Plasma from patients with Lambert-Eaton myasthenic syndrome (LEMS), an 
autoimmune disease of neuromuscular transmission, contains antibodies that bind 
to the synaptic vesicle protein synaptotagmin. Synaptotagmin associates with 
calcium channels and appears to regulate synaptic vesicle docking at the plasma 
membrane prior to rapid neurotransmitter release. Autoantibodies directed 
against a synaptotagmin-calcium channel complex may be involved in the etiology 
of LEMS. In the majority of patients LEMS is associated with small cell lung 
cancer (SCLC). We have detected the expression of proteins of the secretory 
pathway, including synaptotagmin, syntaxin and N-type calcium channels, in a 
panel of SCLC tumor lines. These observations are compatible with the hypothesis 
that the initial autoimmune response in LEMS is triggered by the tumor.