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1 pecially lung, ovarian and breast, can cause paraneoplastic cerebellar degeneration.
2 n and may be involved in the pathogenesis of paraneoplastic cerebellar degeneration.
3 thophysiology were described 10 years ago in paraneoplastic cerebellar degeneration.
5 was the cause of death of 65% HuAb positive paraneoplastic cerebellar degeneration and 10% HuAb nega
8 e anti-Tr immune response is associated with paraneoplastic cerebellar degeneration and Hodgkin lymph
9 litis, 1 paraneoplastic encephalomyelitis, 1 paraneoplastic cerebellar degeneration, and 1 opsoclonus
10 rum and cerebrospinal fluid of patients with paraneoplastic cerebellar degeneration associated with c
11 rocessed HLA-A2.1 restricted epitopes of the paraneoplastic cerebellar degeneration breast/ovarian ca
12 immunomodulation did not alter the course of paraneoplastic cerebellar degeneration, but improved Lam
13 at patients with the same tumour can develop paraneoplastic cerebellar degeneration by different immu
14 patients who differed from the HuAb negative paraneoplastic cerebellar degeneration cohort, HuAb posi
15 m of 57 patients with presenting symptoms of paraneoplastic cerebellar degeneration for the presence
17 /or serum samples from 5 other patients with paraneoplastic cerebellar degeneration, HL, and anti-Tr.
18 In patients with small-cell lung cancer, paraneoplastic cerebellar degeneration may occur with or
19 and immunological developments, focusing on paraneoplastic cerebellar degeneration, opsoclonus-myocl
21 erebellar degeneration and 10% HuAb negative paraneoplastic cerebellar degeneration patients (P < 0.0
23 0% of HuAb positive and 20% of HuAb negative paraneoplastic cerebellar degeneration patients, the tum
26 among the better described autoantibodies in paraneoplastic cerebellar degeneration (PCD) combined wi
33 era from patients with Hodgkin's disease and paraneoplastic cerebellar degeneration resulted in the i
35 bodies associated with different cancers and paraneoplastic cerebellar degeneration suggests that sev