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Leccia F, Batisse-Lignier M, Sahut-Barnola I, et al. Mouse Models Recapitulating Human Adrenocortical Tumors: What Is Lacking?. Front Endocrinol (Lausanne). 2016;7:93doi: 10.3389/fendo.2016.00093.
Leccia, F., Batisse-Lignier, M., Sahut-Barnola, I., Val, P., Lefrançois-Martinez, A. M., & Martinez, A. (2016). Mouse Models Recapitulating Human Adrenocortical Tumors: What Is Lacking?. Frontiers in endocrinology, 793. https://doi.org/10.3389/fendo.2016.00093
Leccia, Felicia, et al. "Mouse Models Recapitulating Human Adrenocortical Tumors: What Is Lacking?." Frontiers in endocrinology vol. 7 (2016): 93. doi: https://doi.org/10.3389/fendo.2016.00093
Leccia F, Batisse-Lignier M, Sahut-Barnola I, Val P, Lefrançois-Martinez AM, Martinez A. Mouse Models Recapitulating Human Adrenocortical Tumors: What Is Lacking?. Front Endocrinol (Lausanne). 2016 Jul 15;7:93. doi: 10.3389/fendo.2016.00093. eCollection 2016. PMID: 27471492; PMCID: PMC4945639.
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Front Endocrinol (Lausanne). 2016 Jul 15;7:93. doi: 10.3389/fendo.2016.00093. eCollection 2016.

Mouse Models Recapitulating Human Adrenocortical Tumors: What Is Lacking?.

Frontiers in endocrinology

Felicia Leccia, Marie Batisse-Lignier, Isabelle Sahut-Barnola, Pierre Val, A-Marie Lefrançois-Martinez, Antoine Martinez

Affiliations

  1. UMR6293, GReD, INSERM U1103, CNRS, Clermont Université , Clermont-Ferrand , France.
  2. UMR6293, GReD, INSERM U1103, CNRS, Clermont Université, Clermont-Ferrand, France; Endocrinology, Diabetology and Metabolic Diseases Department, Centre Hospitalier Universitaire, School of Medicine, Clermont-Ferrand, France.

PMID: 27471492 PMCID: PMC4945639 DOI: 10.3389/fendo.2016.00093

Abstract

Adrenal cortex tumors are divided into benign forms, such as primary hyperplasias and adrenocortical adenomas (ACAs), and malignant forms or adrenocortical carcinomas (ACCs). Primary hyperplasias are rare causes of adrenocorticotropin hormone-independent hypercortisolism. ACAs are the most common type of adrenal gland tumors and they are rarely "functional," i.e., producing steroids. When functional, adenomas result in endocrine disorders, such as Cushing's syndrome (hypercortisolism) or Conn's syndrome (hyperaldosteronism). By contrast, ACCs are extremely rare but highly aggressive tumors that may also lead to hypersecreting syndromes. Genetic analyses of patients with sporadic or familial forms of adrenocortical tumors (ACTs) led to the identification of potentially causative genes, most of them being involved in protein kinase A (PKA), Wnt/β-catenin, and P53 signaling pathways. Development of mouse models is a crucial step to firmly establish the functional significance of candidate genes, to dissect mechanisms leading to tumors and endocrine disorders, and in fine to provide in vivo tools for therapeutic screens. In this article, we will provide an overview on the existing mouse models (xenografted and genetically engineered) of ACTs by focusing on the role of PKA and Wnt/β-catenin pathways in this context. We will discuss the advantages and limitations of models that have been developed heretofore and we will point out necessary improvements in the development of next generation mouse models of adrenal diseases.

Keywords: PKA; WNT; adrenal; mouse models; tumor

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