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Citations to this article

Inhibition of tumor cell glutamine uptake by isolated neutrophils.
D B Learn, E L Thomas
D B Learn, E L Thomas
Published September 1, 1988
Citation Information: J Clin Invest. 1988;82(3):789-796. https://doi.org/10.1172/JCI113680.
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Research Article

Inhibition of tumor cell glutamine uptake by isolated neutrophils.

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Abstract

Antitumor activity of phorbol myristate acetate-(PMA) stimulated neutrophils was measured against CCRF-CEM cells. Neutrophils and tumor cells were incubated (a) as a suspension with continuous mixing to maximize the availability of oxygen or (b) after centrifugation as a pellet to maximize cell-cell contact. The cells were then incubated briefly as a suspension with [14C]glutamine under conditions that blocked further damage to the tumor cells. When cells were incubated as a suspension, inhibition of tumor-cell glutamine uptake was mediated by the myeloperoxidase/hydrogen peroxide/chloride system of stimulated neutrophils. Inhibition was blocked by adding catalase, an inhibitor of myeloperoxidase, or compounds that scavenge hypochlorous acid or chloramines. When cells were incubated as a pellet, a portion of the inhibition could not be blocked in this way, indicating that a nonoxidative mechanism contributed to inhibition. In both systems, inhibition of glutamine uptake was rapid and was obtained at effector-cell/target-cell ratios as low as 0.5:1. This inhibition was obtained under conditions that did not result in 51Cr release from cells labeled with [51Cr]-chromate, indicating that inhibition of glutamine uptake measured cytotoxicity rather than cytolysis. 51Cr release was observed only when cells were incubated together for an hour or more as a pellet at high E/T ratios. This cytolysis was mediated by the myeloperoxidase system, and a nonoxidative contribution to cytolysis was not observed. The results indicate that stimulated neutrophils are potent antitumor effectors cells when cytotoxicity rather than cytolysis is the measure of activity. Because glutamine is required for growth of many tumor cells, inhibition of glutamine uptake may represent a significant tumoristatic or tumoricidal effect.

Authors

D B Learn, E L Thomas

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Total citations by year

Year: 2012 2010 1994 1992 1991 1990 Total
Citations: 1 1 1 2 2 1 8
Citation information
This citation data is accumulated from CrossRef, which receives citation information from participating publishers, including this journal. Not all publishers participate in CrossRef, so this information is not comprehensive. Additionally, data may not reflect the most current citations to this article, and the data may differ from citation information available from other sources (for example, Google Scholar, Web of Science, and Scopus).

Citations to this article (8)

Title and authors Publication Year
Glutamine as a supplemental treatment in pediatric and adult oncology patients
T Stachowicz-Stencel, A Synakiewicz
Expert Opinion on Investigational Drugs 2012
Use of attenuated paramyxoviruses for cancer therapy
PJ Lech, SJ Russell
Expert Review of Vaccines 2010
Glutamine metabolism and utilization: relevance to major problems in health care
B Moskovitz, Y Katz, P Singer, O Nativ, B Rosenberg
Pharmacological research : the official journal of the Italian Pharmacological Society 1994
Inhibition of the human leukocyte enzymes myeloperoxidase and eosinophil peroxidase by dapsone
PM Bozeman, DB Learn, EL Thomas
Biochemical Pharmacology 1992
Relevance of glutamine metabolism to tumor cell growth
MA Medina, F Sánchez-Jiménez, J Márquez, AR Quesada, I de Castro Núñez
Molecular and Cellular Biochemistry 1992
Disparate effects of interferon-gamma and tumor necrosis factor-alpha on early neutrophil respiratory burst and fungicidal responses to Candida albicans hyphae in vitro
RD Diamond, CA Lyman, DR Wysong
Journal of Clinical Investigation 1991
Inhibition by monochloramine of the transport of glutamine and glucose in HeLa cells and lymphocytes
TJ Piva, EA Newsholme, L Goldstein
International Journal of Biochemistry 1991
Mechanisms of hypochlorite injury of target cells
IU Schraufstätter, K Browne, A Harris, PA Hyslop, JH Jackson, O Quehenberger, CG Cochrane
Journal of Clinical Investigation 1990

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