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1. OR12-3 Identification of Predictive Criteria for the Primary Bilateral Macronodular Adrenal Hyperplasia Gene ARMC5: A European Series of 352 Unselected Patients.

2. OR04-3 Genetic Alterations of ARMC5 and KDM1A Are Associated With Different Expression Profiles of Illegitimate Receptors in Primary Bilateral Macronodular Adrenal Hyperplasia

3. Noninvasive Prenatal Diagnosis of a Paternally Inherited MEN1 Pathogenic Splicing Variant

4. Clinical Characteristics of 86 Patients with Multiple Endocrine Neoplasia Type 1 (MEN-1) and Insulinomas

6. Frequency and Incidence of Carney Complex Manifestations: A Prospective Multicenter Study With a Three-Year Follow-Up

8. DNA methylation is an independent prognostic marker of survival in adrenocortical cancer

9. DNA methylation is an independent prognostic marker of survival in adrenocortical cancer

12. Pituitary Lesion of Unknown Origin: Think Epithelioid Angiosarcoma

13. DNA methylation is an independent prognostic marker of survival in adrenocortical cancer

15. ARMC5Mutations in a Large Cohort of Primary Macronodular Adrenal Hyperplasia: Clinical and Functional Consequences

17. A Concomitant False-Negative18F-FDG PET Imaging in an Adrenocortical Carcinoma and a High Uptake in a Corresponding Liver Metastasis

18. Outpatient Thyroid Remnant Ablation Using Repeated Low 131-Iodine Activities (740 MBq/20 mCi × 2) in Patients with Low-Risk Differentiated Thyroid Cancer

19. Wnt/β-Catenin Pathway Activation in Adrenocortical Adenomas Is Frequently due to Somatic CTNNB1-Activating Mutations, Which Are Associated with Larger and Nonsecreting Tumors: A Study in Cortisol-Secreting and -Nonsecreting Tumors

20. Frequent Phosphodiesterase 11A Gene (PDE11A) Defects in Patients with Carney Complex (CNC) Caused byPRKAR1AMutations:PDE11AMay Contribute to Adrenal and Testicular Tumors in CNC as a Modifier of the Phenotype

21. Wnt/β-Catenin Pathway Activation in Adrenocortical Adenomas Is Frequently due to Somatic CTNNB1-Activating Mutations, Which Are Associated with Larger and Nonsecreting Tumors: A Study in Cortisol-Secreting and -Nonsecreting Tumors

22. Systematic Analysis of G Protein-Coupled Receptor Gene Expression in Adrenocorticotropin-Independent Macronodular Adrenocortical Hyperplasia Identifies Novel Targets for Pharmacological Control of Adrenal Cushing’s Syndrome

23. Management of Cushing’s Syndrome due to Ectopic Adrenocorticotropin Secretion with 1,Ortho-1, Para′-Dichloro-Diphenyl-Dichloro-Ethane: Findings in 23 Patients from a Single Center

24. Adrenocortical Tumor with Two Distinct Elements Revealed by Combined 18F-Fluorodeoxyglucose Positron Emission Tomography and 131I Nor-Cholesterol Scintigraphy

25. The Paradoxical Increase in Cortisol Secretion Induced by Dexamethasone in Primary Pigmented Nodular Adrenocortical Disease Involves a Glucocorticoid Receptor-Mediated Effect of Dexamethasone on Protein Kinase A Catalytic Subunits

26. Mutations in Regulatory Subunit Type 1A of Cyclic Adenosine 5′-Monophosphate-Dependent Protein Kinase (PRKAR1A): Phenotype Analysis in 353 Patients and 80 Different Genotypes

27. 18F-Fluorodeoxyglucose Positron Emission Tomography for the Diagnosis of Adrenocortical Tumors: A Prospective Study in 77 Operated Patients

29. Wnt/β-Catenin and 3′,5′-Cyclic Adenosine 5′-Monophosphate/Protein Kinase A Signaling Pathways Alterations and Somatic β-Catenin Gene Mutations in the Progression of Adrenocortical Tumors

30. Expression of Serotonin7Receptor and Coupling of Ectopic Receptors to Protein Kinase A and Ionic Currents in Adrenocorticotropin-Independent Macronodular Adrenal Hyperplasia Causing Cushing’s Syndrome

32. APRKAR1AMutation Associated with Primary Pigmented Nodular Adrenocortical Disease in 12 Kindreds

33. In Vivo and in Vitro Screening for Illegitimate Receptors in Adrenocorticotropin-Independent Macronodular Adrenal Hyperplasia Causing Cushing’s Syndrome: Identification of Two Cases of Gonadotropin/Gastric Inhibitory Polypeptide-Dependent Hypercortisolism

36. The Ectopic Expression of the Gastric Inhibitory Polypeptide Receptor Is Frequent in Adrenocorticotropin-Independent Bilateral Macronodular Adrenal Hyperplasia, but Rare in Unilateral Tumors

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