Spontaneous remission of a non-small cell lung cancer possibly caused by anti-NY-ESO-1 immunity.

Spontaneous remission of malignant tumors is rare and the biological mechanism of such remission has not been addressed. We report the case of a 71-year-old Japanese patient with non-small cell lung cancer with a right hilar tumor and pleural dissemination that spontaneously regressed. NY-ESO-1 is a cancer/testis antigen that can elicit specific immune responses in patients with cancer. Strong anti-NY-ESO-1 immunity was detected in this patient. His tumor cells expressed NY-ESO-1 and MHC class I molecules. Anti-NY-ESO-1 immunity might have contributed to spontaneous remission in this patient

Plasma Thrombopoietin Levels are Unlikely to Account for the Platelet-sparing Effect of Paclitaxel in Lung Cancer Patients

Purpose: The present study was designed to determine whether the combination of carboplatin (CBDCA) with paclitaxel (PTX) spared CBDCA-induced thrombocytopenia by increased plasma thrombopoietin (TPO) levels. Methods: Patients with non-small-cell and small-cell lung cancer were consecutively assigned to CBDCA with PTX regimen (CBDCA/PTX) and CBDCA with irinotecan (CPT-11) regimen (CBDCA/CPT-11), respectively. Results: Ten patients were entered into either CBDCA/PTX (n=5) or CBDCA/CPT-11 (n=5). CBDCA/PTX showed a lesser reduction of platelet counts than CBDCA/CPT-11 (p<0.05), although more severe neutropenia was observed in CBDCA/PTX (p<0.01). The plasma TPO levels were inversely correlated with circulating platelet counts in CBDCA/PTX and CBDCA/CPT-11. However, the increased rate of plasma TPO levels in CBDCA/PTX was not significantly different from that in CBDCA/CPT-11. Conclusions: These findings suggest that the increased plasma TPO levels in CBDCA/PTX result secondarily from thrombocytopenia, and that circulating TPO is probably not involved in the platelet-sparing effect of PTX

Etiological factors in primary hepatic B-cell lymphoma

Sixty-four cases of malignant lymphoma involving the liver were examined. Of these, 20 cases were histologically confirmed to be primary hepatic B-cell lymphoma. Twelve of these 20 cases were diffuse large B-cell lymphoma (DLBCL) and eight cases were mucosa-associated lymphoid tissue (MALT) lymphoma. Of the 12 cases of DLBCL, six were immunohistologically positive for CD10 and/or Bcl6 (indicating a germinal center phenotype), six were positive for Bcl2, and five were positive for CD25. Eight of the 12 DLBCL cases (66.7%) and two of the eight MALT lymphoma cases (25%) had serum anti-hepatitis C virus (HCV) antibodies and HCV RNA. The incidence of HCV infection was significantly higher in the hepatic DLBCL cases than in systemic intravascular large B-cell cases with liver involvement (one of 11 cases, 9.1%) and T/NK-cell lymphoma cases (one of 19 cases, 5.3%) (p < 0.01 for both). Two hepatic DLBCL cases (16.7%) had rheumatoid arthritis treated with methotrexate, and four MALT lymphoma cases (50%) had Sjögren’s syndrome, primary biliary cirrhosis, or autoimmune hepatitis; one case in each of these two groups was complicated by chronic HCV-seropositive hepatitis. Although primary hepatic lymphoma is rare, persistent inflammatory processes associated with HCV infection or autoimmune disease may play independent roles in the lymphomagenesis of hepatic B cells