Amplification by macrophages of prostaglandin-mediated immunosuppression in mice bearing syngeneic tumors

Plescia, Otto J.; Pontieri, G. M.; Brown, J. H.; Racis, S.; Ippoliti, Flora; Bellelli, L; Sezzi, Maria Luisa; Lipari, Marcella

doi:10.1016/0262-1746(84)90072-6

Cited by 12 publications

(2 citation statements)

References 27 publications

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“…Many studies have shown that PGE2-producing host cells such as macrophages inhibit host antitumor immunity and also enhance tumor growth and metastases [1,31,33,42]. Several reports have shown that high amounts of prostaglandins, especially PGE2, are secreted by some clinical cancers, such as large-bowel/rectum cancer, mammary cancer and head and neck cancer [2,3,11,18].…”

Section: Discussionmentioning

confidence: 99%

Regression mechanisms of mouse fibrosarcoma cells after in vitro exposure to quercetin: Diminution of tumorigenicity with a corresponding decrease in the production of prostaglandin E2

Okada

Hosokawa

Hasegawa

et al. 1990

Cancer Immunol Immunother

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We have previously reported that both regressor (QR) and progressor (metastatic, QP) clones were obtained after the in vitro exposure of a mouse fibrosarcoma BMT-11 cl-9 to quercetin. In this study, we investigated possible mechanisms of spontaneous regression of QR clones as compared with tumorigenic QP and BMT-11 cl-9 tumor clones. We observed that BMT-11 cl-9 cells produced relatively high amounts of prostaglandin E2 (PGE2) during in vitro culture. The average production by 11 subclones of BMT-11 cl-9 cells was 9236 +/- 2829 pg/ml whereas that by 9 QR clones was 3411 +/- 2213 pg/ml (P less than 0.02). Indomethacin not only inhibited in vitro PGE2 synthesis by QP clones (high-PGE2 producers) but also the s.c. growth of QP clones in mice. Chronological changes in host immune responses to tumor-associated antigen were measured by cytotoxic T lymphocyte (CTL) activity examined after mixed lymphocyte/tumor cell culture of spleen cells obtained from tumor-bearing mice. The CTL activity disappeared abruptly in the spleen of QP-clone-bearing mice 21 days after the inoculation of tumors, whereas the spleen cells of QR-clone-inoculated mice retained their CTL activity. We determined that the mechanism responsible for the regression of these regressor clones is not due to any qualitative or quantitative increase in pre-existing membrane antigens, nor the emergence of new antigen(s) on the cell surface of the QR clones: nor was it due to enhanced susceptibility of QR clones to natural killer cells, lymphokine-activated killer cells and macrophages. These finding suggest that the regression mechanism of QR clones may be the diminished inhibition of host response to tumor-associated antigen caused by the reduced production of PGE2 by QR clones.

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Section: Discussionmentioning

confidence: 99%

Regression mechanisms of mouse fibrosarcoma cells after in vitro exposure to quercetin: Diminution of tumorigenicity with a corresponding decrease in the production of prostaglandin E2

Okada

Hosokawa

Hasegawa

et al. 1990

Cancer Immunol Immunother

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“…Young and Dizer [69] treated 3LL tumor-bearing mice with antibodies to PGE2 and found restoration of depressed lymphocyte mitogenesis and mac rophage migration, and reduction of tumor growth. Plesia et al [70] observed that 3LL cells stimulated PGE production by host macrophages. Differences in prostacyclin production have been observed between cells of primary tumor versus cells of metastases [10], 3LL cells can directly activate platelets [71,72], This aggregation is biphasic.…”

Section: The Lewis Lung Carcinomamentioning

confidence: 99%

Basis for Selection of Anticoagulant Drugs for Therapeutic Trials in Human Malignancy

Zacharski¹

1986

Pathophysiol Haemos Thromb

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Evidence indicates that progression of the Lewis lung carcinoma in mice and small cell carcinoma of the lung in humans is retarded by warfarin administration. This suggests that vitamin K-dependent pathways are of importance in the pathogenesis of these tumors. Available data were reviewed for these tumor types in an attempt to explore mechanisms and to gain insights that might guide the selection of other coagulation-reactive drugs for testing in future controlled clinical trials in small cell carcinoma of the lung. While many differences exist between the Lewis lung tumor and small cell carcinoma of the lung, both are rapidly growing malignancies of pulmonary origin that metastasize early to kill the host after a short time. Both are favorably influenced by combination chemotherapy and radiation therapy as well as anticoagulant treatment. Peripheral blood changes indicative of disseminated intravascular coagulation occur in each of these tumor types, and tumor cells from both are capable of interacting with the coagulation mechanism. While many details concerning the host-tumor interaction remain to be elucidated, the considerable and diverse information available for these tumor types provides a secure base for future investigation. It is postulated that certain drugs in addition to warfarin might reasonably be studied in controlled clinical trials of small cell carcinoma of the lung and that drugs other than warfarin might be effective for tumor types that are not responsive to this agent.

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Tumor-Mediated Immunosubversion: Role of Dietary Essential Fatty Acid

Plescia

Brown

Lombardi

et al. 1989

Carcinogenesis and Dietary Fat

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Amplification by macrophages of prostaglandin-mediated immunosuppression in mice bearing syngeneic tumors

Cited by 12 publications

References 27 publications

Regression mechanisms of mouse fibrosarcoma cells after in vitro exposure to quercetin: Diminution of tumorigenicity with a corresponding decrease in the production of prostaglandin E2

Regression mechanisms of mouse fibrosarcoma cells after in vitro exposure to quercetin: Diminution of tumorigenicity with a corresponding decrease in the production of prostaglandin E2

Basis for Selection of Anticoagulant Drugs for Therapeutic Trials in Human Malignancy

Tumor-Mediated Immunosubversion: Role of Dietary Essential Fatty Acid

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