Untreated patients with Hodgkin’s lymphoma in stages I-IIIA with risk factors (large mediastinal mass, massive splenic involvement, extranodal disease) were entered into the HD1 protocol and received a combined chemoradiotherapy [2 × (COPP+ABVD) + 40 Gy extended field irradiation (EF) vs 2 × (COPP+ABVD) + 20 Gy EF]. Patients in stages IIIB/IV (HD3 protocol) received induction chemotherapy [3 × (COPP+ABVD)] and were randomized into consolidation by radiotherapy [20 Gy involved field irradiation (IF)] vs chemotherapy [1 × (COPP+ABVD)]. Seventy-three of 89 evaluable patients (82%) treated according to the HD1 protocol achieved a complete remission. Freedom from progression and survival of patients in stages I-IIIA with risk factors treated according to HD1 were no worse than those of patients in stages I and II without risk factors who received only radiotherapy. Eighty-six of 137 patients (63%) treated according to the HD3 protocol achieved complete remission after induction chemotherapy with COPP+ABVD. This is significantly better than the 31% complete remission rate observed in a previous pilot study with COPP alone (P < 0.01). Including salvage therapy (radiotherapy in case of persisting nodal disease; chemotherapy with 4 × CEVD in case of persisting disseminated disease), a total of 76% complete remissions in stages IIIB/IVAB were achieved. A high erythrocyte sedimentation rate (> 80 mm h−1) was the most significant risk factor for achieving freedom from progression.

In a national multicentre trial in the FRG patients with Hodgkin's lymphoma in stages CS/PS III B/IV were entered into the HD 3 protocol and received induction chemotherapy with 3× (COPP+ABVD). Patients in complete remission (CR) received consolidation therapy by either radiotherapy (20 Gy IF) or chemotherapy (COPP+ABVD). Patients not in CR received salvage therapy (40 Gy in case of persisting nodal disease, else 4× CEVD chemotherapy). Between July 1983 and May 1987 230 untreated patients aged 15 to 60 qualified for this HD 3 protocol. This analysis is based on the first 137 patients evaluable for response. Of these, 86 (63%) achieved CR after induction chemotherapy. Including salvage therapy a total of 104 patients (76%) achieved CR. Univariate and multivariate prognostic risk factor analyses were performed using freedom from treatment failure (FFTF) as endpoint. Sex, age, splenectomy, bone marrow, liver and bone involvement had no prognostic impact nor had stage according to the Ann Arbor classification. In contrast, a pretreatment erythrocyte sedimentation rate (ESR) above 80 mm/h and a serum alkaline phosphatase (AP) above 230 IU/ml appeared as significant risk factors (p<0.01, relative risk 2.3). The two parameters were not independent. Comparing a group A (ESR ≤ 80 and AP ≤ 230) versus a pooled group B (ESR>80 and/or AP>230) increased the difference (p<0.001, relative risk of 2.8) which was also significant for survival (p<0.04).

A polypeptide complex (p52) belonging to the D-subspecificity of the EBV-induced early antigens (EA-D) was purified from chemically induced P3HR-1 cells. Rabbit antisera raised against the isolated polypeptides reacted with components of EA-D as could be shown by indirect immunofluorescence and immunoperoxidese staining of IdU-induced EA positive Raji cells, ELISA, and immunoblotting. In one-dimensional immunoblots the rabbit antisera detected a predominant polypeptide complex of 52 kDa. Two-dimensional immunoblots prepared with proteins from IdU-induced Raji cells showed that the rabbit sera detect three series of polypeptides of 52 kDa (p/ 8.5–6.2), 55–58 kDa (p/ 6.2–4.5), and 48–50 kDa (pi 6.0–4.5). These three groups of polypeptides could also be identified by 50 high titered anti-EA-D positive human sera and a specific monoclonal antibody (R3) as being the main components of EA-D in Raji and B95-8 cells. All polypeptides of the p50/58 complex showed DNA binding properties either by themselves or by an interaction with other proteins. When TPA or IdU-induced Raji cells were labeled with 12P1, two phosphorylated polypeptides pp50 and pp58 could be immunoprecipitated with the rabbit sera and a high anti-EA titered human serum. The time course of the synthesis of polypeptides associated with the EA-D complex was studied by 2-D immunoblots: EA polypeptides of 52 kDa appeared as early as 6 hr after the addition of IdU to Raji cells in culture, polypeptides of 55–58 and 48–50 kDa after 18 and 25 hr, respectively. The coordinated appearance of these groups of polypeptides and their similar size and reactivity with human sera and rabbit antisera produced against the isolated p52 as well as with a monoclonal antibody (R3) suggested that most of these polypeptides are derived from post-translational modifications of one or a few initially synthesized polypeptides, possibly p52. Phosphorylation seems to be at least one possibility of post-translational modification.

This is a preliminary analysis of the AIO-Testicular Tumour Study Group trial in patients with disseminated bulky testicular cancer. Treatment plan: cisplatin 35 mg/m2 days 1-5, VP-16 120 mg/m2 days 1-5 (two daily divided doses), bleomycin 15 mg/m2 days 1, 8, 15. Of 98 patients at present evaluable 63% had complete remission or have no evidence of disease (CR/NED), 30% had partial remission (PR) and 7% had no change or progressive disease (NC/P). Relapse-free survival is 93% for the CR/NED group after a median follow up of 2.2 years: the overall survival for the entire patient population is 70%. Toxicity included predominantly granulocytopenic fever and infection with septicaemia, thrombocytopenia, nausea, vomiting, neurotoxicity and lung toxicity, with 7% fatal toxicity. A prospective randomized trial is warranted to evaluate the apparent superior activity of ultra high dose cisplatin in combination with VP-16 and bleomycin.

Antibody liters to Epstein‐Barr virus (EBV)‐associated early antigens (EA) and the viral capsid antigen (VCA) were determined by ELISA on 263 sera obtained from healthy donors, patients with Hodgkin's disease (HD), non‐Hodgkin lymphomas (NHL), infectious mononucleosis (IM), Burkitt's lymphoma (BL), and nasopharyngeal carcinoma (NPC). As expected, most lymphoma patients showed markedly elevated anti‐VGA IgG and anti‐EA IgG antibody liters. Only one patient in the NHL group (n = 56) consisting of patients with lymphomas other than chronic lymphocytic leukemia (CLL) and hairy‐cell leukemia (HCL), and 3 patients with HCL (n = 19) had high antibody titers of the IgA class to VCA and EA. Seventeen out of 48 patients (36%) with CLL had high IgA anti‐VCA titers and 10 of these sera (21%) also contained IgA anti‐EA. The geometric mean titer (GMT) of IgA anti‐VCA was 2,510, the GMT of IgA anti‐EA was 780. These antibody titers were about 10 times lower than the corresponding GMT of the NPC patients investigated in this study. The elevated IgG and IgA antibody titers to VCA and EA in CLL and HCL patients seem to reflect an immunodeficiency secondary to the malignant disease leading to reactivation of latent EBV infection. The possibility that at least some of these B‐cell lymphomas are associated with EBV cannot be excluded.