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The interim analysis revealed no major differences in acute toxicity and local efficacy between the two evaluated strategies.

In some patients, chemotherapy (CHT) of cancer can result in pulmonary inflammation and fibrosis, eventually leading to respiratory insufficiency.As animal studies have underlined the importance of major histocompatibility complex (MHC) genes in the susceptibility to bleomycin (BLM)-induced pulmonary fibrosis, the authors typed human leukocyte antigen-DR (HLA-DR) and tumor necrosis factor (TNF) genes in patients treated for Hodgkin's disease by a therapy including bleomycin.Patients were divided into pulmonary responders (PR) (n=21) or nonresponders (PNR) (n=20) on the basis of pulmonary alterations detected on chest radiography and the cumulated amount of BLM injected. The incidence of TNFa2, a microsatellite allele in the promoter region of the TNFB gene reported to be associated with increased TNF-α production, was significantly higher in PR than PNR (65%versus19%). HLA-DRB1*15 showed a weak but nonsignificant association with the PR phenotype (50%versus14%), as well as HLA-DRB1*03 (30%versus19%) and TNFA-308*2 (30%versus14 %). TNFa2 and DR15 were independent risk factors and the occurrence of either genetic marker was 85%versus29% in the PR and PNR groups respectively.Thus, the polymorphic TNFa2 microsatellite is associated with a risk of chemotherapy-induced pulmonary fibrosis.