Cytostasis of tumor cell lines by human granulocytes

Korec, S; Herberman, Ronald B.; Dean, Jack H.; Cannon, Grace B.

doi:10.1016/0008-8749(80)90430-x

Cited by 44 publications

(27 citation statements)

References 22 publications

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“…On the basis of these observations, we investigated the ability of PMN to kill IL-2-transfected tumor cells since direct killing of lymphokine gene-transduced tumor cells by PMN in vitro has not been reported. Moreover, very few reports describe spontaneous anti-tumor cytostatic and tumoricidal activities of granulocytes (Korec et al, 1980;Cameron, 1983;Lichtenstein and Kahle, 1985;Fady et al,, 1990;Midorikama et al, 1990). PMN are commonly viewed as cells that do not directly kill target cells without an additional stimulus (van Kessel and Verhoef, 1990).…”

Section: Direct Killing Of Interleukin-2-transfected Tumor Cells By Hmentioning

confidence: 99%

Direct killing of interleukin-2-transfected tumor cells by human neutrophils

Pericle

Kirken²,

Epling-Burnette

et al. 1996

Int. J. Cancer

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Section: Direct Killing Of Interleukin-2-transfected Tumor Cells By Hmentioning

confidence: 99%

Direct killing of interleukin-2-transfected tumor cells by human neutrophils

Pericle

Kirken²,

Epling-Burnette

et al. 1996

Int. J. Cancer

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“…However, some reports de scribed spontaneous cytostatic and cytotoxic activities of PMN from cancer patients [13,49,76] and spontaneous tumor cell lysis by murine inflammatory peritoneal PMN [81].…”

Section: Cytotoxicitymentioning

confidence: 99%

A View to a Kill: Cytotoxic Mechanisms of Human Polymorphonuclear Leukocytes Compared with Monocytes and Natural Killer Cells

Kessel¹,

Verhoef²

1990

Pathobiology

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Polymorphonuclear leukocytes (PMN) are able to exert cell-mediated cytotoxic reactions in order to eliminate tumor cells and virus-infected cells. Appropriate stimulation is needed to activate the potential cytotoxic arsenal of the PMN in contrast to the spontaneous cytotoxicity mediated by natural killer cells. Stimulation with phorbol esters induces an oxygen-dependent killing mechanism which results in highly efficient lysis of red blood cell targets. Tumor target cells are more resistant to oxygen-dependent killing mechanisms due to effective antioxidant capacities. Antibody-coated tumor target cells are easily recognized and bound by PMN via a cooperative action of Fc receptors and adhesion molecules. This firm contact and receptor occupation result in efficient killing of the tumor cells which does not require production of oxygen radicals. The mechanisms of PMN-mediated cytotoxicity are discussed and compared with data known from natural killer cells and monocytes.

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“…Since the sixties, as reviewed by Levy and Wheelock (1974), Keller (1977), Schulz and Chirigos (1980), Johnson et al (1984), and Adams and Hamilton (1988), a wealth of reports have established that macrophages play a major role in resistance against tumor cells, in either immunologically specific or non-specific situations. Surprisingly, despite the fact that polymorphonuclear leukocytes (PMNs) are very often associated with macrophages, the importance of PMNs in host resistance against tumors has only recently been emphasized (Pickaver et al, 1972; Takasugi et al., 1975;Clark and Klebanoff, 1975;Fisher and Saffer, 1978;Chee et al, 1978;Hafeman and Lucas, 1979;Nathan et al, 1979;Korec et al, 1980;Gerrard et al, 1981;Katano and Torisu, 1982;Weiss and Slivka, 1982;Watanabe et al, 1984;Chapes and Haskill, 1984;Lichtenstein and Kahle, 1985).Preliminary findings had shown that when Lewis tumor cells are injected with a polyacrylamide gel which does not inhibit growth of these cells in vitro, tumor growth is strikingly decreased or even inhibited.Taking advantage of a technique which allows recovery of PMNs and macrophages without lymphocytes in polyacrylamide-bead-induced granuloma (Fauve et al, 1983), we have investigated the interactions of a PMN and macrophage population with the cells from one of the most malignant murine tumors: the Lewis tumor. The major findings were: (1) an inverse correlation between the number of granuloma cells and the incorporation of lZ5I-UdR by Lewis tumor cells; (2) the importance of the contact between macrophages and PMNs; (3) the presence in the supernatant of a cytostatic substance with a low molecular weight which is active against normal and tumor cells.…”

mentioning

confidence: 99%

Inflammation and anti‐tumor resistance. V. Production of a cytostatic factor following cooperation of elicited polymorphonuclear leukocytes and macrophages

Hevin

Friguet

Fauve

1990

Intl Journal of Cancer

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When Lewis tumor cells (3LL) included in a gel of polyacrylamide microbeads are injected into mice and recovered 1 day later, incorporation of 125I-UdR is strongly reduced. In contrast, no reduction is observed in irradiated mice. The cytostatic effect is non-existent in 6 hr-old granuloma (granulocytes 90%, macrophages 10%), but is maximal in 48 hr-old granuloma (granulocytes 50%, macrophages 50%). When 6 hr-old granuloma cells (which are not cytostatic) are incubated with bone-marrow-derived macrophages (BMs) (which are slightly cytostatic), considerable cytostasis against 3LL is observed, such an effect being strongly reduced if the 2 cell populations are separated. This suggests that close contact of live polymorphs with macrophages is necessary for full expression of cytostasis. No increase in cytostasis of bone-marrow macrophages is observed when BMs are incubated with a cell-free extract of freeze-thawed 6-hr-old granuloma cells. Cell contact is not necessary between granuloma cells and 3LL since the cytostatic activity is found in the supernatant of incubated phagocytic cells. Cytostasis is also observed with B16, P815, J774 cells and normal mouse bone-marrow cells. An active cytostatic fraction has been purified from the supernatant of 48-hr-old granuloma cells following molecular filtration and HPLC. The cytostatic factor has a low molecular weight (400-500 daltons), is not a peptide and presents maximum absorption at 267 nm.

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Cytostasis of tumor cell lines by human granulocytes

Cited by 44 publications

References 22 publications

Direct killing of interleukin-2-transfected tumor cells by human neutrophils

Direct killing of interleukin-2-transfected tumor cells by human neutrophils

A View to a Kill: Cytotoxic Mechanisms of Human Polymorphonuclear Leukocytes Compared with Monocytes and Natural Killer Cells

Inflammation and anti‐tumor resistance. V. Production of a cytostatic factor following cooperation of elicited polymorphonuclear leukocytes and macrophages

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