ライフサイエンスコーパス: LMS

1 mic hybridization (aCGH) was performed on 20 LMS samples and showed that the molecular subtypes defin

2 ene expression profiling was performed on 51 LMS samples.

3 siRNA to knock down versican expression in a LMS human cell line, SK-LMS-1.

4 ed rise in the incidence of metastasis after LMS(+) tumors reach 2 cm.

5 7 offers an opportunity to turn TAMs against LMS cells by allowing the phagocytic behavior of residen

6 Although LMS is easily recognized histopathologically, the cause

7 ostic method to distinguish between GIST and LMS and has the potential to be rapidly implemented in a

8 assifier that distinguishes between GIST and LMS with an accuracy of 99.3% on the microarray samples

9 nd 62% of metastatic GIST, embryonal RMS and LMS samples, respectively.

10 tic and benign counterparts of GIST, RMS and LMS tumors, and DMD deletions inactivate larger dystroph

11 oice for most patients with three-vessel and LMS disease and especially in those with the most severe

12 Mimulus cardinalis LMS (McLMS) is weakly expressed and has a nonsense mutat

13 motes primary tumor growth that enriches for LMS(+) cells, and it allows for intravasation after reac

14 agnosis, genomics, and treatment options for LMS.

15 reasing trend to use drug-eluting stents for LMS stenosis rather than CABG despite very little high-q

16 es with poor prognosis in both gynecological LMS (P = 0.00006) and nongynecological LMS (P = 0.03).

17 In gynecological LMS, a similar trend was noted but did not reach statist

18 In gynecological LMS, the coordinate expression of these four markers was

19 ant elevated expression of versican in human LMS versus benign leiomyomas.

20 ith CD47 increases phagocytosis of two human LMS cell lines, LMS04 and LMS05, in vitro.

21 We have identified LMS as the first human disease, to our knowledge, caused

22 ntification of novel agents with activity in LMS is clearly needed.

23 nzymes, PSS1, were described as causative in LMS patients.

24 racellular matrix proteoglycan, increases in LMS.

25 Currently, the only curative option in LMS is surgery and despite progress in systemic therapy

26 reviously shown that the presence of TAMs in LMS is associated with poor clinical outcome and the ove

27 al outcome and the overall effect of TAMs in LMS therefore appears to be protumorigenic.

28 Leiomyosarcoma (LMS) is a mesenchymal cancer that occurs throughout the

29 Leiomyosarcoma (LMS) is a soft tissue tumor with a significant degree of

30 Leiomyosarcoma (LMS) is a tumor of smooth muscle that can express varyin

31 Leiomyosarcoma (LMS) is one of the most common subtypes of soft tissue s

32 , rhabdomyosarcoma (RMS) and leiomyosarcoma (LMS), feature myogenic differentiation.

33 diagnosis of the more common leiomyosarcoma (LMS) anatomic variants, potentially useful prognostic ma

34 therapy agents are active in leiomyosarcoma (LMS), particularly LMS that has progressed after doxorub

35 f uterine sarcomas including leiomyosarcoma (LMS), endometrial stromal sarcoma, high-grade undifferen

36 rognosis in nongynecological leiomyosarcoma (LMS).

37 Uterine leiomyosarcoma (LMS) is staged by the modified International Federation

38 acting management of uterine leiomyosarcoma (LMS).

39 rrent and metastatic uterine leiomyosarcoma (LMS).

40 Mimulus lewisii LMS (MlLMS) and OS (MlOS) are expressed most strongly in

41 Plateau, including the uplifted Longmenshan (LMS) orogenic belt, is accurately imaged in spite of the

42 ogy of lutein ester loaded saponin micelles (LMS), cryo-TEM micrographs showed depending on the compo

43 and IHC, we characterized distinct molecular LMS subtypes, provided insight into their pathogenesis,

44 This association of LHON and MS (LMS) raises an important question about whether there co

45 gical LMS (P = 0.00006) and nongynecological LMS (P = 0.03).

46 n important role in the clinical behavior of LMS that may open a window for new therapeutic reagents.

47 and TGCT-associated proteins in 149 cases of LMS.

48 h the predicted dominant de novo etiology of LMS, we identified causative heterozygous missense mutat

49 he primary aim was to define MRI features of LMS and LHON, and to assess the proportions of individua

50 restored cell proliferation to the level of LMS controls, increased the pericellular coat and the re

51 erapy is not based on the anatomic origin of LMS.

52 xpression was accompanied by slower rates of LMS cell proliferation and migration, increased adhesion

53 Here we show that in a subset of LMS cases, CSF1 is expressed by the malignant cells.

54 cover and characterize molecular subtypes of LMS.

55 f control in the management and treatment of LMS.

56 xorubicin holds promise for the treatment of LMS.

57 oxorubicin holds promise in the treatment of LMS.

58 gical biomarkers in the diagnostic workup of LMS.

59 Immunohistochemistry (IHC) was performed on LMS tissue microarrays (n=377) for five markers with hig

60 active in leiomyosarcoma (LMS), particularly LMS that has progressed after doxorubicin treatment.

61 A set of reestimated LMS parameters that incorporated a smoothed 99th percent

62 The reestimated LMS parameters had several drawbacks and no clear advant

63 Linkage studies suggest that the related LMS and ADULT syndromes are also caused by mutations in

64 ervised clustering showed three reproducible LMS clusters.

65 CDC) growth charts included lambda-mu-sigma (LMS) parameters intended to calculate smoothed percentil

66 "lung metastasis gene-expression signature" (LMS) that mediates experimental breast cancer metastasis

67 lines (DBTRG, U373 and SNB19), as well as SK-LMS-1 human leiomyosarcoma cells are also sensitive to f

68 In experiments with human SK-LMS-1 leiomyosarcoma cells, we show that the Akt kinase

69 of both uPA and its cellular receptor in SK-LMS-1 cells.

70 ing in the human leiomyosarcoma cell line SK-LMS-1 enhances its in vivo tumorigenicity, an effect for

71 a into the human leiomyosarcoma cell line SK-LMS-1.

72 ican expression in a LMS human cell line, SK-LMS-1.

73 ressing cancer cells, including the lines SK-LMS-1 (human leiomyosarcoma), U118 (human glioblastoma),

74 te cancer (PC-3 and TR6LM, human sarcoma (SK-LMS-1), glioblastoma (DBTRG), and gastric cancer (MKN45)

75 separation of conditioned medium from the SK-LMS-1 human leiomyosarcoma cell line.

76 two-thirds of patients with left main stem (LMS) disease have a survival benefit and marked reductio

77 ery disease with unprotected left main stem (LMS) stenosis, coronary artery bypass grafting (CABG) is

78 anic aerosols in the lowermost stratosphere (LMS) had not been considered.

79 rcentiles extrapolated from the CDC-supplied LMS parameters did not match well to the empirical data

80 Extrapolation from the CDC-supplied LMS parameters does not provide a good fit to the empiri

81 Lenz-Majewski syndrome (LMS) is a rare disease characterized by complex craniofa

82 Lenz-Majewski syndrome (LMS) is a syndrome of intellectual disability and multip

83 eft lip/palate (EEC), Limb-mammary syndrome (LMS) and split hand-foot malformation (SHFM) dysplasias.

84 (EEC; OMIM 604292), limb--mammary syndrome (LMS; OMIM 603543), acro-dermato-ungual-lacrimal-tooth sy

85 tion at two loci, LIMONENE-MYRCENE SYNTHASE (LMS) and OCIMENE SYNTHASE (OS).

86 The LMS method was used to derive 10 smoothed skinfold-thick

87 indication that the lower crust beneath the LMS was folded and pushed upwards and the upper crust wa

88 ood of metastatic recurrence provided by the LMS may help to explain observations of prognostic gene

89 well approximated by extrapolations from the LMS values.

90 eric aerosol optical depth originated in the LMS during the period 2008-2011.

91 ite of the extreme topographic relief in the LMS region and thick sedimentary covers in the neighbour

92 derstanding of the underlying biology of the LMS variants, improved diagnostics and more effective, l

93 lution measurement methods, we show that the LMS makes an important contribution to the overall volca

94 Experimentally, we demonstrate that the LMS promotes primary tumor growth that enriches for LMS(

95 km-long profile that is perpendicular to the LMS.

96 ation and density were obtained by using the LMS (lambda, mu, sigma) method.

97 endicular skeletal muscle mass utilizing the LMS statistical procedure.

98 crystalline basement was uplifted within the LMS orogenic belt, and that the neighbouring Songpan-Gan

99 ychev and Nabro eruptions is attributable to LMS aerosol.

100 Clinically, this corresponds to LMS(+) tumors being larger at diagnosis compared with LM

101 he development of drugs that are specific to LMS and has begun to shed light on the similarities and

102 ber of systemic therapies available to treat LMS has increased over the last decade, but the selectio

103 rcutaneous revascularization for unprotected LMS; 2) assess the underlying justification for randomiz

104 s of stenting versus surgery for unprotected LMS; and 3) examine the optimum approach to informed con

105 in good surgical candidates with unprotected LMS stenosis.

106 Patients with unresectable LMS of uterine (n = 29) or other (n = 5) primary sites w

107 ch patients, suggesting a need for a uterine LMS-specific staging system to better target patients fo

108 management of patients with advanced uterine LMS is divided between those with localized and those wi

109 le unique aspects of soft tissue and uterine LMS.

110 tes of stage-specific PFS and OS for uterine LMS were altered substantially when using the AJCC versu

111 lso underway for targeted therapy in uterine LMS.

112 Despite the infrequency of uterine LMS, several recent investigations have advanced our und

113 nowledge of the molecular biology of uterine LMS.

114 Patients with uterine LMS typically present with vaginal bleeding, pain, and a

115 nosis and surveillance in women with uterine LMS.

116 When LMS cells stably expressing versican siRNA were injected

117 mors being larger at diagnosis compared with LMS(-) tumors and to a marked rise in the incidence of m

118 Of these, all patients with LMS and 25% with LHON were found to have an MRI appearan

119 All patients with LMS and 26% of patients with LHON had white matter lesio

120 entional brain MRIs shows that patients with LMS have a scan appearance indistinguishable from MS.

121 , 31 patients with LHON and 11 patients with LMS was conducted by three independent experts in the fi

122 predict disease recurrence in patients with LMS which may allow us to identify a subset of patients

123 Patients with LMS-expressing primary tumors selectively fail in the lu

124 mcitabine plus docetaxel among patients with LMS.

125 ctive in treated and untreated patients with LMS.