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1 with short-gut syndrome caused by recurrent desmoid tumor.
2 usion, CTNNB1 mutations are highly common in desmoid tumors.
3 familial adenomatous polyposis (FAP)-related desmoid tumors.
4 and in 29% of HG-FS cases but only in 4% of desmoid tumors.
5 and trisomy 20 are nonrandom aberrations in desmoid tumors.
6 margins is the treatment of choice for most desmoid tumors.
7 ctively followed 206 patients with extremity desmoid tumors.
8 ents with recurrent, refractory, progressive desmoid tumors.
13 t certain patients with FAP at high risk for desmoid tumors and could be future targets for research.
16 t mortality in patients with intra-abdominal desmoid tumors and identified additional risk factors ab
18 tality rate of patients with intra-abdominal desmoid tumors and to identify prognostic factors for th
27 not metastasize; however, locally aggressive desmoid tumors can cause severe morbidity and loss of fu
29 plex multidisciplinary management needed for desmoid tumor control may underlie significantly increas
30 22 specimens from 19 patients diagnosed with desmoid tumor, desmoplastic fibroma, periosteal desmoid
31 three intermediate connective tissue tumors: desmoid tumor (DT) or aggressive fibromatosis, tenosynov
33 and/or radiation and diagnosis of multifocal desmoid tumors highlight the need to develop effective s
36 of mesenchymal tumors, we hypothesized that desmoid tumors may arise in patients with FAP after MSCs
37 Hedgehog and Notch signaling, suggests that desmoid tumors may respond to therapies targeting these
38 the treatment of 10 children for progressive desmoid tumor not amenable to standard surgical or radia
39 moid tumor, desmoplastic fibroma, periosteal desmoid tumor, osteofibrous dysplasia, or fibrous dyspla
40 Patients and Methods Seventeen patients with desmoid tumors received PF-03084014 150 mg orally twice
42 the 10 recipients experienced intraabdominal desmoid tumor recurrence or developed de novo visceral a
43 ly higher percentages and numbers of primary desmoid tumor referrals to UTMDACC was observed in the m
50 ospective review of 189 consecutive cases of desmoid tumor treated with surgical resection, resection
51 MSC cell line derived from an FAP-associated desmoid tumor, we confirmed an expected loss in the expr
52 current lack of effective treatment against desmoid tumors, we advocate that endostatin gene therapy
53 ith stage I, II, III, and IV intra-abdominal desmoid tumor were 95%, 100%, 89%, and 76% respectively
54 (two patients) or recurrent (eight patients) desmoid tumor were treated with VBL and MTX for 2 to 35
56 rse of a patient with Gardner's syndrome and desmoid tumor who had multiple enterectomies and gradual
58 gut with duodenal adenomatosis and extensive desmoid tumors with pancreaticoduodenal involvement dict
59 otherapy with VBL and MTX appears to control desmoid tumor without significant acute or long-term mor
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