Tumors Associated With Oncogenic Osteomalacia Express Genes Important in Bone and Mineral Metabolism

Oncogenic osteomalacia (OOM) is associated with primitive mesenchymal tumors that secrete phosphaturic factors resulting in low serum concentrations of phosphate and calcitriol, phosphaturia, and defective bone mineralization. To identify overexpressed genes in these tumors, we compared gene express...

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Published inJournal of bone and mineral research Vol. 17; no. 6; pp. 1102 - 1110
Main Authors De Beur, Suzanne M. Jan, Finnegan, Richard B., Vassiliadis, John, Cook, Brian, Barberio, Dana, Estes, Scott, Manavalan, Partha, Petroziello, Joseph, Madden, Stephen L., Cho, Justin Y., Kumar, Rajiv, Levine, Michael A., Schiavi, Susan C.
Format Journal Article
LanguageEnglish
Published Washington, DC John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR) 01.06.2002
American Society for Bone and Mineral Research
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Abstract Oncogenic osteomalacia (OOM) is associated with primitive mesenchymal tumors that secrete phosphaturic factors resulting in low serum concentrations of phosphate and calcitriol, phosphaturia, and defective bone mineralization. To identify overexpressed genes in these tumors, we compared gene expression profiles of tumors resected from patients with OOM and histologically similar control tumors using serial analysis of gene expression (SAGE). Three hundred and sixty‐four genes were expressed at least twofold greater in OOM tumors compared with control tumors. A subset of 67 highly expressed genes underwent validation with an extended set of OOM and control tumors using array analysis or reverse‐transcription polymerase chain reaction (RT‐PCR). Ten of these validated genes were consistently overexpressed in all OOM tumors relative to control tumors. Strikingly, genes with roles in bone matrix formation, mineral ion transport, and bone mineralization were highly expressed in the OOM tumors.
AbstractList Abstract Oncogenic osteomalacia (OOM) is associated with primitive mesenchymal tumors that secrete phosphaturic factors resulting in low serum concentrations of phosphate and calcitriol, phosphaturia, and defective bone mineralization. To identify overexpressed genes in these tumors, we compared gene expression profiles of tumors resected from patients with OOM and histologically similar control tumors using serial analysis of gene expression (SAGE). Three hundred and sixty-four genes were expressed at least twofold greater in OOM tumors compared with control tumors. A subset of 67 highly expressed genes underwent validation with an extended set of OOM and control tumors using array analysis or reverse-transcription polymerase chain reaction (RT-PCR). Ten of these validated genes were consistently overexpressed in all OOM tumors relative to control tumors. Strikingly, genes with roles in bone matrix formation, mineral ion transport, and bone mineralization were highly expressed in the OOM tumors.
Oncogenic osteomalacia (OOM) is associated with primitive mesenchymal tumors that secrete phosphaturic factors resulting in low serum concentrations of phosphate and calcitriol, phosphaturia, and defective bone mineralization. To identify overexpressed genes in these tumors, we compared gene expression profiles of tumors resected from patients with OOM and histologically similar control tumors using serial analysis of gene expression (SAGE). Three hundred and sixty-four genes were expressed at least twofold greater in OOM tumors compared with control tumors. A subset of 67 highly expressed genes underwent validation with an extended set of OOM and control tumors using array analysis or reverse-transcription polymerase chain reaction (RT-PCR). Ten of these validated genes were consistently overexpressed in all OOM tumors relative to control tumors. Strikingly, genes with roles in bone matrix formation, mineral ion transport, and bone mineralization were highly expressed in the OOM tumors.
Author Petroziello, Joseph
Manavalan, Partha
Kumar, Rajiv
Levine, Michael A.
Cook, Brian
Estes, Scott
Vassiliadis, John
Barberio, Dana
Cho, Justin Y.
De Beur, Suzanne M. Jan
Madden, Stephen L.
Finnegan, Richard B.
Schiavi, Susan C.
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Issue 6
Keywords Human
Hydroelectrolytic balance disorder
Diseases of the osteoarticular system
Nutrition disorder
Mesenchyma
Vitamin deficiency
Bone disease
Gene expression
Metabolism
Density
Inorganic element
Osteoarticular system
Metabolic disorder
Hypophosphatemia
Tumor
Bone
Osteomalacia
Tumor cell
Nutritional status
Language English
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Notes Dr. Levine is a co‐inventor with Genzyme of certain DNA sequences. He also has patents pending. All other authors have no conflict of interest
Dr. Kumar has a grant from Genzyme
Dr. Finnegan, Dr. Vassilladis, Dr. Cook, Dr. Manavalan, and Dr. Schiavi have financial interests in the form of stock ownership
Dr. Jan de Beur serves as a consultant to Genzyme. She is also a co‐inventor with Genzyme scientists of a patent derived from this work
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PublicationTitle Journal of bone and mineral research
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American Society for Bone and Mineral Research
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Snippet Oncogenic osteomalacia (OOM) is associated with primitive mesenchymal tumors that secrete phosphaturic factors resulting in low serum concentrations of...
Abstract Oncogenic osteomalacia (OOM) is associated with primitive mesenchymal tumors that secrete phosphaturic factors resulting in low serum concentrations...
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SubjectTerms Base Sequence
Biological and medical sciences
Bone and Bones - metabolism
Bone Neoplasms - genetics
Bone Neoplasms - metabolism
Calcitriol - metabolism
Calcium - metabolism
Diseases of the osteoarticular system
DNA Primers
gene expression
Gene Expression Profiling
Humans
hypophosphatemia
Medical sciences
mesenchymal tumors
mineral metabolism
osteomalacia
Osteomalacia - genetics
Osteomalacia - metabolism
Parathyroid Hormone - metabolism
Phosphorus - metabolism
Reproducibility of Results
Reverse Transcriptase Polymerase Chain Reaction
Tumors of striated muscle and skeleton
Title Tumors Associated With Oncogenic Osteomalacia Express Genes Important in Bone and Mineral Metabolism
URI https://onlinelibrary.wiley.com/doi/abs/10.1359%2Fjbmr.2002.17.6.1102
https://www.ncbi.nlm.nih.gov/pubmed/12054166
https://search.proquest.com/docview/18404327
https://search.proquest.com/docview/71801662
Volume 17
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