title:Development of new preclinical models to advance adrenocortical carcinoma research.
[So] Source:Endocr Relat Cancer;25(4):437-451, 2018 Apr.
[Is] ISSN:1479-6821
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Adrenocortical cancer (ACC) is an orphan malignancy that results in heterogeneous clinical phenotypes and molecular genotypes. There are no curative treatments for this deadly cancer with 35% survival at five years. Our understanding of the underlying pathobiology and our ability to test novel therapeutic targets has been limited due to the lack of preclinical models. Here, we report the establishment of two new ACC cell lines and corresponding patient-derived xenograft (PDX) models. CU-ACC1 cell line and PDX were derived from a perinephric metastasis in a patient whose primary tumor secreted aldosterone. CU-ACC2 cell line and PDX were derived from a liver metastasis in a patient with Lynch syndrome. Short tandem repeat profiling confirmed consistent matches between human samples and models. Both exomic and RNA sequencing profiling were performed on the patient samples and the models, and hormonal secretion was evaluated in the new cell lines. RNA sequencing and immunohistochemistry confirmed the expression of adrenal cortex markers in the PDXs and human tumors. The new cell lines replicate two of the known genetic models of ACC. CU-ACC1 cells had a mutation in and secreted cortisol but not aldosterone. CU-ACC2 cells had a mutation and loss of consistent with the patient's known germline mutation causing Lynch syndrome. Both cell lines can be transfected and transduced with similar growth rates. These new preclinical models of ACC significantly advance the field by allowing investigation of underlying molecular mechanisms of ACC and the ability to test patient-specific therapeutic targets.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180303
[Lr] Last revision date:180303
[St] Status:In-Data-Review
[do] DOI:10.1530/ERC-17-0447


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