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Biomedical subjects

J W Proctor

Publications and source records attributed to J W Proctor.

32 records · Page 2Linked to original sources
PubMed1976

The distribution and fate of blood-borne 125IUdR-labelled tumour cells in immune syngeneic rats.

Radiolabelled sarcoma cells injected into the tail veins of normal rats were held up almost exclusively in the lung, and were not observed to pass through into the systemic circulation. Intramuscularly injected tumour cells were retained at the site of injection. Radioactivity was lost from both sites though more rapidly from the lung than from muscular tissue and was probably the result of tumour-cell death. Alveolar macrophages did not take part in the destruction of tumour cells in the lung. There was an increased rate of radiolabel loss from the lungs of hyperimmune, post-excision and tumour-bearing rats, as compared with normal rats. The destruction was immunologically specific; it was detected earlier, was more comprehensive in the hyperimmune and post-excision animals than in tumour-bearing animals, and correlated with the ability of the hyperimmune and post-excision animals to reject larger numbers of intravenous unlabelled tumour cells, than the tumour-bearing rats.

Animals↗
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

Rat sarcoma model supports both "soil seed" and "mechanical" theories of metastatic spread.

Following injection into the portal venous or vena caval systems, tumour cells are held up almost exclusively in the liver or lung respectively, and subsequent outgrowth of tumour only occurs in these organs. Following systemic arterial injection, cells are distributed, and subsequently grow, in a variety of organs. However, the adrenal gland supports tumour growth from much fewer cells than the lung, and this is partly due to the fact the rate of tumour cell loss in the initial 48 h is very high in the latter compared to the former organ.

Adrenal Gland Neoplasms↗
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

Endrocrine factors and the growth and spread of B16 melanoma.

B16 melanomas grew more slowly in female than in male syngeneic C57BL/6J mice. After oophorectomy, the growth rate was similar to that in normal and castrated male mice and was not altered in pregnant mice. The growth in vitro was similar in the presence of serum from normal and castrated male and female mice.

Adrenal Glands↗
PubMed1976

Immunotherapy for cancer: an overview.

Immunotherapy of cancer is of interest to oncologists because it is specifically directed to cancer cells, sparing normal cells. While it is ineffective in most patients, especially those with widespread metastatic disease, it occasionally produces good results. Each of the available methods has inherent problems and, recently, attempts have been made to overcome some of these. There is a strong case for small-scale experimental trials in highly selected groups of patients who are intensively investigated for their immunologic status in relation to their tumour. Despite the lack of success in general, immunotherapy still appears to have a future as an adjunct to existing therapy in order to control as much as to cure residual tumour.

Adjuvants, Immunologic↗
PubMed1975

Host responses with solid tumors. I. Monocytic effector cells within rat sarcomas.

Morphologic studies of two unrelated progressively growing sarcomas in rats revealed the presence of a large proportion of host cells distinct from tumor cells. Enzymatically or mechanically dispersed tumor suspensions were fractionated by the velocity sedimentation method, which resulted in a separation of host and tumor cells. The host cells had the typical morphology of macrophages and also were adherent to a plastic surface after a short incubation period. The proportion of host cells was greater in a young (10 or 12 days) than in an older tumor (35 days). These macrophage-like host cells isolated from sarcomas 12 and 35 days after implantation inhibited the colony formation of tumor cells in vitro in the nonspecific manner ascribed to activated marcrophages. In addition to these effector cells, the host fraction contained macrophage precursors able to proliferate in vitro but apparently inhibited by the presence of tumor cells. The results indicated that these macrophage-like effector cells may be the predominant host reaction within some rat sarcomas, and also that thymus- and bone marrow-derived lymphocytes act only indirectly if they are involved.

Animals↗
PubMedDate not supplied

Development of a bioassay for anti tumor activity of biological response modifiers of the reticuloendothelial stimulant class: reproducibility of the bioassay.

Intravenously administered DiLuzio glucan, Wellcome C. parvum, and Glaxo BCG caused dose dependent increases in the tumor cell loss from the lungs of C57BL/6J and DBA/2J mice challenged respectively with intravenous 125IuDR labelled B16 or T 1699 mammary carcinoma cells. The results were reproducible with respect to the optimal doses and the magnitudes and shapes of the dose response curves.

Adjuvants, Immunologic↗