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1 biologic agents (infliximab, adalimumab, and natalizumab).
2 ts given fingolimod, and 1160 patients given natalizumab.
3 multiple sclerosis (MS) who are treated with natalizumab.
4 rials established the efficacy and safety of natalizumab.
5 onance imaging MS activity after 24 doses of natalizumab.
6 score remained stable for patients receiving natalizumab.
7  died of PML after receiving 45 infusions of natalizumab.
8 far unreported amongst patients treated with natalizumab.
9 atients treated with the monoclonal antibody natalizumab.
10 lateral blindness following his 44th dose of natalizumab.
11 cal leukoencephalopathy (PML) in patients on natalizumab.
12  or multiple sclerosis patients treated with natalizumab.
13  being treated or considering treatment with natalizumab.
14 atients with multiple sclerosis treated with natalizumab.
15 ultiple sclerosis (MS) patients treated with natalizumab.
16 ncreases with the duration of treatment with natalizumab.
17 ith multiple sclerosis who were treated with natalizumab.
18 lso showed significantly improved HRQoL with natalizumab.
19 nce imaging, and improved significantly with natalizumab.
20  (MS): glatiramer acetate, mitoxantrone, and natalizumab.
21 -339.3, p < 0.0001) in patients treated with natalizumab.
22 r probability of disability improvement than natalizumab (0.35 [0.20-0.59], p=0.0006).
23 , fingolimod (1.27 [0.60-2.70], p=0.67), and natalizumab (0.81 [0.47-1.39], p=0.60).
24             Within 1.5 years of cessation of natalizumab, 1.8% (rituximab) and 17.6% (fingolimod) of
25 es of PML among 99,571 patients treated with natalizumab (2.1 cases per 1000 patients).
26 lity Status Scale score at the initiation of natalizumab, 3.6).
27 s received an initial i.v. bolus of placebo, natalizumab (30 mg/kg), or vedolizumab (30 mg/kg) before
28 ceived interferon beta-1a (IFN-beta-1a) plus natalizumab 300 mg (n = 589), or IFN-beta-1a plus placeb
29  Sclerosis (AFFIRM) study, patients received natalizumab 300 mg (n = 627) or placebo (n = 315); in th
30 centrations were randomized (1:1) to receive natalizumab 300 mg or placebo intravenously at Weeks 0,
31                                              Natalizumab, a humanized monoclonal antibody targeting a
32                                              Natalizumab, a new addition to the armamentarium for tre
33 e tested Plerixafor, a CXCR4 antagonist, and natalizumab, a VLA-4 antibody.
34                              INTERPRETATION: Natalizumab administered up to 9 h after stroke onset di
35                               Efalizumab and natalizumab administration is associated with CD4+ T lym
36 e decision was made to continue or interrupt natalizumab after 24 doses.
37 alemtuzumab, interferon beta, fingolimod, or natalizumab), age 65 years or younger, Expanded Disabili
38 e, we review the bench-to-bedside journey of natalizumab, along with the lessons learned from postmar
39        We assessed the effect of one dose of natalizumab, an antibody against the leukocyte adhesion
40            Our objective was to test whether natalizumab, an antibody against very late activating an
41           Week 4 response rates were 51% for natalizumab and 37% for placebo (P = .001).
42                                         Both natalizumab and alemtuzumab seem highly effective and vi
43 risk of developing PML during treatment with natalizumab and detect early suspected PML using MRI inc
44  the disability-time curve) differed between natalizumab and fingolimod (-0.12 vs 0.04 per year, resp
45 d relapse rates decreased from 1.5 to 0.2 on natalizumab and from 1.3 to 0.4 on fingolimod, with 50%
46 d high-titer neutralizing antibodies against natalizumab and had to stop therapy.
47 ct the potential immunosuppressive effect of natalizumab and hence be associated with a reduced risk
48 ith multiple sclerosis who were treated with natalizumab and in whom PML later developed.
49 r or with approved second-line drugs such as natalizumab and mitoxantrone.
50 rapies in MS include interferon, glatiramer, natalizumab and mitoxantrone.
51                                              Natalizumab and placebo groups had similar incidences of
52 ) or immunoabsorption to hasten clearance of natalizumab and shorten the period in which natalizumab
53 ed out, the shared reason for switching from natalizumab and the preferential use of either rituximab
54  modulatory monoclonal antibodies rituximab, natalizumab, and efalizumab have received regulatory app
55                                 Alemtuzumab, natalizumab, and fingolimod were associated with the gre
56 e achieved within 1 day of the first dose of natalizumab, and similar levels were continuously mainta
57                                              Natalizumab antibody to alpha4-integrins is used in ther
58 responders among disabled MS subjects in the natalizumab arms than in the placebo or IM IFNbeta-1a ar
59 pse rates were observed in patients who used natalizumab as first MS therapy, in patients with lower
60 strating the early and sustained efficacy of natalizumab as induction therapy in patients with elevat
61            AIJCV was assessed in 37 cases of natalizumab-associated PML and 89 MS-patients treated wi
62         Twenty-six of 37 (70%) patients with natalizumab-associated PML exhibited an AIJCV > 1.5, whe
63 CR for JCV DNA, 11 of 20 (55%) patients with natalizumab-associated PML had an AIJCV > 1.5.
64  pattern facilitates an earlier diagnosis of natalizumab-associated PML in an asymptomatic stage asso
65                     18 patients with MS with natalizumab-associated PML lesions on MRI were included.
66                                 Asymptomatic natalizumab-associated PML manifestations on MRI show a
67 ients with multiple sclerosis, who developed natalizumab-associated PML or GCN with regard to JC vira
68                    Identifying patients with natalizumab-associated PML poses a diagnostic challenge
69 tudy assessing brain MRI of 26 patients with natalizumab-associated PML presenting with lesions sugge
70                                 Fortunately, natalizumab-associated PML remains a rare entity compare
71                    WHERE NEXT?: Diagnosis of natalizumab-associated PML requires optimised clinical v
72 more common and more severe in patients with natalizumab-associated PML than it is in patients with H
73 ancement is the most common earliest sign of natalizumab-associated PML-IRIS with a frequent imaging
74 should be included in the case definition of natalizumab-associated PML.
75 been identified that aid in the diagnosis of natalizumab-associated PML.
76 al presentation, diagnosis, and treatment of natalizumab-associated PML.
77  antibody index (AIJCV ) in the diagnosis of natalizumab-associated PML.
78                               BACKGROUND AND Natalizumab-associated progressive multifocal leukoencep
79 constitution inflammatory syndrome (IRIS) in natalizumab-associated progressive multifocal leukoencep
80 lerosis who received 12 or more infusions of natalizumab at an academic multiple sclerosis center.
81                             IDG discontinued natalizumab at once and initiated another disease modify
82 currently being treated with, or initiating, natalizumab, based on their anti-JCV antibody status.
83                         Patients who stopped natalizumab because of poor tolerance or lack of efficac
84 l to monitor the risk incurred during use of natalizumab beyond 3 years.
85 nized anti-alpha4 integrin antibody known as Natalizumab, blocks homing of mononuclear cells to the C
86                                              Natalizumab can be a therapeutic option in patients with
87   We sought to determine whether exposure to natalizumab causes subclinical reactivation and neurotro
88 sitive multiple sclerosis (MS) patients from natalizumab clinical studies and postmarketing sources.
89 lished using sera from >800 MS patients from natalizumab clinical studies.
90 le from 2,113 multiple sclerosis patients in natalizumab clinical studies.
91  from nearly 1,400 patients participating in natalizumab clinical trials were tested for JCV DNA usin
92          Follow-up for at least 4 years from natalizumab commencement in 468 patients and at least 2
93 izumab (n = 81), with a protective effect of natalizumab continuation on both outcomes (odds ratio [O
94 ect of natalizumab on the risk of relapse in natalizumab continuers compared with natalizumab quitter
95                     In the as-treated group, natalizumab continuers received natalizumab, natalizumab
96  .03) MS activity was significantly lower in natalizumab continuers than in natalizumab switchers or
97 ncephalopathy (PML) following treatment with natalizumab develop IRIS which carries a high morbidity
98 unotherapies, including cyclophosphamide and natalizumab, did not improve her cognitive deficits, nec
99  benefits of disease control, we initiated a natalizumab discontinuation study.
100                                              Natalizumab discontinuation therapy was associated with
101  therapy >/=24 months and were contemplating natalizumab discontinuation were enrolled.
102                                        After natalizumab discontinuation, 1 patient developed progres
103 creased risk of MS activity resumption after natalizumab discontinuation.
104  alemtuzumab, and dimethyl fumarate, whereas natalizumab disproportionally increases them in the bloo
105                                              Natalizumab dosage interruption is associated with clini
106                                  At the time natalizumab dosing was suspended, JCV DNA was detected i
107 utcomes for all RRMS patients switching from natalizumab due to JC virus antibody positivity at 3 Swe
108 imod in stable RRMS patients who switch from natalizumab due to JC virus antibody positivity.
109 apies, and natalizumab quitters discontinued natalizumab during the study year.
110  and thrombocytopenia in newborns exposed to natalizumab during the third trimester.
111 ive multiple sclerosis who were treated with natalizumab during their third trimester of pregnancy, w
112          Recently, the monoclonal antibodies natalizumab, efalizumab, and rituximab--used for the tre
113 -infected CD8-depleted macaques treated with natalizumab either early (the day of infection) or late
114 ur l'Introduction du Fingolimod en Relais au Natalizumab (ENIGM) study, a survey-based, observational
115 ge, comprehensive data about third-trimester natalizumab exposure are scant.
116                                      Neither natalizumab exposure nor prior immunosuppressant use app
117 alence was similar in patients regardless of natalizumab exposure or prior immunosuppressant use, p =
118 mpared the effectiveness of alemtuzumab with natalizumab, fingolimod, and interferon beta in patients
119  We review each of the newly approved agents-natalizumab, fingolimod, teriflunomide, dimethyl fumarat
120         Treatment of multiple sclerosis with natalizumab first involves risk stratifying patients.
121                                   The use of natalizumab for highly active relapsing-remitting multip
122 mple was drawn from 23 MS patients receiving natalizumab for more than 24 months and from 18 healthy
123 virus (JCV), can occur in patients receiving natalizumab for multiple sclerosis (MS).
124 diction of risk of PML in patients receiving natalizumab for multiple sclerosis, supporting yearly be
125 s review article summarizes the evolution of natalizumab from target molecule discovery through regul
126                          Two patients in the natalizumab group died because of adverse events assesse
127                                              Natalizumab has been available as a multiple sclerosis t
128             Two weeks after his 45th dose of natalizumab, he developed hemiplegia that evolved into q
129                                              Natalizumab improves ambulatory function in disabled RRM
130 e Sclerosis [AFFIRM], Safety and Efficacy of Natalizumab in Combination With Interferon Beta-1a in Pa
131 ebo (n = 315); in the Safety and Efficacy of Natalizumab in Combination with Interferon Beta-1a in Pa
132  regression was observed after the switch to natalizumab in comparison to fingolimod (p < 0.001).
133 anisms that may contribute to the benefit of natalizumab in MS, as well as candidate therapeutics tha
134 rapeutic choices is needed after 24 doses of natalizumab in patients with multiple sclerosis (MS).
135 e use of intense immunosuppressant drugs and natalizumab in patients with rapidly worsening MS and pr
136                                              Natalizumab induced response and remission at Week 8 tha
137 o-controlled trial evaluated the efficacy of natalizumab induction therapy in patients with Crohn's d
138 e modifying therapy (DMT) following the last natalizumab infusion, while the TG received two more nat
139 d at baseline, 6 and 12 months from the last natalizumab infusion.
140 natalizumab to fingolimod after a mean of 31 natalizumab infusions (female to male ratio, 2.36; mean
141                     Annual PML risks (per 12 natalizumab infusions) for patients without PML in the p
142 mab infusion, while the TG received two more natalizumab infusions, at 6 and 8 weeks (14 weeks from s
143 eucoencephalopathy reported, following 11-44 natalizumab infusions.
144 s were continuously maintained under monthly natalizumab infusions.
145  intervals to 10 months during the course of natalizumab infusions.
146                                              Natalizumab inhibits the trafficking of lymphocytes from
147  .001) and with less disease activity before natalizumab initiation (P = .03).
148 r median Expanded Disability Status Scale at natalizumab interruption was 3.0 and increased to 6.0 du
149                                              Natalizumab is an effective treatment for patients with
150             With ongoing safety evaluations, natalizumab is being reevaluated by the US Food and Drug
151         Treatment of multiple sclerosis with natalizumab is complicated by rare occurrence of progres
152                                              Natalizumab is effective in anti-TNF failures and patien
153 le disease-modifying therapies, switching to natalizumab is more effective than switching to fingolim
154 bsample of 5 mother-child pairs, we analyzed natalizumab levels in the umbilical cord blood.
155 cases occurred during the first two years of natalizumab marketing but, by the end of November, 2009,
156                       Our data indicate that natalizumab may be safe and effective against MS in pedi
157 CV-seropositive MS patients, including 32 on natalizumab monotherapy >18 months, 6 on interferon beta
158                    The risks and benefits of natalizumab must be reassessed with continued therapy du
159 s significantly lower in patients continuing natalizumab (n = 43) than in patients interrupting natal
160 zumab (n = 43) than in patients interrupting natalizumab (n = 81), with a protective effect of natali
161 2015, 161 patients were randomly assigned to natalizumab (n=79) or placebo (n=82).
162 ncluded patients, 578 patients were matched (natalizumab, n = 407; fingolimod, n = 171).
163 eated group, natalizumab continuers received natalizumab, natalizumab switchers changed to different
164                                              Natalizumab, no treatment, interferon beta, glatiramer a
165 modifying treatments for multiple sclerosis, natalizumab (NTZ) is highly effective, well tolerated an
166                                              Natalizumab (NTZ), a monoclonal antibody to human alpha4
167 ultiple sclerosis (MS) patients treated with natalizumab (NTZ).
168                                 The Tysabri (natalizumab) Observational Program (TOP) is an open-labe
169                        Assess the effects of natalizumab on ambulatory function in disabled subjects
170  quitters, confirming a protective effect of natalizumab on the risk of relapse in natalizumab contin
171 ing infusions of the CD49d-blocking antibody natalizumab) on levels of circulating HSPCs after a sing
172 e, clinicians often switch therapy to either natalizumab or fingolimod.
173 onths immediately preceding switch to either natalizumab or fingolimod.
174 andomly assigned (1:1) to 300 mg intravenous natalizumab or placebo with stratification by treatment
175 ith multiple sclerosis who were treated with natalizumab over an 18-month period, performing quantita
176 f PML increases with duration of exposure to natalizumab over the first 3 years of treatment.
177               These data confirm that JCV in natalizumab-PML patients is similar to that observed in
178                                              Natalizumab prevented CNS inflammation and demyelination
179                   Chemotherapy combined with Natalizumab prolonged survival of NOD/SCID recipients of
180 apse in natalizumab continuers compared with natalizumab quitters (OR, 4.40; 95% CI, 1.72-11.23) and
181 witchers changed to different therapies, and natalizumab quitters discontinued natalizumab during the
182           No disease rebound was observed in natalizumab quitters.
183 spended pending a safety review when several natalizumab recipients were diagnosed as having progress
184 opeller and thigh domain fragment shows that natalizumab recognizes human-mouse differences on the ci
185     In a 48-week study testing the safety of natalizumab redosing, JCV DNA was detected in plasma of
186                                              Natalizumab reduces multiple sclerosis relapses very eff
187 ongitudinal clinical course of patients with natalizumab-related progressive multifocal leukoencephal
188  natalizumab and shorten the period in which natalizumab remains active (usually several months).
189    Therapy discontinuation after 24 doses in natalizumab-responding patients should be considered onl
190 d treatment with the CD49d-blocking antibody natalizumab resulted in significantly decreased migratio
191 ebrospinal fluid of MS patients treated with natalizumab revealed that transmigration of this subset
192                     Interim TOP data confirm natalizumab's overall safety profile and the low relapse
193                                       In the Natalizumab Safety and Efficacy in Relapsing Remitting M
194 tively analyzed data from 3 clinical trials (Natalizumab Safety and Efficacy in Relapsing-Remitting M
195              INTERPRETATION: Alemtuzumab and natalizumab seem to have similar effects on annualised r
196                                              Natalizumab seems superior to alemtuzumab in enabling re
197  Treatment decisions between alemtuzumab and natalizumab should be primarily governed by their safety
198                   Thus patients treated with natalizumab show clinical benefit even in the presence o
199                                              Natalizumab significantly improved SF-36 PCS and Mental
200                                          The natalizumab story highlights both the opportunities and
201  sclerosis (RRMS) patients who are stable on natalizumab switch to other therapies to avoid progressi
202  quitters (OR, 4.40; 95% CI, 1.72-11.23) and natalizumab switchers (OR, 3.28; 95% CI, 0.99-10.79).
203 natalizumab continuers received natalizumab, natalizumab switchers changed to different therapies, an
204 ntly lower in natalizumab continuers than in natalizumab switchers or quitters, confirming a protecti
205                                              Natalizumab, the first anti-integrin antibody tested for
206                               Fingolimod and natalizumab therapies efficiently targeted autoreactive
207 with multiple sclerosis (MS) who had been on natalizumab therapy >/=24 months and were contemplating
208 r long-term anti-very late antigen-4 (VLA-4)/natalizumab therapy (LTNT) and from CNS specimens.
209 n the 12 months prior to baseline to 0.31 on natalizumab therapy (p<0.0001), remaining low at 5 years
210 lopathy risk associated with >/=24 months of natalizumab therapy against the benefits of disease cont
211           The mean (SD) age at initiation of natalizumab therapy was 16.7 (1.1) years, and the mean (
212 gulated in developing B cells in response to natalizumab therapy, a known risk factor for PML.
213  immunosuppressants before the initiation of natalizumab therapy, and had received 25 to 48 months of
214                 After the discontinuation of natalizumab therapy, relapse activity occurred in 6 of 8
215                           After 12 months of natalizumab therapy, the prevalence of JC virus in the u
216 s of immunosuppression that may occur during natalizumab therapy.
217 In total, 333 patients with MS switched from natalizumab to fingolimod after a mean of 31 natalizumab
218    The safety and efficacy of switching from natalizumab to fingolimod have not yet been evaluated in
219                In this study, switching from natalizumab to fingolimod was associated with a risk of
220 cipants were patients for whom a switch from natalizumab to fingolimod was planned.
221 ocyte traffic, was diminished in DRGs of all natalizumab-treated animals.
222 A was detectable within cell compartments of natalizumab-treated MS patients after treatment inceptio
223   In this retrospective review, the first 40 natalizumab-treated MS patients diagnosed with PML in th
224 sive multifocal leukoencephalopathy (PML) in natalizumab-treated MS patients is linked to JC virus (J
225 NA was detected in the CSF of 2 of 27 (7.4%) natalizumab-treated MS patients who had no symptoms or m
226                         In our evaluation of natalizumab-treated MS patients, 53.6% tested positive f
227 tomatic JCV reactivation may occur in CSF of natalizumab-treated MS patients.
228 y in screening and early diagnosis of PML in natalizumab-treated MS patients.
229 kely to be useful for predicting PML risk in natalizumab-treated MS patients.
230 ring JC virus (JCV) DNA in blood or urine of natalizumab-treated multiple sclerosis (MS) patients to
231                                              Natalizumab-treated patients also had significantly high
232       Sustained remission occurred in 26% of natalizumab-treated patients and 16% of patients receivi
233 sustained through Week 12 occurred in 48% of natalizumab-treated patients and 32% of patients receivi
234 25.6%) subjects without a difference between natalizumab-treated patients and controls.
235                                              Natalizumab-treated patients in both studies were more l
236                                      Data on natalizumab-treated patients were pooled from four large
237  frequencies in untreated and fingolimod- or natalizumab-treated patients with MS.
238 characteristics of PML-IRIS manifestation in natalizumab-treated patients with multiple sclerosis and
239                              We report on 20 natalizumab-treated patients with multiple sclerosis who
240 istry to estimate the incidence of PML among natalizumab-treated patients with multiple sclerosis, ac
241 sociated with distinct levels of PML risk in natalizumab-treated patients with multiple sclerosis.
242 eactivation of JC virus occurs frequently in natalizumab-treated patients with multiple sclerosis.
243 pse rate and stabilised disability levels in natalizumab-treated patients with RRMS in clinical pract
244  were evaluated in a single center cohort of natalizumab-treated patients.
245 gher at subsequent assessments (P < .001) in natalizumab-treated patients.
246 ted >6 months prior to PML diagnosis from 71 natalizumab-treated PML patients and 2,522 non-PML anti-
247 rmine the presence of anti-JCV antibodies in natalizumab-treated PML patients where serum samples wer
248               Using biofluid samples from 17 natalizumab-treated PML patients, we sequenced multiple
249  DNA sequences in blood, CSF and/or urine of natalizumab-treated PML patients.
250                                 The blood of natalizumab-treated subjects also contained SCID-repopul
251 le sclerosis patient who developed PML under natalizumab treatment and a vigorous immune response aga
252 therapy, and had received 25 to 48 months of natalizumab treatment had the highest estimated risk (in
253 ML) is a serious side effect associated with natalizumab treatment in multiple sclerosis (MS).
254 ve multifocal leukoencephalopathy (PML) with natalizumab treatment is associated with the presence of
255 ver, severe disease activity may return once natalizumab treatment is withdrawn, as recommended durin
256                         Sometimes restarting natalizumab treatment may be the best option for the mot
257 orted here sought to determine the effect of natalizumab treatment on relapse activity in the minorit
258                                              Natalizumab treatment resulted in a decrease in the numb
259 ults, close clinical vigilance is indicated, natalizumab treatment should be suspended, and JCV polym
260                                              Natalizumab treatment significantly reduced the annualis
261 itive patients who wish to begin or continue natalizumab treatment to be managed with a more individu
262             These data link the mechanism of natalizumab treatment with progressive multifocal leukoe
263 mmunosuppressants, and increased duration of natalizumab treatment, alone or in combination, were ass
264  (JC) antibodies, with prolonged duration of natalizumab treatment, and with prior exposure to immuno
265             These analyses demonstrated that natalizumab treatment, both alone (AFFIRM) and in combin
266              Clinical data were collected on natalizumab treatment, duration and management of the wa
267 eveloped, progressive cerebellar signs under natalizumab treatment, especially in cases where cerebel
268 thology showed diminished DRG pathology with natalizumab treatment, including decreased inflammation,
269 te neurological disability despite long-term natalizumab treatment.
270 atus, prior immunosuppression, and length of natalizumab treatment.
271  infections have been rarely reported during natalizumab treatment.
272 munosuppressants, and increasing duration of natalizumab treatment.
273 leukoencephalopathy (PML) is associated with natalizumab treatment.
274 tion, and 19% (16/84) had no interruption in natalizumab treatment.
275  any of these 1,094 patients before or after natalizumab treatment.
276 +) T lymphocytes in DRGs was not affected by natalizumab treatment.
277 t suffer this opportunistic infection during natalizumab treatment.
278 and 55 (25%) were positive after 48 weeks of natalizumab, treatment.
279 f FAE and bsAb formation using Hz6F4-2v3 and natalizumab, two humanized IgG4s which bind to human Jun
280 at target the cell adhesion molecules VLA-4 (natalizumab; Tysabri for multiple sclerosis and Crohn's
281              Shortly after initial approval, natalizumab use was suspended pending a safety review wh
282  more personalized decision making and safer natalizumab use.
283  in patients being treated with rituximab or natalizumab warrants early assessment for JCV infection.
284                               Treatment with natalizumab was associated with reductions in mean annua
285                                              Natalizumab was detectable in all 5 newborns.
286                                              Natalizumab was granted approval by the US Food and Drug
287                                              Natalizumab was later reintroduced with required adheren
288                     After the safety review, natalizumab was reintroduced to the market in 2006.
289 us success of a molecular targeted approach, natalizumab was the first mAb approved for the treatment
290                                              Natalizumab was well tolerated in this study.
291 wever, only a few months after its approval, natalizumab was withdrawn from the market because of an
292 ML probability over 6 years (72 infusions of natalizumab) was 2.7% (95% CI 1.8-4.0) in patients with
293 unders (age, sex, disability status, time on natalizumab, washout time, follow-up time, and study cen
294 pha(4)beta(1) and alpha(4)beta(7) antagonist natalizumab were compared with those of the alpha(4)beta
295 n patients with multiple sclerosis receiving natalizumab were stratified by three risk factors: anti-
296             Response and remission rates for natalizumab were superior to those for placebo at Weeks
297 d leukocyte traffic by treating animals with natalizumab, which binds to alpha4-integrins.
298                                              Natalizumab, which binds very late antigen-4 (VLA-4), is
299 sis patients treated with the anti-VLA-4 mAb natalizumab, which selectively inhibits cell migration a
300 sociated PML and 89 MS-patients treated with natalizumab without PML.

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