Differential sensitivity of two murine leukaemia sublines to cytolysis by Corynebacterium parvum-activated macrophages

Berd, David; Mastrangelo, Michael J.

doi:10.1038/bjc.1981.280

Cited by 3 publications

(3 citation statements)

References 15 publications

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“…Similar findings have been reported by Cabilly & Gallily (1981) using syngeneic murine embryonic fibroblasts as target cells. These observations are in contrast to other reports (Alexander & Evans, 1971;Nathan et al, 1979aNathan et al, , 1980Berd & Mastrangelo, 1981;Koren et al, 1981a) in which antibody-mediated contact with activated mp led to lysis of lymphoid tumour cells from established cell lines. The reason for lack of cytotoxicity in L2C cells is unclear.…”

Section: Discussioncontrasting

confidence: 99%

“…In common with other investigators (Nathan et al, 1979a(Nathan et al, , 1980Berd & Mastrangelo, 1981;Koren et al, 1981a), we have not observed phagocytosis of the lymphoid tumour cells. Even when L2C cells were sensitized with antibodies which were not susceptible to surface redistribution, phagocytosis did not occur.…”

Section: Discussionsupporting

confidence: 93%

“…Several reports that activated macrophages (m(p) are capable of mediating antibody-dependent cellular cytotoxicity (ADCC) towards lymphoid tumour cells (Alexander & Evans, 1971;Nathan et al, 1979aNathan et al, , 1980Berd & Mastrangelo, 1981;Koren et al, 1981a) have prompted us to investigate their activity against neoplastic B lymphocytes of the guinea pig L2C leukaemia. Previous findings from this laboratory have demonstrated the susceptibility of these cells in vitro to antibody-dependent cytotoxicity-both extracellular killing by human peripheral blood leukocytes (Stevenson & Elliott, 1978) and complement-mediated lysis .…”

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Macrophages induce antibody-dependent cytostasis but not lysis in guinea pig leukaemic cells

Lawson¹,

Stevenson²

1983

Br J Cancer

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionsupporting

confidence: 93%

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Macrophages induce antibody-dependent cytostasis but not lysis in guinea pig leukaemic cells

Lawson¹,

Stevenson²

1983

Br J Cancer

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Tumor heterogeneity: biological implications and therapeutic consequences

1983

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It is now appreciated that cancers can be composed of multiple clonal s~bpopulations of cancer cells which differ among themselves in many properties, including karyotype, growth rate, ability to metastasize, immunological characteristics, production and expression of markers, and sensitivity to therapeutic modalities. Such tumor heterogeneity has been demonstrated in a wide variety of animal tumors of differing etiology, tissue and cellular origin, and species. It has been shown in autochthonous, as well as transplanted, tumors. Similar results have been reported for human cancers, although much of the evidence that heterogeneity of human cancers, also reflects, at least in part, the existence of clonal subpopulations, is still indirect. Heterogeneity is not a unique property of malignancy. Preneoplastic tumors, as well as normal tissues, are also composed of cellular subpopulations.Proposed mechanisms for the origin of tumor heterogeneity include coalescence of multiple loci of cancer clones and the generation of diverse subpopulations from a single clone. This latter process could be due to genetic errors arising from classical genetic mechanisms or to the production of cellular variants as in normal tissue differentiation. Indeed, certain tumor subpopulations have been shown to produce variants at high frequency. In some cases this frequency can be modified by environmental circumstances. Nontumor cells may also contribute to production of cancer cell variants, perhaps, in the case of infiltrating phagocytic cells, by producing mutagens or by somatic hybridization with cancer cells. Production of tumor cell variants is a dynamic process which can occur at any time.Although tumors are mixed populations of cells, knowledge of the characteristics of individual components is not sufficient to predict the behavior of the whole. Individual cancer subpopulations can interact to affect each other's growth, immunogenicity, ability to metastasize, sensitivity to drugs, and clonal stability. The existence of multiple, interactive subpopulations provides a basis for the well-known phenomenon of 'tumor progression' in which tumors undergo qualitative changes in characteristics over the course of time. Selection of subpopulations better able to survive changing environmental circumstances allows for such changes as autonomy in regard to endogenous growth regulation, more "malignant' behavior, and loss of response to therapy. Tumor subpopulation interactions may play a regulatory role in this process.Tumor heterogeneity has obvious consequences to the design of effective therapy. It provides one rationale for combination therapies and suggests that initial treatment should be early and comprehensive. The continuing emergence of new clones suggests that treatment which is unsuccessful at one point might be effective later. Assays to predict effective therapy for individual patients need to address the multiplicity of tumor subpopulations and the ability of these subpopulations to influence each other. Subpopulation interacti...

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Intratumor immunologic heterogeneity

Miller

1982

Cancer Metast Rev

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Tumor cells express a great variety of antigens including tumor specific transplantation antigens, tumor-associated antigens, differentiation antigens, histocompatibility antigens, lectin-binding sites and receptors for natural killer cells and natural antibodies. These antigens are distributed unevenly on tumor subpopulations and each subpopulation may induce different immune responses to the same determinant. Intratumor immunologic heterogeneity arises early in cancer, possibly during preneoplasia, and exists throughout the course of progression. Metastatic subpopulations are not generally less antigenic than subpopulations within primary tumors. Different arrays of antigenic determinants are displayed by subpopulations but variability in cell surface expression of a single determinant is also a fundamental type of immunologic heterogeneity. Antigenic specificity patterns commonly reveal one-way cross-reactions between tumor subpopulations. One-way cross-reactions might occur due to quantitative differences, cell-cycle variations, modulation, masking, H-2 expression and restriction phenomena, or alteration in the carbohydrate side-chains of glycoproteins. Interactions which occur when subpopulations co-exist may alter immune responses so that the response to the mixture is not the sum of the responses to the individual subpopulations. It is suggested that the exploitation of the mechanisms involved in immunologic heterogeneity may lead to new therapeutic approaches and that the great diversity of determinants expressed by tumor cells could lead to development of multivalent panel of monoclonal antisera which, acting synergistically, could preferentially lyse tumor cells.

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Differential sensitivity of two murine leukaemia sublines to cytolysis by Corynebacterium parvum-activated macrophages

Cited by 3 publications

References 15 publications

Macrophages induce antibody-dependent cytostasis but not lysis in guinea pig leukaemic cells

Macrophages induce antibody-dependent cytostasis but not lysis in guinea pig leukaemic cells

Tumor heterogeneity: biological implications and therapeutic consequences

Intratumor immunologic heterogeneity

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