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Press Officer and Head of Press and Public Relations

Dr. Stefanie Seltmann
Dr. Stefanie Seltmann

Im Neuenheimer Feld 280
69120 Heidelberg

Phone: +49 6221 422854
Fax: +49 6221 422968

E-Mail: s.seltmann@dkfz.de
or presse@dkfz.de

Recent Press Releases

No. 35 | 28. July 2015 | by Koh

Fatty acid increases performance of cellular powerhouse – Fundamentally new biological signaling pathway discovered

Fatty acid increases performance of cellular powerhouse – Fundamentally new biological signaling pathway discovered

Scientists from the German Cancer Research Center (DKFZ) have discovered an entirely new control mechanism that regulates the function of mitochondria, the powerhouses of the cell. Surprisingly, a fatty acid is playing a key role in this process. The scientists have now reported in the journal Nature that using fatty acid as a food additive improved disease symptoms in flies that suffer from Parkinson’s-like symptoms due to dysfunctional mitochondria.

No. 34 | 23. July 2015 | by AM/FB

Selective agent keeps blood vessels in check

Selective agent keeps blood vessels in check

Blood vessels in the eye that grow out of control and damage the retina may cause blindness in certain affected people. Scientists from the German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ) have now discovered that a molecule, called semaphorin 3C (Sema3C), may halt this process. Sema3C is produced by the body and its normal function is to control the growth of neurons. In an animal model, this protein effectively inhibits pathogenic angiogenesis.

No. 33c3 | 20. July 2015 | by Koh

Researchers discover a possible reason for drug resistance in breast tumors

Researchers discover a possible reason for drug resistance in breast tumors

HER2 membrane proteins play a special role in certain types of breast cancer: amplified levels of HER2 drive unrestricted cell growth. HER2-tailored antibody-based therapeutics aim to prevent cancer cell growth. However, two-thirds of HER2 positive breast cancer patients develop resistance against HER2-targeting drugs. The reason for this is not yet understood. Researchers now found out, that HER2 dimers appeared to be absent from a small sub-population of resting SKBR3 breast cancer cells. This small subpopulation may have self-renewing properties that are resistant to HER2-antibody therapy and thus able to seed new tumor growth.

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