miR-372 is aberrantly expressed in most parathyroid tumours and might contribute to parathyroid tumourigenesis by inhibiting CDKN1A/p21 and LATS2

2015 ◽  
Author(s):  
Chiara Verdelli ◽  
Irene Forno ◽  
Valentina Vaira ◽  
Vito Guarnieri ◽  
Alfredo Scillitani ◽  
...  
Keyword(s):  
Parathyroid Tumours

Molecular pathogenesis of parathyroid tumours

2018 ◽  
Vol 32 (6) ◽  
pp. 891-908 ◽  
Author(s):  
Luigia Cinque ◽  
Flavia Pugliese ◽  
Antonio Stefano Salcuni ◽  
Alfredo Scillitani ◽  
Vito Guarnieri
Keyword(s):  
Molecular Pathogenesis ◽  
Parathyroid Tumours

Acute change in parathyroid function in primary hyperparathyroidism following ultrasonically guided ethanol injection into solitary parathyroid adenomas

1993 ◽  
Vol 129 (5) ◽  
pp. 377-380 ◽  
Author(s):  
Steen Karstrup ◽  
Laszlo Hegedüs ◽  
Hans H Holm
Keyword(s):  
Primary Hyperparathyroidism ◽  
Normal Serum ◽  
Ultrasound Guided ◽  
Percutaneous Injection ◽  
Ethanol Injection ◽  
Parathyroid Function ◽  
Parathyroid Adenomas ◽  
Acute Change ◽  
Parathyroid Tumours ◽  
Acute Changes

Ultrasonically guided percutaneous injection of 96% ethanol into solitary parathyroid tumours in patients with primary hyperparathyroidism may be used as an alternative to surgery in selected patients. Contrary to surgical parathyroidectomy, the acute changes in parathyroid function following ultrasound-guided chemical parathyroidectomy have never been described. Seven consecutive and highly selected patients with primary hyperparathyroidism were treated with ultrasonically guided injection of ethanol (96%) into solitary and biopsy-verified parathyroid tumours. Basic treatment included a maximum of three injections separated by intervals of 24 h. In six of the seven patients normal serum values of ionized calcium were achieved within 36–120 h (median 36 h) and normal serum values of intact parathyroid hormone within 6–78 h (median 24 h). Three patients received two injections and three patients three injections. One patient remained hypercalcaemic in spite of three injections. Subsequent surgery showed the patient to have two parathyroid adenomas, of which only one had been detected ultrasonically. The present study has demonstrated a fast normalization of parathyroid function following two to three ethanol injections into solitary parathyroid tumours in selected patients with primary hyperparathyroidism.

Percutaneous ethanol injection therapy in the treatment of thyroid and parathyroid diseases

1997 ◽  
Vol 136 (3) ◽  
pp. 240-250 ◽  
Author(s):  
Finn Noe Bennedbæk ◽  
Steen Karstrup ◽  
Laszlo Hegedüs
Keyword(s):  
Standard Therapy ◽  
Thyroid Nodules ◽  
Percutaneous Ethanol Injection ◽  
Ultrasound Guided ◽  
Ethanol Injection ◽  
Experimental Procedure ◽  
Percutaneous Ethanol Injection Therapy ◽  
Ethanol Injection Therapy ◽  
Parathyroid Tumours

Abstract Relevant English language articles published from 1966 to 1995 regarding ethanol therapy in the treatment of thyroid and parathyroid diseases were identified through a MEDLINE search and manual searches of identified articles. The sclerosing properties of ethanol have been recognized for many years and have offered interventional possibilities in the management of various benign as well as malignant lesions. The mechanism of action of ethanol appears to be related to a direct coagulative necrosis and local partial or complete small vessel thrombosis. Ultrasound-guided percutaneous ethanol injection therapy (PEIT) is rapid and performed on an out-patient basis and has now gained wide acceptance due to the accumulating evidence of the efficacy and safety of this therapeutic tool. Yet, there is a lack of prospective, randomized clinical trials comparing PEIT with 131I therapy or surgery with regard to its effects, especially long-term ones and it should therefore still be considered an experimental procedure. In benign endocrine diseases, PEIT has shown promising results in the treatment of autonomous thyroid nodules, benign solitary cold solid as well as cystic thyroid nodules and parathyroid tumours. Its use in pretoxic and toxic thyroid nodules has been evaluated in several uncontrolled studies, all demonstrating a high success rate in spite of the large number of treatments needed. So far efficacy and cost-effectiveness seem inferior to 131I and surgery. Short-term results of PEIT in benign cystic thyroid nodules are convincing with a high cure rate, but no controlled studies with long-term results are available. Preliminary results suggest that PEIT could become an alternative to surgical excision or levothyroxine therapy in the symptomatic solid cold benign thyroid nodule. Ultrasound-guided PEIT of parathyroid tumours has proven to be a useful method in highly selected patients in whom surgery has been found non-attractive and medical treatment ineffective. However, no prospective randomized trials have been published comparing the results of PEIT in parathyroid tumours with conventional surgical and medical treatments. PEIT has never been tested against standard therapy, but seems inferior to 131I and surgery. Side-effects caused by ethanol injection are generally few and transient and are related to the injection into solid nodules rather than cysts. Ethanol injection into solid profund nodules may seriously jeopardize subsequent surgery because of perinodular fibrosis. As an experimental procedure, not yet evaluated sufficiently, it should be reserved for patients who cannot or will not undergo standard therapy. Caution in routine use is advisable. European Journal of Endocrinology 136 240–250

scholarly journals Molecular Alterations in Sporadic Primary Hyperparathyroidism

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Maria Inês Alvelos ◽  
Maria Mendes ◽  
Paula Soares
Keyword(s):  
Primary Hyperparathyroidism ◽  
Molecular Mechanisms ◽  
Benign Lesion ◽  
Protein Overexpression ◽  
Endocrine Disorder ◽  
Molecular Alterations ◽  
Familial Form ◽  
Somatic Alterations ◽  
Sporadic Primary Hyperparathyroidism ◽  
Parathyroid Tumours

Primary hyperparathyroidism (PHPT) is a frequent endocrine disorder characterized by an excessive autonomous production and release of parathyroid hormone (PTH) by the parathyroid glands. This endocrinopathy may result from the development of a benign lesion (adenoma or hyperplasia) or from a carcinoma. Most of the PHPT cases occur sporadically; however, approximately 10% of the patients present a familial form of the disease. The molecular mechanisms underlying the pathogenesis of sporadic PHPT are incompletely understood, even though somatic alterations in MEN1 gene and CCND1 protein overexpression are frequently observed. The MEN1 gene is mutated in about 30% of the parathyroid tumours and the protooncogene CCND1 is implicated in parathyroid neoplasia by rearrangements, leading to an overexpression of CCND1 protein in parathyroid cells. The aim of this work is to briefly update the molecular alterations underlying sporadic primary hyperparathyroidism.

scholarly journals Frequency of somatic MEN1 gene mutations in monoclonal parathyroid tumours of patients with primary hyperparathyroidism

2000 ◽  
pp. 47-54 ◽  
Author(s):  
S Miedlich ◽  
K Krohn ◽  
P Lamesch ◽  
A Muller ◽  
R Paschke
Keyword(s):  
Primary Hyperparathyroidism ◽  
Gene Mutation ◽  
X Chromosome ◽  
Somatic Mutations ◽  
Genetic Defect ◽  
Gene Mutations ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation ◽  
Men1 Gene ◽  
Parathyroid Tumours

OBJECTIVES: Investigation of small numbers of parathyroid tumours by X-chromosome inactivation analysis suggests that the majority of them are monoclonal lesions most likely caused by a somatic mutation. Somatic mutations in the MEN1 gene located on chromosome 11q13 have recently been identified in 12-17% of solitary parathyroid tumours in patients with sporadic primary hyperparathyroidism, and they may be the precipitating genetic defect leading to monoclonal cell proliferation in these tumours. DESIGN: To determine the prevalence of MEN1 gene mutations in monoclonal parathyroid neoplasias we investigated 33 parathyroid tumours of patients with primary hyperparathyroidism for clonality and mutations in the MEN1 gene. METHODS: X-chromosome inactivation analysis was used to assess the clonal status of the tumours, direct sequencing of the complete coding region was applied to identify mutations in the MEN1 gene. RESULTS: Twenty-eight female patients (26 patients with solitary adenoma, 2 patients with hyperplasia) were informative for the polymorphism of the androgen receptor on the X-chromosome and could be tested for inactivation pattern. Nineteen of twenty-six (73%) solitary adenomas were monoclonal. Somatic mutations in the MEN1 gene were identified in nine cases. Six of them were found in the relatively large second exon of the MEN1 gene (A49D, 193del36, 402delC, 482del22, 547delT, W126X). One was found in exon 5 (904del9), one in exon 7 (Y327X) and one in exon 9 (R415X). Of the monoclonal tumours, 5 out of 19 (26%) harboured a somatic MEN1 gene mutation. CONCLUSIONS: In summary, 73% of the solitary parathyroid adenomas were monoclonal. In 26% of the monoclonal tumours a somatic MEN1 gene mutation has been identified. However, for 74% of monoclonal tumours of the parathyroids the underlying genetic defects are still not known.

Loss of heterozygosity in sporadic parathyroid tumours: involvement of chromosome 1 and the MEN1 gene locus in 11q13.

2000 ◽  
Vol 53 (1) ◽  
pp. 85-92 ◽  
Author(s):  
Trisha Dwight ◽  
Stephen Twigg ◽  
Leigh Delbridge ◽  
Fung-Ki Wong ◽  
Filip Farnebo ◽  
...  
Keyword(s):  
Loss Of Heterozygosity ◽  
Gene Locus ◽  
Chromosome 1 ◽  
Men1 Gene ◽  
Parathyroid Tumours

PREOPERATIVE LOCALISATION OF PARATHYROID TUMOURS

The Lancet ◽  
1971 ◽  
Vol 298 (7735) ◽  
pp. 1172-1175 ◽  
Author(s):  
J.L.H O'Riordan ◽  
B.E Kendall ◽  
J.S Woodhead
Keyword(s):  
Parathyroid Tumours ◽  
Preoperative Localisation

Pre-Operative Localisation of Parathyroid Tumours Using Neck Vein Catheterisation and Radioimmunoassay for Parathyroid Hormone: The Glasgow Experience

1983 ◽  
Vol 28 (2) ◽  
pp. 146-152 ◽  
Author(s):  
G. H. Beastall ◽  
N. McKellar ◽  
I. T. Boyle ◽  
S. N. Joffe ◽  
J. S. F. Hutchison ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Renal Osteodystrophy ◽  
Single Site ◽  
Neck Exploration ◽  
Tumour Localisation ◽  
Repeated Surgery ◽  
Parathyroid Tumour ◽  
Parathyroid Hormone Assay ◽  
Parathyroid Tumours

Reliable pre-operative localisation of parathyroid tumours can be of value in surgery for primary hyperparathyroidism, and particularly so where re-exploration of the neck is required. Neck vein catheterisation and parathyroid hormone radioimmunoassay have been suggested as a sensitive means of tumour localisation, and we report our experience of the technique over the last five years. A total of 46 patients with primary hyperparathyroidism had 50 studies performed with positive localisation and a pre-operative prediction made on 38 occasions (76%). Forty-two operations were carried out and a parathyroid tumour confirmed in 39 cases for a localisation efficiency of 69 per cent. No negative neck exploration followed a positive localisation. Twelve studies were performed in patients with renal osteodystrophy and localisation to a single site was achieved on only three occasions. It is concluded that neck vein catheterisation and parathyroid hormone assay can correctly localise parathyroid tumours in most cases of primary hyperparathyroidism, but is is suggested that its use be restricted to selected cases such as those subjects with previous negative neck exploration or patients for whom prolonged or repeated surgery may be a particular hazard.

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