ライフサイエンスコーパス: osteochondroma

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1 cause, the persistence of cartilage caps in osteochondromas.

2 collagens, in the matrix of EXT1-associated osteochondromas.

3 the human phenotype of multiple metaphyseal osteochondromas.

4 We show that these mice develop multiple osteochondromas and characteristic bone deformities in a

5 Osteochondromas and enchondromas are the most common tum

6 rocytes is sufficient for the development of osteochondromas and other skeletal defects associated wi

7 multiple cartilage-capped bony protrusions (osteochondroma) and characteristic bone deformities.

8 alyses reveal that chondrocytes constituting osteochondromas are mixtures of mutant and wild-type cel

9 Osteochondromas can occur as multiple lesions, such as t

10 lso confirm homozygous disruption of Ext1 in osteochondroma chondrocytes and their origin in prolifer

11 Moreover, osteochondromas do not possess many typical neoplastic p

12 status of human MHE, are highly resistant to osteochondroma formation, especially in long bones.

13 m used as a cutoff for distinguishing benign osteochondromas from chondrosarcomas, the sensitivities

14 ty of both modalities for differentiation of osteochondromas from chondrosarcomas.

15 Evaluated were 67 benign osteochondromas (from 49 male patients and 18 female pat

16 The pathogenesis of these osteochondromas has remained unclear.

17 Because the observed osteochondromas in our mouse model do not arise from clo

18 that cause MO, occasionally develop solitary osteochondroma-like structures on ribs.

19 We report a mouse model of multiple osteochondromas (MO), an autosomal dominant disease in h

20 etectable beta-catenin in cartilage cells of osteochondromas obtained from hereditary multiple exosto

21 s unclear, especially with regard to whether osteochondroma results from loss of heterozygosity of th

22 ment technique, 101 pathologically confirmed osteochondromas were retrospectively reviewed.

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