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JNCI Journal of the National Cancer Institute 1993 85(22):1836-1839; doi:10.1093/jnci/85.22.1836
© 1993 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 85, No. 22, 1836-1839, November 17, 1993
© 1993 Oxford University Press

Quantitative Study of Monocyte Chemoattractant Protein-1 (MCP-1) in Cerebrospinal Fluid and Cyst Fluid From Patients With Malignant Glioma

Jun-ichi Kuratsu, Kimio Yoshizato, Teizo Yoshimura, Edward J. Leonard, Hideo Takeshima, Yukitaka Ushio

Department of Neurosurgery, Kumamoto University Medical School Japan
Laboratory of Immunobiology, Division of Cancer Biology, Diagnosis, and Centers, National Cancer Institute, NCI-Frederick Cancer Research and Development Center Frederick, Md.

Correspondence to: Jun-ichi Kuratsu, M.D., Department of Neurosurgery, Kumamoto University Medical School, 1-1-1 Honjyo Kumamoto 860, Japan.

Background: Monocyte chemoattractant protein-1 (MCP-1) is a 76-amino acid protein that attracts monocytes. In vitro studies have reported high levels of MCP-1 messenger RNA expression, as well as the presence of MCP-1, in malignant glioma cells. Purpose: Our purpose was to determine whether an MCP-1 assay could be used in a clinical setting 1) to differentiate malignant from benign gliomas and from nontumor disorders of the central nervous system and 2) to detect subarachnoid dissemination of glioma cells. Methods: MCP-1 levels in cerebrospinal fluid (CSF) and cyst fluid were measured with a sandwich enzyme-linked immunosorbent assay (ELISA) that we had previously developed. We measured MCP-1 levels in CSF samples from 19 patients with malignant glioma (glioblastoma, 10; anaplastic astrocytoma, six; anaplastic oligodendroglioma, two; and ependymoblastoma, one), nine patients with benign glioma, and seven patients with nontumor disorders of the central nervous system. Cyst fluids from four patients with malignant glioma (anaplastic astrocytoma) were also tested. The correlation between MCP-1 concentration in the CSF and subarachnoid dissemination of malignant glioma cells was also studied. Results: The MCP-1 concentration (mean ± SE) in CSF samples from patients with malignant glioma (2.3 ± 0.4 ng/mL) was significantly higher than that from patients with benign glioma (0.6 ± 0.1 ng/mL) (P<.01) or from patients with no tumor (0.5 ± 0.1 ng/mL) (P<.01). Furthermore, CSF samples from patients with subarachnoid dissemination of malignant glioma contained significantly higher amounts of MCP-1 than those from patients without dissemination (P<.05). Cyst fluids from four of the patients with malignant glioma contained high concentrations of MCP-1. Conclusions: These results indicate that MCP-1 is produced by malignant glioma in vivo as well as in vitro and suggest that testing for MCP-1 in CSF may be useful in the clinic to differentiate malignant glioma from benign glioma and to detect subarachnoid dissemination of the tumor cells. Implications: The MCP-1 ELISA in CSF may lead to more accurate diagnosis of malignant glioma and detection of subarachnoid dissemination of tumor cells, facilitating selection of patients with these conditions for appropriate therapy. [J Natl Cancer Inst 85:1836–1839, 1993]


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