BACKGROUND: Differential diagnosis between adenoma and hyperplasia in primary hyperparathyroidism (pHPT) remains a dilemma. The aim of this study was to assess differences in transcriptional genomic expression profiles between sporadic (nonfamilial) parathyroid hyperplasia (SPH), adenoma, and normal tissue. METHODS: Parathyroid tissue from 12 patients with parathyroid adenoma, 3 with SPH, and 2 with normal glands was selected for analysis. Histopathology was reviewed in all cases, and all patients with adenomas presented normocalcemia for a minimum of 6 months after one gland resection. Hybridizations were performed in a microarray containing 19,968 human cDNA clones including contiguous replicates. Direct comparisons were performed with reverse labeling for every different pooled sample entity. Expression levels were analyzed using the SAM, SMA, LIMMA, Cluster, and PAM packages in the R environment for statistical computing. RESULTS: There were significant statistical differences between SPH and adenomas. In the direct comparison, a total of 200 genes showed differential expression (P < 0.03): 61 genes were upregulated (> 1.65-fold increase) and 139 were downregulated (> 1.58-fold decrease) with a B value > 4.68 (99.08% probability of real differential expression). When SPH was compared to normal parathyroid tissue, 50 genes were differentially expressed: 42 were upregulated (> 1.89) and 8 were downregulated (> 1.7) with a B > 4.26 (98.6% probability of real differential expression). At least 17 genes were differentially expressed and able to discriminate SPH from adenoma or normal tissue. Upregulated genes were related to apoptosis inhibition, cell proliferation, transcriptional activity and cell adhesion, among other activities. Downregulated genes were mainly related to ion channel activity, lipopolysaccharides, prostaglandin-d synthase, and integral membrane proteins. CONCLUSIONS: Our data suggest that SPH and adenoma have a singular molecular signature that, theoretically, could be used for the differential diagnosis of these entities and normal parathyroid tissue.
BACKGROUND: Differential diagnosis between adenoma and hyperplasia in primary hyperparathyroidism (pHPT) remains a dilemma. The aim of this study was to assess differences in transcriptional genomic expression profiles between sporadic (nonfamilial) parathyroid hyperplasia (SPH), adenoma, and normal tissue. METHODS: Parathyroid tissue from 12 patients with parathyroid adenoma, 3 with SPH, and 2 with normal glands was selected for analysis. Histopathology was reviewed in all cases, and all patients with adenomas presented normocalcemia for a minimum of 6 months after one gland resection. Hybridizations were performed in a microarray containing 19,968 human cDNA clones including contiguous replicates. Direct comparisons were performed with reverse labeling for every different pooled sample entity. Expression levels were analyzed using the SAM, SMA, LIMMA, Cluster, and PAM packages in the R environment for statistical computing. RESULTS: There were significant statistical differences between SPH and adenomas. In the direct comparison, a total of 200 genes showed differential expression (P < 0.03): 61 genes were upregulated (> 1.65-fold increase) and 139 were downregulated (> 1.58-fold decrease) with a B value > 4.68 (99.08% probability of real differential expression). When SPH was compared to normal parathyroid tissue, 50 genes were differentially expressed: 42 were upregulated (> 1.89) and 8 were downregulated (> 1.7) with a B > 4.26 (98.6% probability of real differential expression). At least 17 genes were differentially expressed and able to discriminate SPH from adenoma or normal tissue. Upregulated genes were related to apoptosis inhibition, cell proliferation, transcriptional activity and cell adhesion, among other activities. Downregulated genes were mainly related to ion channel activity, lipopolysaccharides, prostaglandin-d synthase, and integral membrane proteins. CONCLUSIONS: Our data suggest that SPH and adenoma have a singular molecular signature that, theoretically, could be used for the differential diagnosis of these entities and normal parathyroid tissue.
Authors: Dmitry I Gabrilovich; Pingyan Cheng; Yuhong Fan; Bin Yu; Ekaterina Nikitina; Allen Sirotkin; Michael Shurin; Tsunehiro Oyama; Yasushi Adachi; Sorena Nadaf; David P Carbone; Arthur I Skoultchi Journal: J Leukoc Biol Date: 2002-08 Impact factor: 4.962
Authors: C Luceri; F Guglielmi; C De Filippo; G Caderni; E Mini; A Biggeri; C Napoli; F Tonelli; F Cianchi; P Dolara Journal: Scand J Gastroenterol Date: 2000-06 Impact factor: 2.423
Authors: Carola J Haven; Viive M Howell; Paul H C Eilers; Robert Dunne; Masayuki Takahashi; Marjo van Puijenbroek; Kyle Furge; Job Kievit; Min-Han Tan; Gert Jan Fleuren; Bruce G Robinson; Leigh W Delbridge; Jeanette Philips; Anne E Nelson; Ulf Krause; Henning Dralle; Cuong Hoang-Vu; Oliver Gimm; Hans Morreau; Deborah J Marsh; Bin T Teh Journal: Cancer Res Date: 2004-10-15 Impact factor: 12.701
Authors: Maria Mizamtsidi; Konstantinos Nastos; Fausto Palazzo; Vasilis Constantinides; Roberto Dina; Megan Farenden; George Mastorakos; Ioannis Vassiliou; Maria Gazouli Journal: In Vivo Date: 2019 Jul-Aug Impact factor: 2.155