Research Topics
Species | T CarlingSummaryAffiliation: University Hospital Country: Sweden Publications
| Collaborators
|
Detail Information
Publications
Vitamin D receptor alleles b, a, and T: risk factors for sporadic primary hyperparathyroidism (HPT) but not HPT of uremia or MEN 1T Carling
Department of Surgery, Uppsala University Hospital, Sweden
Biochem Biophys Res Commun 231:329-32. 1997..0006-0.0001), whereas HPT of MEN 1 and uremia seemed unrelated to the VDR polymorphisms (p = 0.26-0.96). The results suggest that the VDR alleles b, a, and T are novel risk factors in the essentially uncharacterized pathogenesis of spHPT...- Vitamin D receptor polymorphisms correlate to parathyroid cell function in primary hyperparathyroidismT Carling
Department of Surgery, Uppsala University Hospital, Sweden
J Clin Endocrinol Metab 82:1772-5. 1997..05). As VDR alleles were unrelated to parathyroid intracellular Ca2+, influences of polymorphic VDR alleles on PTH secretion seem to involve mechanisms other than the Ca2+-sensing protein of the parathyroid cell surface... - Vitamin D receptor (VDR) and parathyroid hormone messenger ribonucleic acid levels correspond to polymorphic VDR alleles in human parathyroid tumorsT Carling
Department of Surgery, Uppsala University Hospital, Sweden
J Clin Endocrinol Metab 83:2255-9. 1998..21.6 +/- 2.2 for PTH; both P < 0.005). The lower VDR mRNA levels associated with the b, a, and T alleles may affect the calcitriol-mediated control of parathyroid function and thereby contribute to the development of sporadic pHPT... - Parathyroid MEN1 gene mutations in relation to clinical characteristics of nonfamilial primary hyperparathyroidismT Carling
Department of Surgery, Uppsala University Hospital, Sweden
J Clin Endocrinol Metab 83:2960-3. 1998.... - Familial hypercalcemia and hypercalciuria caused by a novel mutation in the cytoplasmic tail of the calcium receptorT Carling
Department of Surgery, Uppsala University Hospital, Sweden
J Clin Endocrinol Metab 85:2042-7. 2000..The hypercalcemic disorder of the present family is caused by an inactivating point mutation in the cytoplasmic tail of the CaR and displays clinical characteristics atypical of FHH and primary HPT... - Reduced parathyroid vitamin D receptor messenger ribonucleic acid levels in primary and secondary hyperparathyroidismT Carling
Department of Surgery, Uppsala University Hospital, Sweden
J Clin Endocrinol Metab 85:2000-3. 2000..Circulating factors like calcium, PTH, and 1,25(OH)2D3 seem to be less likely candidates mediating the decreased VDR gene expression in HPT... - Mutation of the multiple endocrine neoplasia type 1 gene in nonfamilial, malignant tumors of the endocrine pancreasO Hessman
Department of Surgery, University Hospital, Uppsala, Sweden
Cancer Res 58:377-9. 1998..These findings support the hypothesis that MEN1 gene mutations contribute to the tumorigenesis of nonfamilial, malignant endocrine pancreatic tumors... - Genetic alterations on 3p, 11q13, and 18q in nonfamilial and MEN 1-associated pancreatic endocrine tumorsO Hessman
Department of Surgery, Endocrine Unit, Uppsala University Hospital, Uppsala, Sweden
Genes Chromosomes Cancer 26:258-64. 1999..The data indicate involvement of tumor suppressor genes on 3p and 18q, in addition to the MEN1 gene at 11q13, in the tumorigenesis of both nonfamilial and MEN 1-associated pancreatic endocrine tumors... - The NeiI polymorphism in the cyclin D1 gene and sporadic primary hyperparathyroidismP Correa
Department of Surgical Sciences, Uppsala University Hospital, Sweden
J Intern Med 250:516-20. 2001..Furthermore, a limited study of 28 primary hyperparathyroidism (pHPT) patients displayed a tendency of NciI influence on HPT development. We hypothesized that the NciI polymorphism may relate to a risk of developing pHPT... - Pathophysiology of primary hyperparathyroidismP Hellman
Department of Surgery, Uppsala University, Sweden
Histol Histopathol 15:619-27. 2000..This review summarizes data on regulation of PTH release, dysregulation in HPT, as well as proliferation of parathyroid cells... 
Tumor formation and inactivation of RIZ1, an Rb-binding member of a nuclear protein-methyltransferase superfamilyG Steele-Perkins
The Burnham Institute, La Jolla, California 92037, USA
Genes Dev 15:2250-62. 2001..These data suggest a direct link between tumor formation and the MTase domain of RIZ1 and describe for the first time a tumor susceptibility gene among methyltransferases...- Tissue distribution of human gp330/megalin, a putative Ca(2+)-sensing proteinS Lundgren
Department of Cell Research, Swedish University of Agricultural Science, Uppsala, Sweden
J Histochem Cytochem 45:383-92. 1997..It may constitute a protein of utmost importance to adult and fetal calcium homeostasis, although other important functions may also be coupled to this exceptionally large protein with highly restricted tissue distribution... - A deletion polymorphism in the RIZ gene, a female sex steroid hormone receptor coactivator, exhibits decreased response to estrogen in vitro and associates with low bone mineral density in young Swedish womenE Grundberg
Department of Medical Sciences, Uppsala University, SE 751 85 Uppsala, Sweden
J Clin Endocrinol Metab 89:6173-8. 2004..02), which was evident also after corrections for fat and lean mass (P = 0.03). We conclude that RIZ1 may be a new candidate gene for involvement in the variation seen in BMD... - Parathyroid surgery in familial hyperparathyroid disordersT Carling
Department of Surgery, Yale University School of Medicine, New Haven, CT, USA
J Intern Med 257:27-37. 2005..However, minimally invasive parathyroidectomy (MIP) techniques that have become routine for sporadic HPT at selected institutions may be extrapolated to a subset of cases of familial HPT...