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Proliferative responses by blood and tumor lymphocytes to plant mitogens and allogeneic leukocyte antigens were tested concomitantly on 12 patients with Hodgkin's disease, 10 with chronic lymphocytic leukemia, and seven with non-Hodgkin's lymphomas. In 13 control studies, 3H-thymidine incorporation by blood and lymph node lymphocytes was brisk and, overall, comparable. With Hodgkin's disease, where extent of disease involvement and lymphocyte-depleted tumor histology were factors in the degree of responsiveness, incorporation was higher or at least comparable by tumor lymphocytes when compared with incorporation by autologous blood lymphocytes. Lymph node lymphocytes, especially with clinically stable disease, were more responsive than blood lymphocytes with chronic lymphocytic leukemia. Conversely, tumor lymphocytes were hyporesponsive compared with autologous blood lymphocytes with non-Hodgkin's lymphomas, where prognosis is usually less favorable than with chronic lymphocytic leukemia. Plasma from four out of 33 patients, although not lymphocytotoxic, inhibited lymphoproliferative responses.

In this survey for rheumatoid factor (RF) seropositivity on patients with neoplasms, an 85% rate of positive screening tests was recorded under certain circumstances. This high rate of RF seropositivity occurred after irradiation and/or chemotherapy of breast and lung cancers. Treated patients with breast cancers who had no evidence of residual tumor had an 89% rate of positive RF tests. Conversely, the incidence of RF seropositivity was low among untreated patients with similar tumors and treated patients with glioblastomas or multiple myeloma. The administration of cytotoxic drugs (e.g., azathiprene) was not itself associated with RF production even in renal allograft recipients. The data indicate that RF production occurs frequently after therapy of certain tumors and suggest that in these circumstances RF may be an expression of tumor-host interaction.Rheumatoid factor (RF) is detected by routine laboratory techniques in serum from <4% of healthy adults under 65 years of age (1-8). About 13-20% of unselected patients with malignancies are RF seropositive (1, 4, 5), and RF has been eluted from neoplastic but not from adjacent normal tissues (5). The relevance of this antibody response to tumor-host interactions is not known, nor are circumstances that cause it to occur.Most RFs are IgM antibodies to antigenic determinants in IgG. In general, IgM is a more effective activator of complement than IgG (6, 7). However, the effect of IgM-RF on complement mediated reactions is variable (8-11). For example, IgM-RF induces complement-mediated neutralization of herpes simplex virus complexed to IgG antibody (9). However, RF may inhibit complement-mediated phagocytosis (10) and lysis (11) administration of various chemotherapeutic agents intravenously in dose schedules dictated by patient weight, clinical status, and drug tolerance. These drugs included cyclophosphamide, vinblastin, methotrexate, 5-fluorouracil, thio-TEPA, and steroids. Multiple myeloma was treated with irradiation, melphalan, and, in selected cases, steroids. Glioblastomas were treated with irradiation to the head and with steroids. Most patients had received prolonged courses of therapy before their serum was tested. Nineteen patients with breast cancer had no apparent residual tumor after radical mastectomy and had received "prophylactic" irradiation and chemotherapy before they were tested. Of the patients receiving cytotoxic drugs, which were administered for immunosuppression, 11 were renal allograft recipients and 10 had multiple sclerosis. The renal allograft recipients were receiving 100-175 mg of azathioprene and up to 20 mg of prednisone daily; patients with multiple sclerosis were receiving azathioprene at 50 mg/day. Sera were tested for RF at 1:20 dilutions with glycine-saline buffer using latex particles coated with Cohns Fraction II (Hyland Laboratories). RESULTSThe results of the serologic survey for RF are listed in Table 1