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Editorial
October 2005

Keeping “Trk” of Paraneoplastic Syndromes

Arch Neurol. 2005;62(10):1508-1509. doi:10.1001/archneur.62.10.1508

Paraneoplastic syndromes are distant effects of known or occult neoplasms. Many of the paraneoplastic syndromes that affect nonneural tissues are caused by the tumor’s secretion of bioactive proteins. An example of this is the syndrome of inappropriate antidiuretic hormone secretion, which occurs in about 5% of patients with small-cell lung carcinoma.1,2 A tumor cell secretory mechanism also occasionally contributes to the pathogenesis of paraneoplastic neurological syndromes. For example, production of vascular endothelial growth factor by neoplastic plasma cells appears to be involved in the cause of neuropathy in POEMS (characterized by polyneuropathy, organomegaly, endocrinopathy/edema, monoclonal gammopathy, and skin changes), the Crow-Fukase syndrome.3 However, most paraneoplastic neurological syndromes are caused, instead, by antibody-mediated and/or T-lymphocyte–mediated responses to tumor epitopes that mimic epitopes expressed by normal neural cells. These paraneoplastic neurological syndromes can thus be thought of as unfortunate adverse effects of autoimmune mechanisms intended to suppress tumor growth.46

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