|
|
 Previous Article | Table of Contents | Next Article 
Tumor cells are the site of erythropoietin synthesis in human renal cancers
associated with polycythemia
JL Da Silva, C Lacombe, P Bruneval, N Casadevall, M Leporrier, JP Camilleri, J Bariety, P Tambourin and B Varet
Institut National de la Sante et de la Recherche Medicale, Hopital
Broussais, Paris, France.
One to five percent of human renal cell carcinomas are associated with
polycythemia. It is generally assumed that polycythemia results from the
secretion of erythropoietin (Epo) by the malignant cells. However, there is
no direct proof supporting this hypothesis. Three patients with typical
renal adenocarcinoma and polycythemia were studied. All three exhibited
high Epo serum levels as measured by radioimmunoassay (RIA). A strong Epo
signal was observed on Northern blot analysis of total RNA extracted from
the renal tumors. The Epo message seemed to be of normal size and no Epo
gene rearrangement was observed with the restriction enzymes tested. Using
the in situ hybridization technique, a significant labeling was constantly
observed on the tumor cells. Immunohistochemical studies showed that these
tumor cells, known to be of tubular origin, were labeled by an
anti-cytokeratin antibody and therefore were of epithelial nature. Thus,
this study demonstrated that malignant cells of tubular origin were able to
produce Epo constitutively, whereas in the mouse hypoxic kidney,
peritubular cells (probably capillary endothelial cells) were the major
site of Epo synthesis.
Volume 75,
Issue 3,
pp. 577-582,
02/01/1990
Copyright © 1990 by The American Society of Hematology
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
E. B. Rankin, D. F. Higgins, J. A. Walisser, R. S. Johnson, C. A. Bradfield, and V. H. Haase
Inactivation of the Arylhydrocarbon Receptor Nuclear Translocator (Arnt) Suppresses von Hippel-Lindau Disease-Associated Vascular Tumors in Mice
Mol. Cell. Biol.,
April 15, 2005;
25(8):
3163 - 3172.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. Hopfl, O. Ogunshola, and M. Gassmann
HIFs and tumors--causes and consequences
Am J Physiol Regulatory Integrative Comp Physiol,
April 1, 2004;
286(4):
R608 - R623.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Y. Yasuda, Y. Fujita, T. Matsuo, S. Koinuma, S. Hara, A. Tazaki, M. Onozaki, M. Hashimoto, T. Musha, K. Ogawa, et al.
Erythropoietin regulates tumour growth of human malignancies
Carcinogenesis,
June 1, 2003;
24(6):
1021 - 1029.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Y. D. Pastore, J. Jelinek, S. Ang, Y. Guan, E. Liu, K. Jedlickova, L. Krishnamurti, and J. T. Prchal
Mutations in the VHL gene in sporadic apparently congenital polycythemia
Blood,
February 15, 2003;
101(4):
1591 - 1595.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. S. Wiesener, M. Seyfarth, C. Warnecke, J. S. Jurgensen, C. Rosenberger, N. V. Morgan, E. R. Maher, U. Frei, and K.-U. Eckardt
Paraneoplastic erythrocytosis associated with an inactivating point mutation of the von Hippel-Lindau gene in a renal cell carcinoma
Blood,
May 15, 2002;
99(10):
3562 - 3565.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
V. H. Haase, J. N. Glickman, M. Socolovsky, and R. Jaenisch
Vascular tumors in livers with targeted inactivation of the von Hippel-Lindau tumor suppressor
PNAS,
February 13, 2001;
98(4):
1583 - 1588.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. L. Ebert and H. F. Bunn
Regulation of the Erythropoietin Gene
Blood,
September 15, 1999;
94(6):
1864 - 1877.
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Krieg, H. H. Marti, and K. H. Plate
Coexpression of Erythropoietin and Vascular Endothelial Growth Factor in Nervous System Tumors Associated With von Hippel-Lindau Tumor Suppressor Gene Loss of Function
Blood,
November 1, 1998;
92(9):
3388 - 3393.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
