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Although cisplatin and etoposide seem to represent the treatment of choice in Small-Cell Lung Cancer, a lot of data exist in literature supporting both the use of anthracycline-containing regimens and the use of alternating regimens where platinum-containing regimens and anthracycline-containing regimens are alternatively used as first line in the same patient. In our paper we review the outcomes of two different series of patients treated with ciclophosphamide-epidoxorubicin-etoposide (CEVP16) or carboplatin-etoposide (CBE) for extended Small-Cell Lung Cancer. Sixty-three patients (53.4%) were treated with CEVP16 and 55 patients (46.6%) with CBE. Response Rate (complete plus partial responses) was greater in patients treated with CEVP16 (49.2%) when compared with the response rate in patients treated with CBE (30.9%) (p=0.04 using the Chi-Square test); no differences were observed in the median time to progression (235 vs 199 days, using the Log-Rank test). Overall survival was greater in the CEVP16 group when compared with the CBE one (281 vs 208 days and 35.6% vs 16.3% of patients alive after 2 years of follow up for CEVP16 and CBE respectively, p=0.02 using the Log-Rank test). Although our data present all the methodological limits of the "case-series", it is interesting to observe how an anthracycline-containing regimen seems to be more effective than a platinum-containing one and how it could still play a role in the treatment of extended Small-Cell Lung Cancer.

Subacute cerebellar degeneration is an autoimmune disorder and represents the paraneoplastic neurologic syndrome most frequently occurring in the central nervous system. To our knowledge, until now, no case of such a paraneoplastic syndrome as been described in patients with mesothelioma; on the contrary, some non-neurologic paraneoplastic syndromes have been described in patients with mesothelioma, and an aberrant production of cytokines has been suggested as the main pathogenetic event. In our report it can be supposed that an aberrant production of cytokines might have triggered an autoimmune reaction, causing anti Purkinje cells antibodies production, neurological damage and clinical outcome.