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1 the expression of cancer/testis antigens in chondrosarcoma.
2 loci may be required for the development of chondrosarcoma.
3 , and one somatic mutation in a patient with chondrosarcoma.
4 ily located at 9q22-31, in a skeletal myxoid chondrosarcoma.
5 been observed in the myxoid variant of human chondrosarcoma.
6 lecules shown to be involved in conventional chondrosarcoma.
7 osarcoma and one (20%) of five patients with chondrosarcoma.
8 ome of the increased VEGF expression seen in chondrosarcoma.
9 the regulation of VEGF by HDAC4 and Runx2 in chondrosarcoma.
10 y are causes of increased VEGF expression in chondrosarcoma.
11 including osteoarthritis, osteosarcoma, and chondrosarcoma.
12 used as markers of prognostic importance in chondrosarcoma.
13 eutic potential in the future for subsets of chondrosarcoma.
14 oncogene, as a frequent change in high-grade chondrosarcoma.
15 tified in samples of enchondroma and grade 1 chondrosarcoma.
16 xostoses undergo malignant transformation to chondrosarcomas.
17 cases, these exostoses progress to malignant chondrosarcomas.
18 ibed in multiple tumors and more recently in chondrosarcomas.
19 are, together constituting 10% to 15% of all chondrosarcomas.
20 ns in IDH1 or IDH2 in nearly half of central chondrosarcomas.
21 2 cm or greater strongly indicated secondary chondrosarcomas.
22 for differentiation of osteochondromas from chondrosarcomas.
23 linical findings in conventional and variant chondrosarcomas.
24 (15%), G3 (20%), and dedifferentiated (21%) chondrosarcomas.
25 ic findings, except for extraskeletal myxoid chondrosarcomas.
26 anges are diagnostic of extraskeletal myxoid chondrosarcomas.
27 ard to isocitrate dehydrogenase mutations in chondrosarcoma, a disease in which currently available s
29 This peptide adheres to and kills cells from chondrosarcoma and cervical and breast cancer cell lines
31 tments may soon be routine for patients with chondrosarcoma and chordoma for whom surgery alone is in
35 Loss of heterozygosity (LOH) analysis of chondrosarcomas and chondroblastomas revealed multiple L
36 rentiated, 23 clear cell, and 23 mesenchymal chondrosarcomas and performed immunohistochemistry to st
37 ns (eg, cemento-ossifying fibroma and myxoid chondrosarcoma) and the association of established trans
39 rphic rhabdomyosarcoma, one dedifferentiated chondrosarcoma, and one malignant peripheral nerve sheat
41 gliomas, acute myeloid leukaemias (AML) and chondrosarcomas, and share a novel enzymatic property of
45 ed genome-wide CpG methylation sequencing of chondrosarcoma biopsies and found that IDH mutations wer
46 ), grade 3 (80%), and dedifferentiated (29%) chondrosarcomas, but was not found in any samples of enc
49 bp segment with recombinant Sox9 or with rat chondrosarcoma cell extracts, confirming the binding of
50 2 expression and its potential role in human chondrosarcoma cell invasion and metastasis have yet to
51 P-12 or MMP-12 overexpression can potentiate chondrosarcoma cell invasion in vitro and the lung colon
53 pursued this possibility using the Swarm rat chondrosarcoma cell line (RCS-LTC) found to express high
54 inity IL-1R sites were identified in a human chondrosarcoma cell line by means of 125I-IL-1beta bindi
55 n of recombinant CRYBP1 in a transfected rat chondrosarcoma cell line inhibited Col2a1 enhancer activ
56 solated human articular chondrocytes and the chondrosarcoma cell line SW-1353 were activated with pol
57 resulted in reduced promoter activity in the chondrosarcoma cell line SW1353 as shown by CpG-free luc
59 red chondrocytes, a stable long-term culture chondrosarcoma cell line, as well as Chinese hamster ova
64 CH1 was not up-regulated or overexpressed in chondrosarcoma cell lines exposed to inflammatory stimul
65 -3 mimetic ABT-737 rendered dedifferentiated chondrosarcoma cell lines sensitive to doxorubicin or ci
68 F repressed COMP gene expression in both rat chondrosarcoma cells and bone morphogenetic protein-2-tr
69 nase 1 (MMP-1) in articular chondrocytes and chondrosarcoma cells and found that IL-1 induction of MM
70 In this study, transient transfection of rat chondrosarcoma cells and NIH-3T3 fibroblasts demonstrate
72 pression of c/EBPbeta, SOX9, and p300 in rat chondrosarcoma cells and primary human articular chondro
74 HrP also increased Col2a1 mRNA levels in rat chondrosarcoma cells as well as 10T1/2 mesenchymal cells
75 ncreased promoter activity of Col11a2 in rat chondrosarcoma cells but not in either BalB/3T3 cells or
77 the activation of the RhoA pathway in SW1353 chondrosarcoma cells increased SOX9(Ser181) phosphorylat
79 We show that reduced expression of HDAC4 in chondrosarcoma cells increases expression of Runx2 leadi
80 BM40 signal peptide in HEK-293 cells and rat chondrosarcoma cells revealed that the BM40 signal pepti
84 an articular chondrocytes (HACs) and SW-1353 chondrosarcoma cells were treated with cytokines and TSA
92 and biochemical analyses of FGF-treated rat chondrosarcoma chondrocytes, we show that FGF inhibits c
99 ll line, RCS-LTC (derived from the Swarm rat chondrosarcoma), deposits a copious extracellular matrix
102 tionable; and late recurrences of clear cell chondrosarcomas emphasize the need for long-term follow
106 erein that, in contrast to osteosarcomas and chondrosarcomas, for which OSM was cytostatic, OSM induc
107 ents; mean age, 23.4 years) and 34 secondary chondrosarcomas (from 27 male patients and seven female
109 -grade gliomas, acute myeloid leukaemia, and chondrosarcomas, has been the identification of early-oc
110 med in rat chondrosarcoma (RCS) cells, human chondrosarcoma (HTB) cells, and NIH/3T3 cells showed tha
111 s of c-fos oncogene-induced osteosarcoma and chondrosarcoma in addition to c-Fos-inducible systems in
112 ongly expressed in joint cartilage, we found chondrosarcoma in the knee joint and remarkable defects
115 s have established that extraskeletal myxoid chondrosarcoma is a unique entity defined by the presenc
117 ukemia, intrahepatic cholangiocarcinoma, and chondrosarcomas, led to intense discovery efforts to del
119 re osteosarcoma (n = 20), lymphoma (n = 18), chondrosarcoma (n = 16), and giant cell tumor (n = 16).
120 y HIF-1alpha, immunohistochemical studies of chondrosarcoma nodules were conducted and revealed that
124 igated such a role for ADAMTS-3 in Swarm rat chondrosarcoma RCS-LTC cells, which fail to process the
125 bits chondrocyte proliferation both in a rat chondrosarcoma (RCS) cell line and in primary murine cho
126 dramatically inhibited proliferation of rat chondrosarcoma (RCS) cells and arrested their cell cycle
127 oter activity in transiently transfected rat chondrosarcoma (RCS) cells and mouse primary chondrocyte
128 sient-transfection analyses performed in rat chondrosarcoma (RCS) cells, human chondrosarcoma (HTB) c
129 K1/2 or the p38 MAPK pathways applied to rat chondrosarcoma (RCS) chondrocytes significantly prevente
130 benefit of chemotherapy for dedifferentiated chondrosarcomas remains questionable; and late recurrenc
133 tation is the first of its kind described in chondrosarcoma, serving as an identifying marker of chon
134 apoptosis-inducing ligand (Apo2L/TRAIL) for chondrosarcoma, small molecule inhibitor crizotinib for
135 esenchymal, clear cell, and dedifferentiated chondrosarcoma subtypes are extremely rare, together con
136 h p-SMAD2 and PAI-1 was highly active in all chondrosarcoma subtypes, which suggests that TGFbeta inh
138 alignancies is an uncommon but real risk for chondrosarcoma survivors; the benefit of chemotherapy fo
140 r distinguishing benign osteochondromas from chondrosarcomas, the sensitivities and specificities wer
142 g role for targeting Bcl-2 family members in chondrosarcoma treatment, irrespective of the subtype.
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