Christine Burns
Mater Misericordiae Hospital
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Featured researches published by Christine Burns.
Cancer Immunology, Immunotherapy | 1987
Peter Hersey; Malcolm MacDonald; Christine Burns; David A. Cheresh
SummaryPrevious studies have shown that monoclonal antibodies (M.Ab) to the ganglioside GD3 may induce partial remissions in tumour growth in patients with melanoma. In vitro studies demonstrated that M.Abs to GD3 may also enhance lymphocyte responses to phytohemagglutinin and interleukin 2 (IL2). The present study extended these findings by showing that the IL2-dependent proliferative and cytotoxic response of T cell clones derived from a melanoma patient and a patient with the Vogt-Koyanagi-Harada syndrome were enhanced by pre-incubation of T cells with M.Ab to GD3. The degree of enhancement increased with the duration of pre-incubation from 2 to 24 h and applied to both T4+ and T8+ clones. The potentiation of these responses was not specific for M.Abs to GD3 but was also seen with M.Abs to GD2 and the T10 structure on T cells but not with M.Abs to the transferrin receptor or an isotype control M.Ab. Incubation of lymphocytes from a melanoma patient with M.Ab to GD3 during culture with autologous melanoma cells enhanced the proliferative response to the tumour. The expression of IL2 receptors (Tac epitope) on the T cells showed variable enhancement after incubation with M.Ab to GD3 but the significance of these findings in relation to the mechanism of the enhanced responses is not known. These results suggest that certain M.Abs may stimulate cell-mediated immune responses against tumour cells and that this may provide an additional mode of action of M.Abs against tumours in vivo
Archive | 1986
Peter Hersey; Malcolm MacDonald; Stephen Schibeci; Christine Burns
SummaryThis study investigates the nature and specificity of cytotoxic T lymphocytes (CTL) in patients with melanoma which are able to kill autologous melanoma cells. Interleukin 2 (IL2)-dependent T cell clones from two melanoma patients and a normal subject were generated in mixed lymphocyte cultures (MLC) or mixed lymphocyte tumor cell cultures (MLTC) and propagated for prolonged periods in tissue culture. Analysis of their phenotype by a wide range of monoclonal antibodies (M.Abs) revealed two main phenotypes which depended on whether they expressed Fc receptors detected by Leu 11 M.Abs or not. Leu 11− T cells (referred to as Type 1) were inhibited by M.Abs to T3, T8, and a common HLA, ABC antigen. Conversely Leu 11+ T cells (referred to as Type 2) were inhibited by M.Ab to Leu 11 but not by M.Ab to T3, T8 and the HLA, ABC antigen. Subtypes among Type 1 cells were recognized which depended on their specificity. The most restricted were CTL [Type 1(a)] clones generated only in MLTC which recognized the autologous melanoma cell plus 1 of 11 other melanoma target cells. Type 1(b) CTL clones recognized a larger proportion (approximately 50%) of the melanoma cells. A third category [Type 1(c)] recognized antigens on melanoma cells shared with that on the EBV-transformed B cells used as stimulators in the MLC. Type 2 CTL clones had broad specificity to melanoma and nonmelanoma cells, characteristic of that described for lymphokine activated killer (LAK) cells. The latter were MHC unrestricted but further studies are required to clarify whether the Type 1 CTL clones are MHC restricted or not. The CTL activity of all clones was inhibited by M.Ab to the sheep red blood cell receptor and to the T10 antigens. It is suggested that recognition of these different types of CTL clones may assist future studies on the immune response against melanoma and the nature of antigens recognized by CTL.
Annals of Clinical Biochemistry | 1990
Maree Gleeson; Lynn Herd; Christine Burns
The effect on the concentrations of specific serum proteins and tumour markers, of heat-treating samples at 56°C for 30 min to inactivate HIV, was investigated. Statistically significant decreases, that may affect clinical decisions, were observed for α-1-antitrypsin, β-2-microglobulin, IgE, fibrinogen, C***1-esterase inhibitor and CA125. Statistical, but not clinically significant, changes were observed for α-1-acid glycoprotein, C3, haptoglobin, IgA, IgG, IgM and transferrin. A significant decrease in the α-1 band was observed on protein electrophoresis.
Journal of Investigative Dermatology | 1987
Peter Hersey; Malcolm MacDonald; Christine Burns; Steven Schibeci; Helen Matthews; F. J. Wilkinson
Cancer Research | 1986
Peter Hersey; Stephen Schibeci; Phillip Townsend; Christine Burns; David A. Cheresh
Cancer Immunology, Immunotherapy | 1986
Peter Hersey; Malcolm MacDonald; Stephen Schibeci; Christine Burns
Cancer Research | 2018
James Sun; Yali Li; Coren A. Milbury; Joel Skoletsky; Christine Burns; Wai-ki Yip; Jun Luo; Ninad Dewal; Adrienne Johnson; Kyle Gowen; Jing Tong; Yuting He; Jie He; Pei Ma; Jared White; Steve Roels; John Truesdell; Eric C. Peters; Houston Gilbert; Charlie Wu; Erica Schleifman; Johannes Noe; Carl Barrett; Kenneth S. Thress; Suzanne Jenkins; Julia A. Elvin; Geoff Otto; Doron Lipson; Jeffrey Ross; Vincent A. Miller
Cancer Research | 2018
Wai-ki Yip; Joel Skoletsky; Pei Ma; Jun Luo; Coren A. Milbury; Christine Burns; John Truesdell; Julia A. Elvin; Geoff Otto; Doron Lipson; Jeffrey Ross; Vincent A. Miller; Philip J. Stephens; Michael Doherty; Christine Vietz; James Sun; Yali Li
Cancer Research | 2018
Ninad Dewal; Joel Skoletsky; Wai-ki Yip; Caitlin Patriquin; Yuting He; Jeffrey S. Ross; Vincent A. Miller; Philip J. Stephens; Christine Burns; Christine Vietz; Yali Li; Colin C. Pritchard; James Sun
Cancer Research | 2018
Yuting He; Matthew Wongchenko; Joel Skoletsky; Christine Burns; Yali Li; Paula Maness; Doris Kim; Doron Lipson; Philip J. Stephens; Vincent A. Miller; Jeffrey Ross; Steven Gendreau; James Sun