International Research Prize

The Austrian Bone and Mineral Society
announces its 2018 International Research Prize

The prize acknowledges an individual whose recent work in the fields of molecular, cellular, material science, (patho)physiological or clinical aspects of bone and mineral metabolism has resulted in a novel finding or concept. Individuals are invited to submit up to three related publications that have appeared since 2015. Papers in press are acceptable if accompanied by an acceptance letter from the journal. Publication must be in English, in refereed journals listed in Current Contents.

Applicants should describe their finding or concept and its background in a brief statement, not to exceed 300 words, emphasizing the importance of their contribution to progress in bone and mineral metabolism. The letter of application should also include a brief biographical sketch, along with a letter stating that co-authors agree to the submission and either wish to share the prize money or waive their claim to it.

The prize of EUR 7,500.00 will be awarded at the Austrian Bone Conference 2018 , which will be held in Vienna, Austria, on November 23–24, 2018. The work of the prize winner will be featured during this conference.


Complete applications must be submitted not later than March 9, 2018 to:
 klaus.klaushofer@osteologie.at

All entries, which comply to the aforementioned regulations, will be forwarded to an international jury which will independently select the prize winner.

 The jury consists of: K. Klaushofer (Vienna, Chair), G. Karsenty (New York), S. Kato (Fukushima), H.M. Kronenberg (Boston), T.J. Martin (Melbourne), H. Takayanagi (Tokyo), A. Teti (L’Aquila), R.V. Thakker (Oxford), E. Wagner (Madrid).

The jury’s decision is final and cannot be appealed.
The winner will be notified by end of July 2018.


Winners of the International Research Prize:

JahrPreisträgerProjekt
2015Prof. Rajesh V. Thakker (Oxford)(1)Receptor-mediated endocytosis and endosomal acidification is impaired in proximal tubule epithelial cells of Dent disease patients. CM Gorvin et al., 2013, Proc Natl Acad Sci U S A 110:7014-9
(2)Mutations in AP2S1 cause familial hypocalciuric hypercalcemia type 3. MA Nesbit et al., 2013, Nat Genet 45:93-7
(3)Mutations affecting G-protein subunit α11 in hypercalcemia and hypocalcemia. MA Nesbit et al., 2013, N Engl J Med 368:2476-86
2012Prof. Henry M. Kronenberg (Boston)(1)Osteoblast precursors, but not mature osteoblasts, move into developing and fractured bones along with invading blood vessels. C. Maes et al., 2010, Dev Cell 19:329-44
(2)Gsα enhances commitment of mesenchymal progenitors to the osteoblast lineage but restrains osteoblast differentiation in mice. JY Wu et al., 2011, J Clin Invest 121:3492-504
(3)Parathyroid hormone/parathyroid hormone-related protein receptor signaling is required for maintenance of the growth plate in postnatal life. T. Hirai et al., 2011, Proc Natl Acad Sci U S A. 108:191-6
2009Prof. Erwin Wagner (Madrid)(1)Osteoclast size is controlled by Fra-2 through LIF/LIF-receptor signaling and hypoxia. A Bozec et al., 2008, Nature 454: 221-5
(2)Epidermal JunB represses G-CSF transcription and affects hematopoiesis and bone formation. A Meixner et al., 2008, Nat Cell Biol 10:1003-11
(3)Role of heterodimerization of c-Fos and Fra1 proteins in osteoclast differentiation. L. Bakiri et al., 2007, Bone 40:867-75
2006Prof. Hiroshi Takayanagi, (Tokyo)(1)Genes & Development, 2003, 17:1979-1991; Nature, 2004, 428:758-763;
Nature Medicine, 2005, 11:880-885
(2)Costimulatory signals mediated by the ITAM motif cooperate with RANKL for bone homeostasis. T Koga et al., 2004, Nature 428:758-63
(3)NFAT and Osterix cooperatively regulate bone formation. T. Koga et al., 2005, Nature Medicine 11:880-5
2003Prof. Josef Penninger(1)The osteoclast differentiation factor osteoprotegerin-ligand is essential for mammary gland development. JE Fata et al., 2000, Cell 103:41-50
(2)Functional human T-cell immunity and osteoprotegerin ligand control alveolar bone destruction in periodontal infection. YA Teng et al., 2000, J Clin Invest 106:R59-R67
2000Prof. Shigeaki Kato (Tokyo)(1)Mice lacking the vitamin D receptor exhibit impaired bone formation, uterine hypoplasia and growth retardation after weaning. T Yoshizawa et al., 1997, Nat Genet 16:391-6
(2)Inactivating mutations in the 25-hydroxyvitamin D3 1alpha-hydroxylase gene in patients with pseudovitamin D-deficiency rickets. S Kitanaka et al., 1998, N Engl J Med 338:653-61
(3)Convergence of transforming growth factor-beta and vitamin D signaling pathways on SMAD transcriptional coactivators. J Yanagisawa et al., 1999, Science 283:1317-21
1997Prof. Gerard Karsenty (New York)(1)Two distinct osteoblast-specific cis-acting elements control expression of a mouse osteocalcin gene. P Ducy, G Karsenty, 1995, Mol Cell Biol 15:1858-69
(2)Osf2/Cbfa1: a transcriptional activator of osteoblast differentiation. P Ducy et al., 1997, Cell 89:747-54
(3)Missense mutations abolishing DNA binding of the osteoblast-specific transcription factor OSF2/CBFA1 in cleidocranial dysplasia. B Lee et al., 1997, Nat Genet 16:307-10
1994Prof. Edward M. Brown (Boston)(1)Mutations in the human Ca(2+)-sensing receptor gene cause familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism. MR Pollak et al., 1993, Cell 75:1297-303
(2)Cloning and characterization of an extracellular Ca(2+)-sensing receptor from bovine parathyroid. EM Brown et al., 1993, Nature 366:575-80
1991Prof. Anna Teti (L’Aquila)(1)Control of cytosolic free calcium in rat and chicken osteoclasts. The role of extracellular calcium and calcitonin. A Malgaroli et al., 1989, J Biol Chem 264:14342-7
Monique Thomasset (Paris)(1)
The rat vitamin-D-dependent calcium-binding protein (9-kDa CaBP) gene. Complete nucleotide sequence and structural organization. C Perret et al., 1988, Eur J Biochem 172:43-51
1988Prof. Thomas Jack Martin (Melbourne)(1)A parathyroid hormone-related protein implicated in malignant hypercalcemia: cloning and expression. L J Suva et al., 1987, Science 237:893-96