ライフサイエンスコーパス: bone sarcoma

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1 kade of NGF reduced weight loss in mice with bone sarcoma.

2 therapy in the treatment of soft tissue and bone sarcoma.

3 anti-angiogenesis agents in soft tissue and bone sarcoma.

4 als with DMS develop MFH, a highly malignant bone sarcoma.

5 atients with advanced soft-tissue sarcoma or bone sarcoma.

6 D-based gene therapy affected soft tissue or bone sarcomas.

7 the prediction of survival before therapy in bone sarcomas.

8 e, which is the most common site for primary bone sarcomas.

9 Unresectable metastatic bone sarcoma and soft-tissue sarcomas (STS) are incurabl

10 To identify putative sCSCs, autologous bone sarcoma and STS cells were engineered with a CSC de

11 nduced killer (CIK) cells against autologous bone sarcoma and STS, including against putative sCSCs.

12 However, patients without bone sarcoma and those able to tolerate therapy for more

13 sponse rate was 40% (95% CI, 24% to 56%) for bone sarcomas and 19% (95% CI, 6% to 32%) for soft tissu

14 are changing the diagnosis and treatment of bone sarcomas and carcinomas metastatic to bone.

15 oad applicability for mechanistic studies of bone sarcomas and exhibits the potential to augment prec

16 ese trials, 27 (61%) were male; 18 (41%) had bone sarcoma, and 26 (59%) had soft tissue sarcoma.

17 steoid osteomas, giant-cell lesions of bone, bone sarcomas, and metastases.

18 Soft tissue and bone sarcomas are malignancies of mesenchymal origin, an

19 ed in the osteosarcoma and Ewing's subset of bone sarcomas at nanomolar concentrations of dasatinib.

20 In addition, 5FC treatment of bone sarcomas caused a significant reduction in cancer-i

21 lso induced apoptosis, indicating that these bone sarcoma cell lines are dependent on Src activity fo

22 types and selectively blocks the survival of bone sarcoma cells.

23 ed 18 years or older to enrol; patients with bone sarcoma could enrol if they were aged 12 years or o

24 ation of the molecular mechanisms underlying bone sarcomas, especially in the case of osteogenic sarc

25 nrolled patients with soft-tissue sarcoma or bone sarcoma from 12 academic centres in the USA that we

26 d 90% CI 21-43), 19 of 54 in IGF-1R-positive bone sarcoma group (35%; one-sided 95% CI lower bound 24

27 Nine (11%) patients (five [12%] in the bone sarcoma group and four [10%] in the soft-tissue sar

28 decreased platelet count (three [7%]) in the bone sarcoma group, and anaemia, decreased lymphocyte co

29 ft-tissue sarcoma (group A), IGF-1R-positive bone sarcomas (group B), or IGF-1R-negative bone and sof

30 Two (5%) of 40 patients with bone sarcoma had an objective response, including one (5

31 CI, 0.23-0.93; P = .03) and those without a bone sarcoma (ie, neither primitive neuroectodermal tumo

32 t discoveries in the molecular mechanisms of bone sarcomas may help to elucidate the pathogenesis of

33 Soft tissue and bone sarcomas of the extremities can be difficult to era

34 entify a gene involved in the development of bone sarcoma, provide evidence of the primate-specific e

35 ), AML (RR = 11.2; 95% CI, 2.1 to 61.2), and bone sarcoma (RR = 7.3; 95% CI, 2.0 to 26.2) were at hig

36 Using a mouse graft model of bone sarcoma, we demonstrate that early treatment with a

37 Bone sarcomas were eliminated in 9 of 10 5FC-treated mic

38 Patients with metastatic soft tissue or bone sarcomas who achieved objective response or stable

39 management of patients with soft tissue and bone sarcomas will be discussed.

40 nd, in patients with advanced soft tissue or bone sarcoma with progressive disease.

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