ライフサイエンスコーパス: desmoid

1 tations were observed in 117 of 138 (85%) of desmoids.

2 als to UTMDACC, especially primary untreated desmoids.

3 matic APC mutation association exists in FAP desmoids.

4 ival was significantly poorer in 45F-mutated desmoids (23%, P < 0.0001) versus either 41A (57%) or no

5 ion has been commonly identified in sporadic desmoids although the incidence of CTNNB1 (the gene enco

6 NNB1 mutations in a large cohort of sporadic desmoids and examined whether mutation type was relevant

7 f molecular alterations in HG-FS, LG-FS, and desmoids appear to be related to biological aggressivene

8 Desmoids are a life threatening extra-colonic manifestat

9 ional study of the molecular determinates of desmoid behavior is needed to guide therapeutic selectio

10 ate for young patients with large, extremity desmoids, but surgery alone is curative for most abdomin

11 common region encompassing 48 % of published desmoid cases and 40 % of the reference population.

12 In addition, the occurrence of desmoid fibromas was strongly enhanced by p53 deficiency

13 ic polyps and extracolonic lesions including desmoid fibromas, osteomas, epidermoid cysts, and congen

14 m1 showed no influence on the development of desmoid fibromas, whereas the combination of piroxicam a

15 he differential diagnosis of GIST, including desmoid fibromatosis (0 of 17) and Schwannoma (0 of 3),

16 Desmoid fibromatosis is a rare, nonmetastatic neoplasm m

17 to colonic polyps, loss of heterozygosity in desmoids involved deletion rather than mitotic recombina

18 amined whether mutation type was relevant to desmoid outcome.

19 t treatments may be associated with improved desmoid patient outcomes.

20 This study compared a large series of desmoid patients treated at a single institution to a pr

21 was used to analyze clinical courses of 189 desmoid patients treated at The University of Texas M.D.

22 om 1995 to 2005 as compared with 189 UTMDACC desmoid patients treated between 1965 and 1994.

23 enin degradation repeats, respectively, most desmoids preferentially retain two repeats (P < 0.001, c

24 y was inversely correlated with incidence of desmoid recurrence (P < 0.01).

25 Molecular determinants of desmoid recurrence remain obscure.

26 ly three-fold increase in annualized UTMDACC desmoid referral volume with significantly higher percen

27 Desmoid specimens (195 tumors from 160 patients, 1985 to

28 1 genotyping was performed on a 138-sporadic desmoid subset.

29 ions in the largest cohort of FAP-associated desmoids to date, and combined our results with previous

30 three intermediate connective tissue tumors: desmoid tumor (DT) or aggressive fibromatosis, tenosynov

31 nown regarding the molecular determinates of desmoid tumor behavior.

32 k has focused on the role of beta-catenin in desmoid tumor biology.

33 ly induces cell death on primary FAP-related desmoid tumor cells in culture.

34 plex multidisciplinary management needed for desmoid tumor control may underlie significantly increas

35 the treatment of 10 children for progressive desmoid tumor not amenable to standard surgical or radia

36 After the transplant, the desmoid tumor recurred in the thoracic wall twice and wa

37 the 10 recipients experienced intraabdominal desmoid tumor recurrence or developed de novo visceral a

38 ly higher percentages and numbers of primary desmoid tumor referrals to UTMDACC was observed in the m

39 The term fibromatosis or desmoid tumor refers to a group of benign fibrous growth

40 ospective review of 189 consecutive cases of desmoid tumor treated with surgical resection, resection

41 ith stage I, II, III, and IV intra-abdominal desmoid tumor were 95%, 100%, 89%, and 76% respectively

42 (two patients) or recurrent (eight patients) desmoid tumor were treated with VBL and MTX for 2 to 35

43 rse of a patient with Gardner's syndrome and desmoid tumor who had multiple enterectomies and gradual

44 otherapy with VBL and MTX appears to control desmoid tumor without significant acute or long-term mor

45 22 specimens from 19 patients diagnosed with desmoid tumor, desmoplastic fibroma, periosteal desmoid

46 moid tumor, desmoplastic fibroma, periosteal desmoid tumor, osteofibrous dysplasia, or fibrous dyspla

47 MSC cell line derived from an FAP-associated desmoid tumor, we confirmed an expected loss in the expr

48 with short-gut syndrome caused by recurrent desmoid tumor.

49 inal crypt multiplicity as well as enhancing desmoid tumorigenesis and epidermoid cyst development.

50 Purpose Desmoid tumors (aggressive fibromatosis) arise from conn

51 Desmoid tumors also contained a subclass of fibrocytes l

52 A cohort of 24 desmoid tumors and 25 low-grade (LG) and 14 high-grade (

53 t certain patients with FAP at high risk for desmoid tumors and could be future targets for research.

54 Medline and Embase to identify subjects with desmoid tumors and FAP.

55 Desmoid tumors and fibrosarcomas (FS) are part of a wide

56 t mortality in patients with intra-abdominal desmoid tumors and identified additional risk factors ab

57 iate between histologically similar cases of desmoid tumors and LG-FS.

58 tality rate of patients with intra-abdominal desmoid tumors and to identify prognostic factors for th

59 Desmoid tumors are a group of benign, invasive, solid tu

60 The biology and natural history of desmoid tumors are an enigma.

61 Desmoid tumors are associated with a variable and unpred

62 Desmoid tumors are locally invasive fibromatous tumors,

63 Desmoid tumors are nonmalignant neoplasms of mesenchymal

64 INTRODUCTION: Intra-abdominal desmoid tumors are one of the leading causes of death in

65 not metastasize; however, locally aggressive desmoid tumors can cause severe morbidity and loss of fu

66 To test this idea, we examined 16 desmoid tumors from FAP-associated and sporadic cases, f

67 and/or radiation and diagnosis of multifocal desmoid tumors highlight the need to develop effective s

68 There is an increased risk for desmoid tumors in individuals with APC mutations between

69 The standard management of desmoid tumors is resection, but many recur locally.

70 of mesenchymal tumors, we hypothesized that desmoid tumors may arise in patients with FAP after MSCs

71 Hedgehog and Notch signaling, suggests that desmoid tumors may respond to therapies targeting these

72 Patients and Methods Seventeen patients with desmoid tumors received PF-03084014 150 mg orally twice

73 Treatment of desmoid tumors remains a challenge, but new chemotherapy

74 Together, our findings argue that desmoid tumors result from the growth of MSCs in a wound

75 In contrast, desmoid tumors showed a normal phenotype with these mark

76 th the increase of tumor aggressiveness from desmoid tumors to LG-FS to HG-FS.

77 A total of 154 patients with intra-abdominal desmoid tumors were included in the study.

78 fit in patients with refractory, progressive desmoid tumors who receive long-term treatment.

79 gut with duodenal adenomatosis and extensive desmoid tumors with pancreaticoduodenal involvement dict

80 In desmoid tumors, aggressive attempts at achieving negativ

81 Given the variable clinical course of desmoid tumors, the interpretation of factors classicall

82 current lack of effective treatment against desmoid tumors, we advocate that endostatin gene therapy

83 usion, CTNNB1 mutations are highly common in desmoid tumors.

84 familial adenomatous polyposis (FAP)-related desmoid tumors.

85 and in 29% of HG-FS cases but only in 4% of desmoid tumors.

86 and trisomy 20 are nonrandom aberrations in desmoid tumors.

87 margins is the treatment of choice for most desmoid tumors.

88 ents with recurrent, refractory, progressive desmoid tumors.

89 ctively followed 206 patients with extremity desmoid tumors.

90 levels of beta-catenin signalling levels in desmoid tumour cells.

91 Many women who present with desmoid-type fibromatosis (DF) have had a recent pregnan

92 this case series, patients (<25 years) with desmoid-type fibromatosis from 57 centres in eight count

93 Vbl) and methotrexate (Mtx) in children with desmoid-type fibromatosis that is recurrent or not amena

94 INTERPRETATION: In paediatric patients with desmoid-type fibromatosis, the EpSSG conservative strate

95 ur progression)-for paediatric patients with desmoid-type fibromatosis.

96 and Mtx are well tolerated in children with desmoid-type fibromatosis.

97 g 1982-2011 for primary or locally recurrent desmoids were identified from a single-institution prosp

98 Desmoids were treated surgically in 495 patients (median

99 In addition, most desmoids with two APC hits (87%, 26/30) had one mutated