Molecular Profiling of Parathyroid Hyperplasia, Adenoma and Carcinoma

Árvai, Kristóf; Nagy, K.; Barti-Juhasz, Helga; Peták, István; Krenács, Tibor; Micsik, Tamás; Végsô, Gyula; Perner, F.; Szende, B.

doi:10.1007/s12253-011-9483-7

Cited by 32 publications

(27 citation statements)

References 18 publications

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“…Parathyroid adenomas and hyperplasias showed overexpression of the FAS gene compared to normal tissue. Hyperplasias demonstrated the highest expression, whereas in adenomas, the expression of the FAS gene was increased compared to normal tissue, but it was lower than in hyperplasias …”

Section: Introductionmentioning

confidence: 83%

“…There are also decoy‐receptors, DcR1 and DcR2, which do not contain a functional cytoplasmic death domain. Studies demonstrated overexpression of TRAIL gene in parathyroid adenomas and hyperplasias compared to normal tissue . The relationship between factors involved in apoptosis and caspases is presented in Figure .…”

Section: Introductionmentioning

confidence: 99%

“…Numerous different mechanisms are responsible for hyperplastic changes: activation of oncogenes, inactivation of tumor‐suppressor genes, epigenetic changes, and disturbance of the balance between growth factors and other transmitter substances, including proteins involved in cell cycle regulation . Although numerous studies on the molecular mechanisms have been developed recently, it is still difficult to differentiate between parathyroid hyperplasia (Figure A), adenoma (Figure B), and carcinoma (Figure C).…”

Section: Introductionmentioning

confidence: 99%

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Molecular profiling in primary hyperparathyroidism

et al. 2014

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Primary hyperparathyroidism (HPT) is one of the most common endocrine disorders, defined by hypersecretion of parathormone. Primary HPT can be caused by adenoma, hyperplasia, and carcinoma. A great amount of mechanisms contribute to the pathogenesis of this disease, such as genetic predispositions because of the germline-inactivating mutations in the multiple endocrine neoplasia type 1 (MEN1) and HRPT2 tumor suppressor genes. Somatic mutations in these genes were found also in sporadic parathyroid neoplasias. Cell cycle regulators, growth factors, apoptosis-inducing ligands, death receptors, and other transmitter substances have also been implicated in the etiology of primary HPT. Parathyroid carcinoma is often misdiagnosed as parathyroid adenoma and long-term survival is conditioned by the extent of the primary surgical resection, therefore, of great interest is the discovery of definitive diagnostic markers for carcinoma. This article presents current state of knowledge of the molecular pathogenesis of primary HPT.

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Section: Introductionmentioning

confidence: 83%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Molecular profiling in primary hyperparathyroidism

et al. 2014

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“…Gene expression profiling of parathyroid adenomas and carcinomas may provide an explanation for the formation of parathyroid carcinomas and aid in the differential diagnosis of these lesions (Arvai et al 2012).…”

Section: Molecular Profilementioning

confidence: 99%

Molecular targeted therapies in adrenal, pituitary and parathyroid malignancies

Angelousi¹,

Dimitriadis²,

Zografos³

et al. 2017

Endocrine-Related Cancer

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Tumourigenesis is a relatively common event in endocrine tissues. Currently, specific guidelines have been developed for common malignant endocrine tumours, which also incorporate advances in molecular targeted therapies (MTT), as in thyroid cancer and in gastrointestinal neuroendocrine malignancies. However, there is little information regarding the role and efficacy of MTT in the relatively rare malignant endocrine tumours mainly involving the adrenal medulla, adrenal cortex, pituitary, and parathyroid glands. Due to the rarity of these tumours and the lack of prospective studies, current guidelines are mostly based on retrospective data derived from surgical, locoregional and ablative therapies, and studies with systemic chemotherapy. In addition, in many of these malignancies the prognosis remains poor with individual patients responding differently to currently available treatments, necessitating the development of new personalised therapeutic strategies. Recently, major advances in the molecular understanding of endocrine tumours based on genomic, epigenomic, and transcriptome analysis have emerged, resulting in new insights into their pathogenesis and molecular pathology. This in turn has led to the use of novel MTTs in increasing numbers of patients. In this review, we aim to present currently existing and evolving data using MTT in the treatment of adrenal, pituitary and malignant parathyroid tumours, and explore the current utility and effectiveness of such therapies and their future evolution.

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“…Gene expression profiling of parathyroid adenomas and carcinomas may provide an explanation for the formation of parathyroid carcinomas and aid the differential diagnosis of these lesions [6,7]. In the current study, we aimed to identify the gene expression profile of parathyroid tumors and investigate potential diagnostic markers.…”

mentioning

confidence: 99%