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

被引:8
作者
Nelson, AE [1 ]
Mason, RS
Hogan, JJ
Diamond, T
Robinson, BG
机构
[1] Univ Sydney, Royal N Shore Hosp, Kolling Inst Med Res, Dept Mol Genet, St Leonards, NSW 2065, Australia
[2] Univ Sydney, Dept Physiol, Sydney, NSW 2006, Australia
[3] Univ Sydney, Inst Biomed Res, Sydney, NSW 2006, Australia
[4] Univ Sydney, Dept Med, Sydney, NSW 2006, Australia
[5] St George Hosp, Dept Endocrinol, Kogarah, NSW 2217, Australia
基金
英国医学研究理事会;
关键词
oncogenic osteomalacia; HEM-1; hypophosphatemia; phosphaturia; PTH-like;
D O I
10.1016/S8756-3282(98)00136-7
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 HEIM-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, (Bone 23:549-553; 1998) (C) 1998 by Elsevier Science Inc. All rights reserved.
引用
收藏
页码:549 / 553
页数:5
相关论文
共 8 条
  • [1] CHAMBON P, 1984, RECENT PROG HORM RES, V40, P1
  • [2] CHOMCZYNSKI P, 1987, ANAL BIOCHEM, V162, P156, DOI 10.1016/0003-2697(87)90021-2
  • [3] Drezner Marc K., 1996, P319
  • [4] A GENE (PEX) WITH HOMOLOGIES TO ENDOPEPTIDASES IS MUTATED IN PATIENTS WITH X-LINKED HYPOPHOSPHATEMIC RICKETS
    FRANCIS, F
    HENNIG, S
    KORN, B
    REINHARDT, R
    DEJONG, P
    POUSTKA, A
    LEHRACH, H
    ROWE, PSN
    GOULDING, JN
    SUMMERFIELD, T
    MOUNTFORD, R
    READ, AP
    POPOWSKA, E
    PRONICKA, E
    DAVIES, KE
    ORIORDAN, JLH
    ECONS, MJ
    NESBITT, T
    DREZNER, MK
    OUDET, C
    PANNETIER, S
    HANAUER, A
    STROM, TM
    MEINDL, A
    LORENZ, B
    CAGNOLI, M
    MOHNIKE, KL
    MURKEN, J
    MEITINGER, T
    [J]. NATURE GENETICS, 1995, 11 (02) : 130 - 136
  • [5] Kumar R, 1995, P ASSOC AM PHYSICIAN, V107, P296
  • [6] MELTON DA, 1984, NUCLEIC ACIDS RES, V12, P7035, DOI 10.1093/nar/12.18.7035
  • [7] Oncogenic osteomalacia: is there a new phosphate regulating hormone?
    Nelson, AE
    Robinson, BG
    Mason, RS
    [J]. CLINICAL ENDOCRINOLOGY, 1997, 47 (06) : 635 - 642
  • [8] Characteristics of tumor cell bioactivity in oncogenic osteomalacia
    Nelson, AE
    Namkung, HJ
    Patava, J
    Wilkinson, MR
    Chang, ACM
    Reddel, RR
    Robinson, BG
    Mason, RS
    [J]. MOLECULAR AND CELLULAR ENDOCRINOLOGY, 1996, 124 (1-2) : 17 - 23