PMID- 9748021
OWN - NLM
STAT- MEDLINE
DCOM- 19981020
LR  - 20190514
IS  - 0028-3878 (Print)
IS  - 0028-3878 (Linking)
VI  - 51
IP  - 3
DP  - 1998 Sep
TI  - A systematic study of oligodendrocyte growth factors as candidates for genetic 
      susceptibility to MS. French Multiple Sclerosis Genetics Group.
PG  - 748-53
AB  - OBJECTIVE: To test 23 genes coding for growth factors and their receptors as 
      candidates for MS genetic susceptibility in 84 multiplex families of French 
      origin by linkage analysis. BACKGROUND: Epidemiologic studies have indicated that 
      genetic susceptibility in MS exists. To identify MS susceptibility genes, 
      association and linkage studies were performed with candidate genes suggested by 
      the pathology of MS. The most consistent result was genetic association and 
      linkage of MS to human leukocyte antigen (HLA) DR15. Recent advances in the 
      knowledge of MS pathology have suggested that the oligodendrocyte, the 
      myelin-forming cell in the CNS, and its growth factors might play a crucial role 
      in MS. METHODS: Fifty-two polymorphic markers within or flanking 23 candidate 
      genes were used. Data were analyzed with the maximum likelihood score (MLS) 
      approach. We also searched for a genetic interaction with HLA. RESULTS: Negative 
      results were obtained for all candidate genes. The lower limits of the relative 
      risk (Xs) possibly excluded for any candidate gene ranged from 1.3 to 2.8. 
      Positive MLS values (up to 0.93) were observed for transforming growth factor 
      beta 3 (TGFbeta3) in HLA DR15-associated families, suggesting a possible role for 
      this growth factor in interaction with HLA. CONCLUSIONS: Oligodendrocyte growth 
      factors do not play a significant role in MS genetic susceptibility, at least in 
      the tested sample. TGFbeta3, the only gene highlighted by this study, deserves 
      further analysis.
FAU - Mertens, C
AU  - Mertens C
AD  - INSERM CJF9608, Groupe Hospitalier Pitie-Salpetriere, Paris, France.
FAU - Brassat, D
AU  - Brassat D
FAU - Reboul, J
AU  - Reboul J
FAU - Eichenbaum-Voline, S
AU  - Eichenbaum-Voline S
FAU - Vuillemin-Azais, C
AU  - Vuillemin-Azais C
FAU - Cournu, I
AU  - Cournu I
FAU - Babron, M C
AU  - Babron MC
FAU - Semana, G
AU  - Semana G
FAU - Edan, G
AU  - Edan G
FAU - Clanet, M
AU  - Clanet M
FAU - Clerget-Darpoux, F
AU  - Clerget-Darpoux F
FAU - Baron-Van Evercooren, A
AU  - Baron-Van Evercooren A
FAU - Lyon-Caen, O
AU  - Lyon-Caen O
FAU - Liblau, R
AU  - Liblau R
FAU - Fontaine, B
AU  - Fontaine B
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Neurology
JT  - Neurology
JID - 0401060
RN  - 0 (Growth Substances)
RN  - 0 (Receptors, Growth Factor)
SB  - IM
MH  - Adult
MH  - Disease Susceptibility
MH  - Female
MH  - Genetic Linkage
MH  - Genotype
MH  - Growth Substances/*genetics
MH  - Humans
MH  - Male
MH  - Multiple Sclerosis/*genetics
MH  - Oligodendroglia/*metabolism
MH  - Polymorphism, Genetic
MH  - Receptors, Growth Factor/*genetics
MH  - Risk
EDAT- 1998/09/25 00:00
MHDA- 1998/09/25 00:01
CRDT- 1998/09/25 00:00
PHST- 1998/09/25 00:00 [pubmed]
PHST- 1998/09/25 00:01 [medline]
PHST- 1998/09/25 00:00 [entrez]
AID - 10.1212/wnl.51.3.748 [doi]
PST - ppublish
SO  - Neurology. 1998 Sep;51(3):748-53. doi: 10.1212/wnl.51.3.748.