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The winner of the “Best Paper Award” of Circulation - Michael Jeltsch

The article of Michael Jeltsch and Kari Alitalo has been selected as the 2014 winner of the “Best Paper Award” in the category of Basic Science in Circulation, the journal of the American Heart Association.

The article of Michael Jeltsch and Kari Alitalo is the winner of the "Best Paper Award" of Circulation.

Academy Research Fellow Michael Jeltsch, the group leader in the Translational Cancer Biology Research Program, has been selected as the 2014 winner of the “Best Paper Award” in the category of Basic Science in Circulation, the journal of the American Heart Association.

The title of the winner article is “CCBE1 Enhances Lymphangiogenesis via A Disintegrin and Metalloprotease With Thrombospondin Motifs-3–Mediated Vascular Endothelial Growth Factor-C Activation”.

Circulation is the leading cardiology journal, and the journal’s “Best Paper Award” is determined by its editors, who consider the paper’s importance in the field and altmetrics (“real usage statistics”) to identify those papers that have the greatest impact. 

Circulation publishes articles related to research in and the practice of cardiovascular diseases, including observational studies, clinical trials, epidemiology, health services and outcomes studies, and advances in applied and basic research.

– The research had been started, when I was working as a postdoc in the group of Academy professor Kari Alitalo, but the important breaktrough was achieved in our further collaboration when I had already set up my own lab, Michael Jeltsch tells. He adds:

– Such recognition is a testimony to the high quality of the research done in the Research Program's Unit of the Medical Faculty of the University of Helsinki and in the Wihuri Research Institute.

Already when the article was published – May 2014 – it was clear that it provided a major overhaul of the understanding of lymphangiogenesis, which got featured by Open Heart, the official blog of Circulation.

The article manages to provide multiple new insights. For example, it identifies how the mutated protein CCBE1 mechanistically contributes to the disease phenotype of the human hereditary disease Hennekam Syndrome.

– Our article also forces the field to re-evaluate much previous research. VEGF-C was viewed in a too simplistic way so far, not appreciating that its different forms might have vastly different properties. This research shows that VEGF-C has not only the ability to promote lymphangiogenesis, but that it could also inhibit lymphangiogenesis if it is not activated by proteases, Jeltsch says.

– Almost half of all publications on VEGF-C have measured VEGF-C and correlated its levels to certain disease outcomes. However, none of these measurements did differentiate between active and inactive VEGF-C.

VEGF-C is evaluated as a potential biopharmaceutical to treat lymphedema, while drugs that inhibit VEGF-C are in clinical trials to treat cancer. The findings of this research indicate, that the current treatment strategies might not be optimal, and that molecules like CCBE1 could be used to improve current drug designs.

The 2014 Best Paper Award will be presented in the symposium, “Groundbreaking Studies in the Practice of Cardiovascular Medicine,” to be held in the American Heart Association’s Scientific Sessions on November 8, 2015, in Orlando, Florida.


Text: Päivi Lehtinen / Michael Jeltsch

Jeltsch Lab
Alitalo Lab

 

Michael Jeltsch, PhD; Sawan Kumar Jha, BSc; Denis  Tvorogov, PhD; Andrey Anisimov, PhD; Veli-Matti Leppänen, PhD; Tanja Holopainen, MD; Riikka Kivelä, PhD; Sagrario Ortega, PhD; Terhi Kärpanen, PhD; Kari Alitalo, MD, PhD: CCBE1 Enhances Lymphangiogenesis via A Disintegrin and Metalloprotease With Thrombospondin Motifs-3–Mediated Vascular Endothelial Growth Factor-C Activation. Circulation. May 31, 2014.