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Biomedical subjects

A Goldin

Publications and source records attributed to A Goldin.

At least 73 records · Page 4Linked to original sources
PubMed1978

Secondary cytotoxic response in vitro against Moloney lymphoma cells antigenically altered by drug treatment in vivo.

Cell-mediated cytotoxic response in vitro to a Moloney strain of murine leukemia virus-induced tumor (LSTRA) altered by 5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide (DTIC) was investigated with the use of mixed-leukocyte tumor cell cultures (MLTC). As assessed by means of a short-term 51Cr-release assay, minimal or no cytolytic activity was generated in primary MLTC. In contrast, high specific cytotoxic response against the altered tumor was obtained in secondary MLTC. Partial cross reactivity was found between the LSTRA and LSTRA/DTIC tumor lines.

Animals↗
PubMed1978

Growth and rejection patterns of murine lymphoma cells antigenically altered following drug treatment in vivo.

Murine leukemia cells transformed by in vivo treatment with 5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide (DTIC) are rejected by histocompatible recipients following inocula of 10(7) cells i.p. Progressive tumor growth or tumor growth and regression was monitored measuring the extent of DNA synthesis in the peritoneal cavity of mice using the [125I]5-iodo-2'-deoxyuridine uptake method. In addition, the results were confirmed by cell count and mortality data. Comparable growth rate was found initially in both DTIC and parental lines in histocompatible hosts. Later, mice challenged with parental lines died, whereas hosts inoculated with DTIC-treated sublines rejected the tumor. On the other hand, lethal growth occurred in mice inoculated with DTIC-treated sublines when immunodepressed by cyclophosphamide given before tumor challenge, or by methotrexate given after challenge of a methotrexate-resistant DTIC-treated subline. The similarity between the growth rate of the parental and DTIC-treated lines in histocompatible hosts does not support the hypothesis of impaired "oncogenic potential" of such DTIC-treated lines. Furthermore, the growth and rejection pattern of a parental line in H-2-incompatible hosts was similar to that observed for DTIC-treated lines in histocompatible hosts, suggesting that comparable immune mechanisms were involved in both cases.

Animals↗
PubMed1978

Chemotherapy modalities and immune condition of the host.

It is clear that it is possible to improve the immune condition of the host and to increase its immunological reactivity by employing a range of modalities. These may involve nonspecific immunostimulation of the host, active or passive immunization, adoptive chemotherapy, alteration of tumor cell antigenicity or other types of approaches. New agents may be sought that will serve as immunostimulants or that may prevent immunosuppression by tumor growth or by chemotherapeutic agents. New analogs of the known antitumor agents may be examined to determine whether they are less immunosuppressant than the parent drug. Any means leading to the net improvement of the immune status of the host may result in diminished drug toxicity for the host, increased antitumor response, and augmentation of immunochemotherapy.

Animals↗
PubMed1978

In vitro lymphocyte stimulation and the generation of cytotoxic lymphocytes with drug-induced antigenic lymphomas.

New antigenic specificities, not detectable on parental cells and transmissible after the withdrawal of the drug treatment, have been induced in mouse lymphomas. Studies were conducted of proliferative stimulation of syngeneic lymphocytes and the generation of cytotoxic lymphocytes (CL's) in a mixed lymphocyte-tumor cell culture system by 5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide (DTIC)-induced antigens in L1210 and EL4 leukemia sublines. The DTIC-induced antigens were observed to stimulate [3H]thymidine uptake by normal and primed syngeneic lymphocytes and to generate specific CL's to DTIC-altered cells. The specificity of the in vitro immune reactivity was demonstrated. Characteristics of lymphocyte triggering, including the optimal ratio of stimulating cells to responding cells, the kinetics of CL activation, and the quantitation of CL activity, were also evaluated. DTIC antigens on leukemic cells can activate syngeneic lymphocytes and can act as target antigens in cell-mediated immunity. The experimental data support the transplantation antigen-like nature of DTIC-induced antigens.

Animals↗
PubMed1977

Cell kinetics and immunoegenicity of lymphoma cells treated with 5-(3,3-dimethyl-1-triazeno) imidazole-4-carboxamide (DIC) in vivo.

A cycle of treatment with antineoplastic compounds may alter the immunologic properties of experimental tumors leading to an increased survival of syngeneic hosts as compared to that observed with the original parental tumors. However, a loss of growth potential in drug-treated tumors might account for this preferential rejection by syngeneic or by allogeneic animals. In the present study the cell cycle kinetics of parental (L1210 and L5178Y) and DIC-altered leukemic cells (L1210/DIC; L5178Y/DIC) has been evaluated by the establishment of labelled mitosis curves. The in vitro DNA synthesis and cell loss were also investigated. The experimental results indicate that no significant differences in the above properties were present for parental and corresponding drug-treated leukemic sublines. Immuno-depressed allogeneic mice were more resistant to lymphoma challenge when inoculated with the DIC-sublines than with the parental lines. On adoptive transfer of immune lymphocytes there was increased survival of allogeneic animals challenged with DIC cells, attributable to an additional immune response to DIC-induced antigens. Thus, parental or DIC-tumors showed similar tumorigenic characteristics, and the increased allogeneic host survival to DIC-cell challenge may be attributed to an additional immune response of the animal DIC-induced antigens.

Animals↗
PubMed1977

Radioresistant inhibition of lymphoma growth in congenitally athymic (nude) mice.

Several murine tumors were used to determine whether the phenomenon of tumor inhibition in athymic "nude" mice reported previously could be extended to other tumor systems in nude as well as conventional mice. The results with the L5MF-22 tumor line were confirmed, and similar data were obtained with the K36 leukemia of AKR mice and the LAF-17 leukemia of B10.A origin. This phenomenon of tumor inhibition has been called, tentatively, radioresistant inhibition of tumor and may be explained by one of several possibilities. The immunological origin of such tumor inhibition is supported by various observations. The data on tumor cell proliferation in spleens and liver of lethally irradiated mice were similar to previous findings on hemopoietic histocompatibility-incompatible lymphomas. Additionally, the nude mice were stronger responders against lymphoma cells than were conventional hosts. Another explanation is that the tumor inhibition is due to natural cytotoxicity.

Animals↗
PubMed1976

Attempt to alter antigenic structure of normal tissues by treatment with dimethyl-triazeno-imidazole-carboxamide in vivo.

The antigenic structure of normal skin and spleen cells has been investigated following in vivo treatment with the compound DIC. In experiments involving skin grafting in the normal and sensitized host, cross sensitization with a DIC-antigenic lymphoma and 3H-thymidine incorporation by lymphocytes cultured with DIC-treated spleen cells, new antigens on DIC-treated tissues were not demonstrated.

Animals↗