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J Clin Endocrinol Metab. 2006 Feb;91(2):580-3. Epub 2005 Nov 1.

Hypercalcemia of malignancy due to ectopic transactivation of the parathyroid hormone gene.

Author information

1
Section of Endocrinology and Metabolism, Department of Medicine, Yale University School of Medicine, TAC S131, 333 Cedar Street, New Haven, CT 06520-8020, USA.

Abstract

CONTEXT:

The physiology of PTH is well described, but regulation of PTH gene expression remains enigmatic. This is, at least in part, because of a lack of suitable cell culture systems.

OBJECTIVE, DESIGN, SETTING, PATIENTS, INTERVENTIONS, AND MAIN OUTCOME MEASURES:

We report a case of severe hyperparathyroidism resulting from the ectopic production of PTH by a pancreatic malignancy. Cells from the primary tumor (PEPP1 cells) were established in culture to examine the etiology of ectopic PTH gene expression in this patient.

RESULTS AND CONCLUSIONS:

We failed to find amplification or rearrangement of the PTH gene but documented hypomethylation of the PTH promoter in tumor tissue. We found that PEPP1 cells support expression of a reporter gene containing regulatory sequences from the human PTH gene promoter. Therefore, this is the first report documenting ectopic PTH production by a tumor as the result of transactivation of the PTH gene. PEPP1 cells may be useful for future studies aimed at elucidating the details of PTH gene regulation.

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PMID:
16263810
DOI:
10.1210/jc.2005-2095
[Indexed for MEDLINE]

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