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Biomedical subjects

R B Faanes

Publications and source records attributed to R B Faanes.

29 records · Page 2Linked to original sources
PubMed1979

Restoration of cyclophosphamide-induced suppression of thymus-derived cytotoxic cell generation by normal thymocytes.

Spleen cells from mice treated with cyclophosphamide (100 to 200 mg/kg) were unable to generate effective cytotoxic thymus-derived cells to allogeneic tumor cells in vitro. The inability of lymphoid cells from cyclophosphamide-treated mice to generate thymus-derived cytotoxic cells became more apparent as the number of responding cells became limited. This depressed response was not due to the elimination of cytotoxic precursor cells since normal response levels were restored by the addition of thymus cells. The added thymus cells did not provide cytotoxic cells in the culture. The thymus cells active in restoring cytotoxic activity were sensitive to mitomycin C, cyclophosphamide, and anti-theta serum and complement. In addition, the active thymus cells were located in the cortisone-resistant pool and did not adhere to nylon wool columns.

Animals↗
PubMed1979

Matching of chemotherapy to mouse strain and lymphoid tumor type to prevent tumor-induced suppression of specific T- and B-cell functions.

Specific immunological and hematopoietic functions were studied during treatment with antineoplastic agents in mice bearing syngeneic lymphoid tumors: 70Z/2, a B-cell lymphoma of C57BL X DBA/2 F1 (hereafter called (BD2F1) mice; EL4, a T-cell lymphoma of C57BL/6 mice; or J774, a macrophage tumor of BALB/c mice. Both B- and T-lymphocyte function (antibody-forming cells and cell-mediated lymphocyte lympholysis toward alloantigens) were suppressed in spleen cells of mice bearing these tumors. Other hematopoietic functions (granulocyte, macrophage, and megakaryocyte progenitor cells) were variably influenced by growth of these lymphoid tumors. J774 enhanced, but 70Z/2 suppressed, megakaryocyte progenitor cells. J774 and 70Z/2 increased levels of granulocyte-macrophage progenitor cells. EL4, the T-cell lymphoma, did not influence either cell type. Significant variation in strain sensitivity to drug toxicity and drug effectiveness in different tumor-host systems was observed. Increased median survival time with reversal of tumor-induced immune dysfunction, without toxicity to hematopoietic progenitor cells, was realized in two tumor-host-drug combinations. Polyinosinic-polycytidylic acid was effective against J774, while actinomycin D was active against 70Z/2. Mitomycin C effectively reduced tumor load, as evidenced by loss of splenic tumor colony-forming cells for all three tumors. This agent prolonged survival and concomitantly restored immunological responsiveness in hosts immunosuppressed by growth of 70Z/2 or J774. Paralleling tumor reduction with mitomycin C therapy, the splenic hematopoietic progenitor and colony-forming B-cells were reduced in tumor-bearing and tumor-free mice, thus compromising its therapeutic effectiveness. 1-beta-D-Arabinofuranosylcytosine reduced tumor load with marginal toxicity toward hematopoietic progenitor and colony-forming B-cells. However, immune responsiveness was only partially restored, and median survival was not increased. The results presented show the diversity of therapeutic drug effectiveness in increasing mean survival time and influencing other life-sustaining parameters (immunological and hematopoietic functions).

Animals↗
PubMed1977

Antigenic changes of DBA/2J mastocytoma cells when grown in the BALB/c mouse.

A 10-day growth period of the DBA/2J strain-specific P815-X2 mastocytoma in the BALB/c mouse altered the antigenicity of the tumor cell surface. The in vivo-modified mastocytoma cells differed from mastocytoma cells grown in the original DBA/2J mice in suspectibility to lysis by immune peritoneal exudate cells, in vitro antigenic recognition by cytotoxic T-cells, and immunizing capacity in allogeneic C57BL/6 mice. Propagation of the altered tumor cells in the original host or maintenance in tissue culture for 40 hours restored complete susceptibility to lymphocyte-mediated cytotoxicity.

Animals↗
PubMed1973

Escape from isoantiserum inhibition of lymphocyte-mediated cytotoxicity.

Isoantiserum (IS) inhibition of lymphocyte-mediated cytotoxicity (LMC) was studied using an in vitro (51)Cr release assay system. In the early phase of incubation, LMC was competitively inhibited by IS. However, as the incubation continued, LMC irreversibly overcame IS inhibition (the "escape" phenomenon). Addition of fresh antiserum did not alter the course of the escape. Low-temperature incubation of isoantibody-coated target cells delayed the onset of the escape. We have excluded the possibility that the escape phenomenon is induced by complement or by LMC mediated by antigen-antibody complex. It is hypothesized that antibody directed toward an actively metabolizing target cell induces an alteration in the cell membrane that alters further interaction with the antibody. However, sensitivity to lymphocyte cytotoxicity is maintained.

Animals↗