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Tumor expression studies indicate that HEM-1 is unlikely to be the active factor in oncogenic osteomalacia.

Abstract
HEM-1 was isolated as a putative factor responsible for oncogenic osteomalacia by Kumar et al. (Proc Assoc Am Phys 107:296-305; 1995). The cDNA was identified on the basis of PTH-like immunoreactivity; however, no studies have been reported of the expression of HEM-1 mRNA in oncogenic osteomalacia tumors. In this study, expression of HEM-1 mRNA was investigated in two oncogenic osteomalacia tumors and in a series of normal tissues. An HEM-1 PCR product was amplified from a cDNA library from one of the tumors, with six base changes identified, as compared with the published sequence. No expression was detected, however, in the oncogenic osteomalacia tumors either by Northern blot analysis or by reverse transcriptase PCR. This indicates that, although a region of HEM-1 sequence is present in the tumor cell cDNA library, any HEM-1 expression must be at very low levels. It is unlikely, therefore, that the HEM-1 product is the active factor responsible for oncogenic osteomalacia. In the normal tissues examined, human placenta, fibroblasts, parathyroid gland, liver, fetal bone, and rat kidney cortex, HEM-1 mRNA was not detected, suggesting that it does not have a physiological role in these tissues.
AuthorsA E Nelson, R S Mason, J J Hogan, T Diamond, B G Robinson
JournalBone (Bone) Vol. 23 Issue 6 Pg. 549-53 (Dec 1998) ISSN: 8756-3282 [Print] United States
PMID9855464 (Publication Type: Case Reports, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • DNA, Neoplasm
  • HEM-1 phosphate transport inhibitor
  • Neoplasm Proteins
  • RNA, Messenger
Topics
  • Adenocarcinoma (complications, metabolism, pathology)
  • Aged
  • Animals
  • Blotting, Northern
  • DNA, Neoplasm (analysis)
  • Hemangiopericytoma (complications, metabolism, pathology)
  • Humans
  • Male
  • Middle Aged
  • Neoplasm Proteins (genetics, metabolism)
  • Osteomalacia (etiology, genetics, metabolism)
  • Prostatic Neoplasms (complications, metabolism, pathology)
  • RNA, Messenger (metabolism)
  • Rats
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tumor Cells, Cultured

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