1                                       Lethal osteosclerotic bone dysplasia (or, Raine syndrome) is an

2 nd the corresponding defect in FAM20C caused osteosclerotic bone dysplasia and a loss of kinase activ

3   Consequently, mutations in Fam20C cause an osteosclerotic bone dysplasia in humans known as Raine s

4            Kenny-Caffey syndrome (KCS) is an osteosclerotic bone dysplasia with associated hypocalcem

5  kinase cause Raine syndrome, an often-fatal osteosclerotic bone dysplasia.

6 Mutations in Fam20C cause Raine syndrome, an osteosclerotic bone dysplasia.

7 human breast cancer cells caused predominant osteosclerotic bone metastases 20-25 weeks after inocula

8 n conclusion, we show that MCF-7 cells cause osteosclerotic bone metastases and that Neu enhances thi

9 eu cells grew without estrogen and developed osteosclerotic bone metastases in 10-12 weeks in animals

10 plays a causative role in the development of osteosclerotic bone metastases in this model.

11 erapeutic target in the treatment of painful osteosclerotic bone metastases of prostate cancer.

12 -6 as a potential new marker and mediator of osteosclerotic deposit formation.

13  the causative role of FAM20C in this lethal osteosclerotic disorder and its crucial role in normal b

14 te cancer (PCa) is frequently accompanied by osteosclerotic (i.e., excessive bone production) bone me

15 y formed osteolytic bone metastases, induced osteosclerotic lesions in the osteolytic bone metastases

16      We review the biology of osteolytic and osteosclerotic lesions, with a focus on endocrine aspect

17 adhesion, and function, and suggest that the osteosclerotic-like phenotype observed in RAGE knockout

18 nstrated increased osteoblast numbers and an osteosclerotic phenotype but normal adipocyte differenti

19 sing to Lrp5(-/-) mice partially rescued the osteosclerotic phenotype of Shn3(-/-) mice; mechanistica

20 sing pycnodysostosis, an autosomal recessive osteosclerotic skeletal dysplasia.