|
|
 Previous Article | Table of Contents | Next Article 
Blood, 15 May 2002, Vol. 99, No. 10, pp. 3851-3853
BRIEF REPORT
Paradoxical secondary polycythemia in von Hippel-Lindau
patients treated with anti-vascular endothelial growth factor
receptor therapy
Stéphane Richard,
Laure Croisille,
Jeannine Yvart,
Nicole Casadeval,
Pascal Eschwège,
Nozar Aghakhani,
Philippe David,
Alain Gaudric,
Paul Scigalla, and
Olivier Hermine
From Génétique Oncologique EPHE, UPRESS
1601, Service d'Urologie, Laboratoire d'Hématologie, Service de
Biophysique et Médecine Nucléaire, and Service de
Neurochirurgie, CHU, Le Kremlin-Bicêtre; Service de
Néphrologie, Service d'Hématologie Clinique, and CNRS UMR
8603, Hôpital Necker, Paris; Laboratoire d'Hématologie,
Hôtel-Dieu, Paris; Service d'Ophtalmologie, Hôpital
Lariboisière, Paris, France; and Sugen Inc, San
Francisco, CA.
Von Hippel-Lindau (VHL) disease is a dominantly inherited familial
cancer syndrome caused by germline mutations in the VHL tumor-suppressor gene. Central nervous system (CNS) and retinal hemangioblastomas are highly vascular tumors that are hallmarks of the
disease. These tumors overexpress vascular endothelial growth factor
(VEGF) and represent a potential target for anti-angiogenic drugs. We
observed, after 3 to 4 months of treatment, secondary paradoxical
polycythemia in 3 VHL patients with CNS or retinal hemangioblastomas
treated by the anti-VEGF receptor SU5416. Hematocrit was normal before
the beginning of the trial, and no progression of hemangioblastomas was
observed. Polycythemia vera and all known causes of secondary
polycythemia were also ruled out. Polycythemia has never been reported
in current SU5416 trials for advanced malignancies and could express a
specific action on red blood cell precursors occurring only in the
absence of a functional VHL gene. These findings could also affect the
inclusion of VHL patients with pre-existing polycythemia in future
anti-VEGF receptor trials.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
D. T. Alexandrescu
In Reply
J. Clin. Oncol.,
March 10, 2009;
27(8):
1340 - 1342.
[Full Text]
[PDF]
|
|
|
|
|
|
|
I. Alexandre, B. Billemont, J. B. Meric, S. Richard, and O. Rixe
Axitinib Induces Paradoxical Erythropoietin Synthesis in Metastatic Renal Cell Carcinoma
J. Clin. Oncol.,
January 20, 2009;
27(3):
472 - 473.
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. T. Alexandrescu and C. A. Dasanu
In Reply
J. Clin. Oncol.,
January 20, 2009;
27(3):
473 - 474.
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. Schuch, M. de Wit, J. Holtje, E. Laack, G. Schilling, D. K. Hossfeld, W. Fiedler, P. Scigalla, and M. S. Jacobs
Difficult Diagnostic Cases: CASE 2. Hemangioblastomas: Diagnosis of von Hippel-Lindau Disease and Antiangiogenic Treatment With SU5416
J. Clin. Oncol.,
May 20, 2005;
23(15):
3624 - 3626.
[Full Text]
[PDF]
|
|
|
|
|
|
|
W. Y. Kim and W. G. Kaelin
Role of VHL Gene Mutation in Human Cancer
J. Clin. Oncol.,
December 15, 2004;
22(24):
4991 - 5004.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. V. Heymach, J. Desai, J. Manola, D. W. Davis, D. J. McConkey, D. Harmon, D. P. Ryan, G. Goss, T. Quigley, A. D. Van den Abbeele, et al.
Phase II Study of the Antiangiogenic Agent SU5416 in Patients with Advanced Soft Tissue Sarcomas
Clin. Cancer Res.,
September 1, 2004;
10(17):
5732 - 5740.
[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]
|
|
|
|
|
|
|
A. Tefferi
Polycythemia Vera: A Comprehensive Review and Clinical Recommendations
Mayo Clin. Proc.,
February 1, 2003;
78(2):
174 - 194.
[Abstract]
[PDF]
|
|
|
|
|
