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1                                              LMS impacts infant weight gain by limiting milk volume,
2                                              LMS PCI performed at NSC was not associated with increas
3 mic hybridization (aCGH) was performed on 20 LMS samples and showed that the molecular subtypes defin
4 ene expression profiling was performed on 51 LMS samples.
5 siRNA to knock down versican expression in a LMS human cell line, SK-LMS-1.
6 retreated population of adults with advanced LMS.
7 ed rise in the incidence of metastasis after LMS(+) tumors reach 2 cm.
8 7 offers an opportunity to turn TAMs against LMS cells by allowing the phagocytic behavior of residen
9                                     Although LMS is easily recognized histopathologically, the cause
10 S: n = 70 [24.4%]; MPNST: n = 27 [9.4%]; and LMS: n = 28 [9.8%]) were randomly assigned to either A+I
11 ostic method to distinguish between GIST and LMS and has the potential to be rapidly implemented in a
12 assifier that distinguishes between GIST and LMS with an accuracy of 99.3% on the microarray samples
13 nd 62% of metastatic GIST, embryonal RMS and LMS samples, respectively.
14 tic and benign counterparts of GIST, RMS and LMS tumors, and DMD deletions inactivate larger dystroph
15 oice for most patients with three-vessel and LMS disease and especially in those with the most severe
16                           Mimulus cardinalis LMS (McLMS) is weakly expressed and has a nonsense mutat
17                                  Here, chlOR(LMS) , chlOR(QY071) and chlOR(L-11A) completely from the
18                    The oxidoreductases ChlOR(LMS) , ChlOR(QY071) and ChlOR(L-11A) were all classified
19 ore effective in metabolizing CHL than ChlOR(LMS) .
20 ge-matched and sex-matched healthy controls (LMS = 0).
21                                   Currently, LMS treatment is not informed by molecular subtyping and
22                   Of these, dedifferentiated LMS with high immune infiltration and tumors primarily o
23           Compared with the robust diffusion LMS (RDLMS), diffusion Normalized Least Mean M-estimate
24 MS PCI volumes at NSC, particularly elective LMS PCI.
25 motes primary tumor growth that enriches for LMS(+) cells, and it allows for intravasation after reac
26 n evidence-based, noninvasive evaluation for LMS is driven by a clear need to avoid such harms while
27                           MRI evaluation for LMS may potentially serve this purpose in symptomatic wo
28 agnosis, genomics, and treatment options for LMS.
29 rectomy) for patients with elevated risk for LMS and, conversely, to safely offer women with no or mi
30 reasing trend to use drug-eluting stents for LMS stenosis rather than CABG despite very little high-q
31 gesting a promising therapeutic strategy for LMS.
32 es with poor prognosis in both gynecological LMS (P = 0.00006) and nongynecological LMS (P = 0.03).
33                             In gynecological LMS, a similar trend was noted but did not reach statist
34                             In gynecological LMS, the coordinate expression of these four markers was
35 ant elevated expression of versican in human LMS versus benign leiomyomas.
36 ith CD47 increases phagocytosis of two human LMS cell lines, LMS04 and LMS05, in vitro.
37                           We have identified LMS as the first human disease, to our knowledge, caused
38 ntification of novel agents with activity in LMS is clearly needed.
39 nzymes, PSS1, were described as causative in LMS patients.
40 lar cardiomyocyte gene expression changes in LMS and mouse models.
41  in HG-MLPS; gemcitabine plus dacarbazine in LMS; high-dose prolonged-infusion ifosfamide in SS; etop
42                There has been an increase in LMS PCI volumes at NSC, particularly elective LMS PCI.
43 racellular matrix proteoglycan, increases in LMS.
44       Currently, the only curative option in LMS is surgery and despite progress in systemic therapy
45 reviously shown that the presence of TAMs in LMS is associated with poor clinical outcome and the ove
46 al outcome and the overall effect of TAMs in LMS therefore appears to be protumorigenic.
47 ssess lower estrogenic potential, indicating LMS as a safe detoxification strategy in food systems.
48       These findings offer key insights into LMS for ZEN degradation and the underlying degradation p
49                              Leiomyosarcoma (LMS) is a mesenchymal cancer that occurs throughout the
50                              Leiomyosarcoma (LMS) is a soft tissue tumor with a significant degree of
51                              Leiomyosarcoma (LMS) is a tumor of smooth muscle that can express varyin
52                              Leiomyosarcoma (LMS) is one of the most common subtypes of soft tissue s
53 C) in patients with advanced leiomyosarcoma (LMS).
54 , rhabdomyosarcoma (RMS) and leiomyosarcoma (LMS), feature myogenic differentiation.
55 diagnosis of the more common leiomyosarcoma (LMS) anatomic variants, potentially useful prognostic ma
56 rating lymphocytes (TILs) in leiomyosarcoma (LMS), a subtype of soft tissue sarcoma that exhibits his
57 therapy agents are active in leiomyosarcoma (LMS), particularly LMS that has progressed after doxorub
58 f uterine sarcomas including leiomyosarcoma (LMS), endometrial stromal sarcoma, high-grade undifferen
59 yxoid liposarcoma (HG-MLPS); leiomyosarcoma (LMS), synovial sarcoma (SS), malignant peripheral nerve
60 rognosis in nongynecological leiomyosarcoma (LMS).
61                      Uterine leiomyosarcoma (LMS) is staged by the modified International Federation
62 ation of unsuspected uterine leiomyosarcoma (LMS) throughout the pelvis of a physician treated for sy
63 acting management of uterine leiomyosarcoma (LMS).
64 rrent and metastatic uterine leiomyosarcoma (LMS).
65                             Leiomyosarcomas (LMS) are genetically heterogeneous tumors differentiatin
66                              Mimulus lewisii LMS (MlLMS) and OS (MlOS) are expressed most strongly in
67 Plateau, including the uplifted Longmenshan (LMS) orogenic belt, is accurately imaged in spite of the
68 ogy of lutein ester loaded saponin micelles (LMS), cryo-TEM micrographs showed depending on the compo
69 pants were further stratified into moderate (LMS < 14, n = 13) and severe (LMS 14, n = 9) inflammatio
70 and IHC, we characterized distinct molecular LMS subtypes, provided insight into their pathogenesis,
71             This association of LHON and MS (LMS) raises an important question about whether there co
72 gical LMS (P = 0.00006) and nongynecological LMS (P = 0.03).
73 n important role in the clinical behavior of LMS that may open a window for new therapeutic reagents.
74 and TGCT-associated proteins in 149 cases of LMS.
75 h the predicted dominant de novo etiology of LMS, we identified causative heterozygous missense mutat
76 he primary aim was to define MRI features of LMS and LHON, and to assess the proportions of individua
77  restored cell proliferation to the level of LMS controls, increased the pericellular coat and the re
78 relevance of the immune microenvironments of LMS and other sarcoma subtypes.
79 erapy is not based on the anatomic origin of LMS.
80 rofiling highlight the very early origins of LMS.
81 ared patient characteristics and outcomes of LMS PCI performed across SC and NSC in England and Wales
82                            The proportion of LMS PCI performed in NSC increased >2-fold.
83 xpression was accompanied by slower rates of LMS cell proliferation and migration, increased adhesion
84             Here we show that in a subset of LMS cases, CSF1 is expressed by the malignant cells.
85        We uncover three specific subtypes of LMS that likely develop from distinct lineages of smooth
86 cover and characterize molecular subtypes of LMS.
87 analyze 70 genomes and 130 transcriptomes of LMS, including multiple tumor regions and paired metasta
88 f control in the management and treatment of LMS.
89 xorubicin holds promise for the treatment of LMS.
90 oxorubicin holds promise in the treatment of LMS.
91 gical biomarkers in the diagnostic workup of LMS.
92  Immunohistochemistry (IHC) was performed on LMS tissue microarrays (n=377) for five markers with hig
93 he highest priorities for future research on LMS evaluation.
94 active in leiomyosarcoma (LMS), particularly LMS that has progressed after doxorubicin treatment.
95 , LMR, CAR) and cumulative scores (NLS, PLS, LMS, NPS, mGPS).
96 den within a retrospective cohort of primary LMS specimens.
97                         A set of reestimated LMS parameters that incorporated a smoothed 99th percent
98                              The reestimated LMS parameters had several drawbacks and no clear advant
99 ctable or metastatic, relapsed or refractory LMS were treated with escalating doses of unesbulin oral
100     Linkage studies suggest that the related LMS and ADULT syndromes are also caused by mutations in
101 ervised clustering showed three reproducible LMS clusters.
102 d sinonasal inflammation (Lund-Mackay score [LMS] 10) and were compared with age-matched and sex-matc
103 into moderate (LMS < 14, n = 13) and severe (LMS 14, n = 9) inflammation groups.
104 at were estimated using the lambda-mu-sigma (LMS) method.
105 CDC) growth charts included lambda-mu-sigma (LMS) parameters intended to calculate smoothed percentil
106 "lung metastasis gene-expression signature" (LMS) that mediates experimental breast cancer metastasis
107 lines (DBTRG, U373 and SNB19), as well as SK-LMS-1 human leiomyosarcoma cells are also sensitive to f
108                 In experiments with human SK-LMS-1 leiomyosarcoma cells, we show that the Akt kinase
109  of both uPA and its cellular receptor in SK-LMS-1 cells.
110 ing in the human leiomyosarcoma cell line SK-LMS-1 enhances its in vivo tumorigenicity, an effect for
111 a into the human leiomyosarcoma cell line SK-LMS-1.
112 ican expression in a LMS human cell line, SK-LMS-1.
113 ressing cancer cells, including the lines SK-LMS-1 (human leiomyosarcoma), U118 (human glioblastoma),
114 te cancer (PC-3 and TR6LM, human sarcoma (SK-LMS-1), glioblastoma (DBTRG), and gastric cancer (MKN45)
115 separation of conditioned medium from the SK-LMS-1 human leiomyosarcoma cell line.
116                 The strain, Nocardioides sp. LMS-CY, Nocardioides sp. QY071 and Nocardioides sp. L-11
117  two-thirds of patients with left main stem (LMS) disease have a survival benefit and marked reductio
118 e complex procedures such as left main stem (LMS) PCI.
119 ery disease with unprotected left main stem (LMS) stenosis, coronary artery bypass grafting (CABG) is
120 he transcription of the pnb operon in strain LMS-CY.
121 rom the actinomycete Nocardioides sp. strain LMS-CY was biochemically confirmed to express 4-NBA degr
122 anic aerosols in the lowermost stratosphere (LMS) had not been considered.
123 rcentiles extrapolated from the CDC-supplied LMS parameters did not match well to the empirical data
124          Extrapolation from the CDC-supplied LMS parameters does not provide a good fit to the empiri
125                             Low milk supply (LMS) is a major barrier to exclusive and continued lacta
126                      Lenz-Majewski syndrome (LMS) is a rare disease characterized by complex craniofa
127                      Lenz-Majewski syndrome (LMS) is a syndrome of intellectual disability and multip
128  production, causing Lenz-Majewski syndrome (LMS).
129 eft lip/palate (EEC), Limb-mammary syndrome (LMS) and split hand-foot malformation (SHFM) dysplasias.
130  (EEC; OMIM 604292), limb--mammary syndrome (LMS; OMIM 603543), acro-dermato-ungual-lacrimal-tooth sy
131 tion at two loci, LIMONENE-MYRCENE SYNTHASE (LMS) and OCIMENE SYNTHASE (OS).
132                            We establish that LMS have generally low and spatially homogenous TIL burd
133                                          The LMS method was used to derive 10 smoothed skinfold-thick
134                                          The LMS values underlying the charts were presented, enablin
135  indication that the lower crust beneath the LMS was folded and pushed upwards and the upper crust wa
136 ood of metastatic recurrence provided by the LMS may help to explain observations of prognostic gene
137 well approximated by extrapolations from the LMS values.
138 eric aerosol optical depth originated in the LMS during the period 2008-2011.
139                                       In the LMS group, despite higher concentrations of HM protein,
140 ite of the extreme topographic relief in the LMS region and thick sedimentary covers in the neighbour
141 derstanding of the underlying biology of the LMS variants, improved diagnostics and more effective, l
142                   After outlier removal, the LMS (Lambda-Mu-Sigma) function within R's GAMLSS package
143 lution measurement methods, we show that the LMS makes an important contribution to the overall volca
144      Experimentally, we demonstrate that the LMS promotes primary tumor growth that enriches for LMS(
145 km-long profile that is perpendicular to the LMS.
146 ation and density were obtained by using the LMS (lambda, mu, sigma) method.
147 endicular skeletal muscle mass utilizing the LMS statistical procedure.
148 crystalline basement was uplifted within the LMS orogenic belt, and that the neighbouring Songpan-Gan
149 ures of wild-type human PSS1 (PSS1(WT)), the LMS-causing Pro269Ser mutant (PSS1(P269S)), and PSS1(WT)
150 olume, underscoring the importance of timely LMS detection to ensure adequate infant nutrition.
151 ychev and Nabro eruptions is attributable to LMS aerosol.
152 tational diabetes mellitus may contribute to LMS and alter human milk (HM) composition, affecting inf
153              Clinically, this corresponds to LMS(+) tumors being larger at diagnosis compared with LM
154 ment, the contribution of genetic factors to LMS subtype, origins, and timing are unknown.
155 ing lethal metastases arise decades prior to LMS diagnosis.
156 he development of drugs that are specific to LMS and has begun to shed light on the similarities and
157 ber of systemic therapies available to treat LMS has increased over the last decade, but the selectio
158  seven hundred forty-four patients underwent LMS PCI during the period, of which 13 922 (34.2%) had t
159 rcutaneous revascularization for unprotected LMS; 2) assess the underlying justification for randomiz
160 s of stenting versus surgery for unprotected LMS; and 3) examine the optimum approach to informed con
161 in good surgical candidates with unprotected LMS stenosis.
162                   Patients with unresectable LMS of uterine (n = 29) or other (n = 5) primary sites w
163 ch patients, suggesting a need for a uterine LMS-specific staging system to better target patients fo
164 management of patients with advanced uterine LMS is divided between those with localized and those wi
165 le unique aspects of soft tissue and uterine LMS.
166 tes of stage-specific PFS and OS for uterine LMS were altered substantially when using the AJCC versu
167 lso underway for targeted therapy in uterine LMS.
168 valence than previously suspected of uterine LMS in resected masses presumed to represent leiomyoma,
169           Despite the infrequency of uterine LMS, several recent investigations have advanced our und
170 nowledge of the molecular biology of uterine LMS.
171                        Patients with uterine LMS typically present with vaginal bleeding, pain, and a
172 nosis and surveillance in women with uterine LMS.
173                                         When LMS cells stably expressing versican siRNA were injected
174 mors being larger at diagnosis compared with LMS(-) tumors and to a marked rise in the incidence of m
175  examined associations of HM components with LMS and maternal factors, and relationships between infa
176                  Of these, all patients with LMS and 25% with LHON were found to have an MRI appearan
177                            All patients with LMS and 26% of patients with LHON had white matter lesio
178 entional brain MRIs shows that patients with LMS have a scan appearance indistinguishable from MS.
179 , 31 patients with LHON and 11 patients with LMS was conducted by three independent experts in the fi
180  predict disease recurrence in patients with LMS which may allow us to identify a subset of patients
181                                Patients with LMS-expressing primary tumors selectively fail in the lu
182 mcitabine plus docetaxel among patients with LMS.
183 ctive in treated and untreated patients with LMS.

 
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