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1  dysmorphism, craniosynostosis, and multiple osteochondromas.
2  collagens, in the matrix of EXT1-associated osteochondromas.
3 the only available treatment for symptomatic osteochondromas.
4  cause, the persistence of cartilage caps in osteochondromas.
5 ectopic endochondral ossification, including osteochondromas.
6  the human phenotype of multiple metaphyseal osteochondromas.
7     We show that these mice develop multiple osteochondromas and characteristic bone deformities in a
8 o understand the pathology and the origin of osteochondromas and develop therapeutic drugs.
9                                              Osteochondromas and enchondromas are the most common tum
10 rocytes is sufficient for the development of osteochondromas and other skeletal defects associated wi
11  multiple cartilage-capped bony protrusions (osteochondroma) and characteristic bone deformities.
12 riant and presented with joint contractures, osteochondromas, and recurrent B-cell lymphoma.
13                                              Osteochondromas are cartilage-capped tumors that arise n
14 alyses reveal that chondrocytes constituting osteochondromas are mixtures of mutant and wild-type cel
15                                              Osteochondromas can lead to skeletal deformity, pain, lo
16                                              Osteochondromas can occur as multiple lesions, such as t
17                                              Osteochondromas characterize the rare pediatric disorder
18 lso confirm homozygous disruption of Ext1 in osteochondroma chondrocytes and their origin in prolifer
19                                    Moreover, osteochondromas do not possess many typical neoplastic p
20 status of human MHE, are highly resistant to osteochondroma formation, especially in long bones.
21 m used as a cutoff for distinguishing benign osteochondromas from chondrosarcomas, the sensitivities
22 ty of both modalities for differentiation of osteochondromas from chondrosarcomas.
23                     Evaluated were 67 benign osteochondromas (from 49 male patients and 18 female pat
24                    The pathogenesis of these osteochondromas has remained unclear.
25  rare pediatric disorder hereditary multiple osteochondromas (HMO).
26                         Because the observed osteochondromas in our mouse model do not arise from clo
27 that cause MO, occasionally develop solitary osteochondroma-like structures on ribs.
28          We report a mouse model of multiple osteochondromas (MO), an autosomal dominant disease in h
29                                              Osteochondroma mouse models have been developed to under
30 etectable beta-catenin in cartilage cells of osteochondromas obtained from hereditary multiple exosto
31 cacy endpoint was the annualized rate of new osteochondromas (OCs).
32 discusses the signaling pathways involved in osteochondroma pathogenesis and their possible interacti
33 s unclear, especially with regard to whether osteochondroma results from loss of heterozygosity of th
34 s have been implicated in the development of osteochondromas, such as bone morphogenetic protein, hed
35             Together, our findings show that osteochondromas usurp a physiological signaling mechanis
36 ment technique, 101 pathologically confirmed osteochondromas were retrospectively reviewed.