PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
27521440-11	2016	In the replication phase, more NfL-positive patients, according to the cutoff, evolved to MS. Every 100-ng/L increase in NfL predicted CDMS (hazard ratio [HR] = 1.009, 95% CI 1.005-1.014) and McDonald MS (HR = 1.009, 95% CI 1.005-1.013), remaining significant for CDMS in the multivariate analysis (adjusted HR = 1.005, 95% CI 1.000-1.011).	cdms	135-139	neurofilament light chain	Homo sapiens	31-34
28182037-7	2017	CONCLUSION: JAK2 V617F mutation is more commonly seen in older age as a risk for complications related to CDMS.	cdms	106-110	Janus kinase 2	Homo sapiens	12-16
27521440-11	2016	In the replication phase, more NfL-positive patients, according to the cutoff, evolved to MS. Every 100-ng/L increase in NfL predicted CDMS (hazard ratio [HR] = 1.009, 95% CI 1.005-1.014) and McDonald MS (HR = 1.009, 95% CI 1.005-1.013), remaining significant for CDMS in the multivariate analysis (adjusted HR = 1.005, 95% CI 1.000-1.011).	cdms	135-139	neurofilament light chain	Homo sapiens	121-124
27521440-11	2016	In the replication phase, more NfL-positive patients, according to the cutoff, evolved to MS. Every 100-ng/L increase in NfL predicted CDMS (hazard ratio [HR] = 1.009, 95% CI 1.005-1.014) and McDonald MS (HR = 1.009, 95% CI 1.005-1.013), remaining significant for CDMS in the multivariate analysis (adjusted HR = 1.005, 95% CI 1.000-1.011).	cdms	264-268	neurofilament light chain	Homo sapiens	31-34
27521440-11	2016	In the replication phase, more NfL-positive patients, according to the cutoff, evolved to MS. Every 100-ng/L increase in NfL predicted CDMS (hazard ratio [HR] = 1.009, 95% CI 1.005-1.014) and McDonald MS (HR = 1.009, 95% CI 1.005-1.013), remaining significant for CDMS in the multivariate analysis (adjusted HR = 1.005, 95% CI 1.000-1.011).	cdms	264-268	neurofilament light chain	Homo sapiens	121-124
25406498-11	2014	CONCLUSIONS: These results validate previous findings for semaphorin 7A and ala-beta-his-dipeptidase, and suggest that these proteins play a role as CSF biomarkers associated with the conversion to CDMS in CIS patients.	cdms	198-202	semaphorin 7A (John Milton Hagen blood group)	Homo sapiens	58-71
25698172-10	2015	In a multivariate model MRI (p=0.0001), chitinase 3-like 1 (p=0.0033) and age (p=0.0194) combined predicted CDMS best.	cdms	108-112	chitinase 3 like 1	Homo sapiens	40-58
25732842-3	2015	RESULTS: High levels of NFL were associated with early conversion from CIS to CDMS (hazard ratio (HR) with 95% confidence interval (CI): 2.69 (1.75 - 4.15); p < 0.0001).	cdms	78-82	neurofilament light chain	Homo sapiens	24-27
25732842-6	2015	CONCLUSIONS: CSF levels of NFL in CIS patients are an independent prognostic marker for conversion to CDMS.	cdms	102-106	neurofilament light chain	Homo sapiens	27-30
23983889-5	2013	In the 3-, 5-, and 10-year extension studies of 2 formulations of IFN-beta, the decreased conversion rate to CDMS remained meaningful when comparing early treatment of CIS to treatment delayed by a median of 2 to 3 years.	cdms	109-113	interferon beta 1	Homo sapiens	66-74
17334662-8	2007	Only in female patients with at least one MRI lesion (n = 34) did the presence of anti-MOG correlate with more frequent (p = 0.028) and more rapid (p = 0.0209) transition to CDMS.	cdms	174-178	myelin oligodendrocyte glycoprotein	Homo sapiens	87-90
21485162-8	2011	However, not every patient with CIS will progress to CDMS; the IFNbeta treatment is appropriately indicated for CIS patients who are diagnosed with MS by McDonald diagnostic criteria based on MRI findings of dissemination in space and time and are at high risk for conversion to CDMS.	cdms	53-57	interferon beta 1	Homo sapiens	63-70
21485162-8	2011	However, not every patient with CIS will progress to CDMS; the IFNbeta treatment is appropriately indicated for CIS patients who are diagnosed with MS by McDonald diagnostic criteria based on MRI findings of dissemination in space and time and are at high risk for conversion to CDMS.	cdms	279-283	interferon beta 1	Homo sapiens	63-70
22185807-5	2012	RESULTS: The frequency of the inhibitory KIR2DL3 gene was significantly reduced in patients with CIS and CDMS (p = 3.1 x 10(-5)).	cdms	105-109	killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 3	Homo sapiens	41-48
22185807-10	2012	CONCLUSION: Absence of the inhibitory KIR2DL3 gene is associated with the development of CIS/CDMS.	cdms	93-97	killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 3	Homo sapiens	38-45
21485162-6	2011	Clinical trials demonstrated that early treatment of CIS patients with the standard dose of interferon beta (IFNbeta) significantly reduced the risk of progression to CDMS by 44 to 50%.	cdms	167-171	interferon beta 1	Homo sapiens	92-107
21485162-6	2011	Clinical trials demonstrated that early treatment of CIS patients with the standard dose of interferon beta (IFNbeta) significantly reduced the risk of progression to CDMS by 44 to 50%.	cdms	167-171	interferon beta 1	Homo sapiens	109-116
21485162-7	2011	After 5 years of followup, the results of the IFNbeta treatment extension studies confirmed that the risk of conversion to CDMS was significantly reduced by 35 to 37% in patients receiving early treatment compared to that in those receiving delayed treatment.	cdms	123-127	interferon beta 1	Homo sapiens	46-53
18425915-12	2008	The metanalyses showed that the proportion of patients converting to CDMS was significantly lower in IFN beta-treated than in placebo-treated patients both after one year (pooled OR 0.53; 95% CI, 0.40 to 0.71; p <0.0001) as well as after two years of follow-up (pooled OR 0.52; 95% CI, 0.38 to 0.70; p <0.0001).	cdms	69-73	interferon beta 1	Homo sapiens	101-109
18425915-15	2008	AUTHORS" CONCLUSIONS: The efficacy of IFN beta treatment on preventing the conversion from CIS to CDMS was confirmed over two years of follow-up.	cdms	98-102	interferon beta 1	Homo sapiens	38-46
16608106-7	2006	The results of interferon beta trials in patients with CIS showed significant benefit of the treatment in decreasing risk of CDMS development.	cdms	125-129	interferon beta 1	Homo sapiens	15-30
16705196-1	2006	AIM: To investigate whether the presence of serum antibodies against myelin oligodendrocyte glycoprotein (MOG) and myelin basic protein (MBP) in patients with a clinically isolated syndrome (CIS) predicts the interval to develop more frequently and earlier a first relapse (clinically definite multiple sclerosis: CDMS) than seronegative patients.	cdms	314-318	myelin oligodendrocyte glycoprotein	Homo sapiens	69-104
16705196-1	2006	AIM: To investigate whether the presence of serum antibodies against myelin oligodendrocyte glycoprotein (MOG) and myelin basic protein (MBP) in patients with a clinically isolated syndrome (CIS) predicts the interval to develop more frequently and earlier a first relapse (clinically definite multiple sclerosis: CDMS) than seronegative patients.	cdms	314-318	myelin oligodendrocyte glycoprotein	Homo sapiens	106-109
16705196-1	2006	AIM: To investigate whether the presence of serum antibodies against myelin oligodendrocyte glycoprotein (MOG) and myelin basic protein (MBP) in patients with a clinically isolated syndrome (CIS) predicts the interval to develop more frequently and earlier a first relapse (clinically definite multiple sclerosis: CDMS) than seronegative patients.	cdms	314-318	myelin basic protein	Homo sapiens	137-140
30412725-11	2019	Biomechanical manipulation of CDMs, generated on physiologically soft substrates, leads to reduction in nuclear translocation of pERK1/2 in KRAS mutated pancreatic cells.	cdms	30-34	KRAS proto-oncogene, GTPase	Homo sapiens	140-144
12100477-4	2002	Patients with CDMS had a higher percentage of CD5- B cells in CSF than did control subjects (P = 0.02).	cdms	14-18	CD5 molecule	Homo sapiens	46-49