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Biomedical subjects

D M Thomson

Publications and source records attributed to D M Thomson.

At least 91 records · Page 5Linked to original sources
PubMed1977

Classification of glomerulonephritis.

A classification of glomerulonephritis which is being used as a basis for the New Zealand National Study of Glomerulonephritis is presented, together with comments about the salient pathological features of each type of glomerular disease.

Biopsy↗
PubMed1977

An overview: antitumor immunity in breast cancer assayed by tube leukocyte adherence inhibition.

The adherence to glass of human peripheral blood leukocytes (PBL) incubated with tumor antigen in vitro, is specifically inhibited if the PBL are sensitized to the antigen. The presence of leukocyte adherence inhibition (LAI) to tumor extracts indicates the presence of systemic antitumor immunity. By the tube leukocyte adherence inhibition assay (tube LAI), it was shown that 85% (191 of 223) Stage I and II, 45% (15 of 34) Stage III and 29% (30 of 103) Stage IV breast cancer patients had LAI reactivity. LAI responsiveness diminished with an increased tumor burden and most patients with advanced cancer exhibited no LAI reactivity. When LAI reactivity was monitored for 1 to 6 months after surgery, 13 of 25 Stage I and II breast cancer patients were negative on the first repeat assay. In general, 7 months after mastectomy most patients clinically free of cancer showed no LAI reactivity. Of thirty-five patients tested between 7 and 18 months after mastectomy, 6 were positive and 4 of the positives had local recurrence. The phenomenon of tube LAI appears to be mediated by monocytes armed with cytophilic antitumor antibody. The serum of patients whose leukocytes responded in the tube LAI assay had free cytophilic antitumor antibody that "armed" or sensitized normal leukocytes to respond in the LAI assay. Serum arming paralleled leukocyte reactivity before and after surgery. Patients with advanced cancer whose leukocytes failed to react in the LAI assay had serum blocking factors (excess tumor antigen) that abrogated the LAI reactivity of leukocytes from reactive patients.

Antibodies, Neoplasm↗
PubMed1976

Tube leukocyte adherence inhibition assay for the detection of anti-tumor immunity. I. Monocyte is the reactive cell.

Peripheral blood leukocytes (PBL) from breast cancer patients with early or localized cancer fail to adhere to glass in the presence of breast cancer extract. The same leukocytes do not react to unrelated tumour extracts. Enrichment and depletion of certain PBL populations from patients with apparently localized breast cancer indicated that the indicator and/or reactive cell manifesting non-adherence in the presence of appropriate tumour antigen was phagocytic, glass adherent in the absence of tumour antigen and had cell surface Fc-receptors. The cell involved, therefore, appears to be the circulating monocyte. These results show that in the tube LAI assay, the peripheral blood monocyte appears to react directly with the tumour antigen resulting in a loss of its property of adherence to glass.

Adenocarcinoma↗
PubMed1976

Tube leukocyte adherence inhibition assay for the detection of anti-tumour immunity. II. Monocyte reacts with tumour antigen via cytophilic anti-tumour antibody.

The peripheral blood monocyte is the reactive cell in the tube LAI assay. The monocyte loses its properties of adherence to glass upon exposure to specific antigen. Two different experiments to determine if lymphocytes, when they reacted with tumour, released mediators that were responsible for inhibiting monocyte glass adherence, gave negative results. The mechanism wherby the specific tumour antigen appeared to be recognized was the binding of cytophilic IgG antitumour antibody to receptors on the cell surface of the monocyte. The results of the experiments indicate that normal peripheral blood monocytes could be made specifically reactive ("armed") to the tumour extract by incubating normal peripheral blood leukocytes with serum from a reactive cancer patient. IgG isolated from "arming" sera was shown to have the capacity to sensitize normal leukocytes. Patients with breast cancer or malignant melanoma with limited tumour burdens had free cytophilic anti-tumour antibody in their serum, whereas the serum of patients with large tumour burdens (metastatic cancer), whose leukocytes did not react in the tube LAI assay, did not "arm".

Adenocarcinoma↗
PubMed1976

Anti-tumour immunity in malignant melanoma assay by tube leucocyte adherence inhibition.

Tumour antigen-induced inhibition of leucocyte adherence was modified for use in glass test tubes (Tube LAI assay) for the study of cell-mediated anti-tumour immunity to human malignant melanoma. Peripheral blood leucocytes (PBL) of 20 out of 25 patients (80%) with active malignant melanoma responded to an extract of malignant melanoma with LAI, whereas only 4-5% of 475 control subjects showed a response. The malignant melanoma patients reacted to both allogeneic and autologous extracts of malignant melanoma which indicates a common cross-reacting antigen. Malignant melanoma patients did not respond to unrelated tumour extracts. The LAI was mediated by PBL (monocytes) "armed" with cytophilic anti-tumour antibody specific for the sensitizing tumour antigen. The anti-tumour response of the malignant melanoma patients was dependent on the stage of the cancer, and 11 out of 13 Stage I patients had a positive NAI, whereas patients with disseminated cancer had decreased response. The diminished LAI in patients with large tumour burdens appeared to be the result of release of tumour antigen systemically. Also, surgery and chemotherapy depressed LAI. Although LAI was depressed after surgical excision of the cutaneous melanoma, most patients showed LAI 1-3 months later. Tumour-free melanoma patients monitored for one year by the Tube LAI assay showed a decline in their anti-tumour immunity 5-6 months after surgery. The NAI was low or negative after the 8th post-surgical month in tumour-free patients. Patients with residual malignant melanoma showed persistent or recurrent LAI after the 8th post-surgical month. LAI reactivity monitored after "curative" surgery for malignant melanoma may assist in determining whether the patient is tumour-free or has a recurrence.

Antigens, Neoplasm↗
PubMed1976

Cellular localization of immunoglobulin within human maglignant melanomata.

The presence of antibody in patients with malignant melanoma is well established if one examines the serum. In this report we have attempted to identify antibody within solid tumours showing that they are rarely present in any appreciable quantity on the surface of tumour cells but can be seen frequently on a number of different types of host cell within the tumours. This is discussed in the light of the role of antibody in the circulation and the possibility of antibody behaving as a blocking factor in vivo.

Antibodies, Neoplasm↗
PubMed1976

The isolation and characterization of tumor-specific antigens of rodent and human tumors.

Putative tumor-specific transplantation antigens (TSTA) from both a carcinogen-induced rodent tumor (MC-1) and 2 human tumors were purified. The antigens were solubilized from the tumor cell membranes by limited papain digestion in a manner similar to that described for the isolation of normal histocompatibility antigens. The antitumor immune response of the tumor-bearing host was used to monitor the purification of the putative TSTA in both the rodent and human tumor systems. In the case of the rodent tumor, a major step in the purification of the TSTA involved affinity chromatography on Sepharose beads coupled to autologous antitumor antiserum. A comparable procedure was utilized in the purification of the TSTA from human tumors by using affinity chromatography on anti-human beta2-microglobulin antiserum coupled to a solid phase. The data obtained indicate that the TSTA of human tumors contains a beta2-microglobulin chain that is immunochemically identical with, and very similar in size to, that found in normal human histocompatibility antigens. A subunit of similar size was also identified in the carcinogen-induced rodent tumor. These results suggest that the TSTA in both humans and rodents may well be altered histocompatibility antigens.

Animals↗
PubMed1975

Soluble tumour-specific antigen and its relationship to tumour growth.

Hooded rats bearing a syngeneic methylcholanthrene-induced tumour were evaluated for extent of in vivo host immunity and this was correlated by in vitro techniques with the levels of circulating tumour antigen and specific antibody. Early tumour growth was associated with detectable immunity, as measured by the capacity of the animal to reject a second direct challenge of the same tumour at a remote site. Radioimmunoassay for circulating tumour antigen and indirect membrane immunofluorescence for antitumour antibody did not detect either component at this stage. Animals with advanced tumours lost immunity as detected by direct tumour challenge, and this closely coincided with the appearance of rising levels of circulating soluble tumour antigen. Although the host possessed the immunologic ability to react against its own neoplasm, this ability was insufficient to produce tumour rejection. Active immunotherapy initiated at the time of, or up to 10 days after, intramuscular challenge with tumour, increased tumour immunity sufficiently for tumour growth to be prevented. Successful immunization was associated with the early appearance (16 days) of measurable levels of antitumour antibody and absence of circulating antigen. It is concluded that soluble tumour antigen present in the local microenvironment of the tumour in the early stages of tumour growth interferes with the ability of immune cells to cause tumour rejection. As the tumour progressively grows, sufficient soluble antigen is produced and released systemically to suppress the effector arm of the host's tumour immune response at distant sites. The levels of circulating soluble tumour antigen attained may be of critical importance in the suppression of rejection responses that prevent metastasis.

Animals↗
PubMed1975

Cell-mediated antitumor immunity in breast cancer patients evaluated by antigen-induced leukocyte adherence inhibition in test tubes.

Tumor antigen-induced inhibition of leukocyte adherence was adapted and modified for use in glass test tubes for the study of cell-mediated antitumor immunity to human adenocarcinoma of the breast. Peripheral blood leukocytes from 40 to 47 patients with proven breast cancer responded to an antigenic extract of breast cancer with significant leukocyte adherence inhibition, whereas only 2 of 32 controls showed a response. Further, 7 patients with histologically proven benign breast disease did not react to the breast adenocarcinoma extract, indicating that only breast cancer patients have leukocytes sensitized to the breast cancer antigen. The cell-mediated antitumor response of the breast cancer patient was dependent on the stage of the cancer, and patients with disseminated cancer had decreased responsiveness. In fact, 4 of 7 breast cancer patients who had no response in the assay had disseminated breast cancer. Also, surgery and irradiation depressed leukocyte adherence inhibition responsiveness. Chromatographic fractionation on Sepharose 4B of the breast cancer extract showed that the antigenic component was greater than 10(6) daltons. The responsive cell in the assay interacts directly with the tumor antigen, and as a result subsequent adherence to glass is inhibited. The assay described is a comparatively simple and sensitive technique for demonstrating cell-mediated antitumor immunity and appears to be immunologically specific.

Adenocarcinoma↗
PubMed1973

Radioimmunoassay of tumour specific transplantation antigen of a chemically induced rat sarcoma: circulating soluble tumour antigen in tumour bearers.

The tumour specific transplantation antigen (TSTA) from a chemically induced rat sarcoma has been isolated as an electrophoretically homogeneous soluble material by affinity chromatography using a Sepharose bound antibody raised to the tumour in syngeneic rats. The TSTA is specific for the particular tumour used (the MC-1 sarcoma) and does not cross-react with material extracted from other rat sarcomata. In addition, a material with different physicochemical properties which cross-reacted with different sarcomata was also eluted from the antibody column and this may be the previously identified onco-embryonic antigen (OEA1) which is immunogenic in the syngeneic host.The purified TSTA labelled with (125)I was used in a radioimmunoassay which detected soluble TSTA in rats bearing a MC-1 sarcoma. The assay shows that tumour transplantation is associated with a persisting release of soluble antigen into the circulation. This antigenic burden is present continuously and renewed as long as the tumour mass exists.

Animals↗