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Journal Article

Overexpression of EagI potassium channels in clinical tumours

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Weseloh,  Rüdiger M.
Molecular biology of neuronal signals, Max Planck Institute of Experimental Medicine, Max Planck Society;

/persons/resource/persons182293

Mello de Queiroz,  Fernanda
Molecular biology of neuronal signals, Max Planck Institute of Experimental Medicine, Max Planck Society;

/persons/resource/persons182388

Sanchez,  Araceli
Molecular biology of neuronal signals, Max Planck Institute of Experimental Medicine, Max Planck Society;

/persons/resource/persons182380

Rubio,  María E.
Molecular biology of neuronal signals, Max Planck Institute of Experimental Medicine, Max Planck Society;

/persons/resource/persons182288

Martin,  Sabine
Molecular biology of neuronal signals, Max Planck Institute of Experimental Medicine, Max Planck Society;

/persons/resource/persons182219

Jenke,  Marc
Molecular biology of neuronal signals, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Stühmer,  Walter
Molecular biology of neuronal signals, Max Planck Institute of Experimental Medicine, Max Planck Society;

/persons/resource/persons182344

Pardo,  Luis A.
Molecular biology of neuronal signals, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Citation

Hemmerlein, B., Weseloh, R. M., Mello de Queiroz, F., Knötgen, H., Sanchez, A., Rubio, M. E., et al. (2006). Overexpression of EagI potassium channels in clinical tumours. Molecular Cancer, 5: 41. doi:10.1186/1476-4598-5-41.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002A-257E-E
Abstract
Background: Certain types of potassium channels (known as Eag1, KCNHO1, Kv10.1) are associated with the production of tumours in patients and in animals. We have now studied the expression pattern of the Eag1 channel in a large range of normal and tumour tissues from different collections utilising molecular biological and immunohistochemical techniques. Results: The use of reverse transcription real-time PCR and specifically generated monoclonal anti-Eag1 antibodies showed that expression of the channel is normally limited to specific areas of the brain and to restricted cell populations throughout the body. Tumour samples, however, showed a significant overexpression of the channel with high frequency (up to 80% depending on the tissue source) regardless of the detection method (staining with either one of the antibodies, or detection of Eag1 RNA). Conclusion: Inhibition of Eag1 expression in tumour cell lines reduced cell proliferation. Eag1 may therefore represent a promising target for the tailored treatment of human tumours. Furthermore, as normal cells expressing Eag1 are either protected by the blood-brain barrier or represent the terminal stage of normal differentiation, Eag1 based therapies could produce only minor side effects.