Defective Monocyte Killing in Cancer Patients

Israël, Lucien; Samak, Raymond; Eedelstein, Richard

doi:10.1016/s0140-6736(80)92385-5

Cited by 5 publications

(2 citation statements)

References 4 publications

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“…This possibility is also suggested by the findings of Kleinerman et that the monocyte functions increase after chemotherapy; Israel et a1. 26 suggest that this enhancement is not due to a simple stimulatory effect, but rather to the reduction of the tumor burden. The increase in cytotoxic cells against certain target cells after radiation treatment for breast cancer also tends to support this view, taking into account that the monocytic cells probably are responsible for the spontaneous cytot~xicity.~~ The effect was not seen immediately after completion of the radiation treatment, also suggesting an indirect and slow effect on the monocyte population.…”

Section: Discussionmentioning

confidence: 91%

Lymphocyte subpopulations in patients with breast cancer after postoperative radiotherapy

Toivanen

Granberg

Nordman

1984

Cancer

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The effects of radiotherapy on the immune competence of patients with mammary cancer was studied using enumeration of the various lymphocyte subpopulations as detected by monoclonal OKT antisera, lymphocyte proliferative responses to phytohemagglutinin, concanavalin A, purified protein derivative to tuberculin (PPD), and serum immunoglobulin levels. The tests were carried out in nine patients with newly diagnosed and operated mammary cancer before and after the radiation therapy, and 6 months later, and in ten patients whose mammary cancer had been diagnosed and treated at least 3 years earlier and who had remained tumor‐free. The number of lymphocytes in the peripheral blood and the various T‐cell subpopulations as well as the OKIa1 cells mostly representing B‐cells decreased. The only population increasing were the OKM1‐positive cells, mostly representing monocytes and null cells. As also described earlier, the responses to mitogens decreased because of the radiotherapy but recovered, except for the responses to PPD which remained low.

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Section: Discussionmentioning

confidence: 91%

Lymphocyte subpopulations in patients with breast cancer after postoperative radiotherapy

Toivanen

Granberg

Nordman

1984

Cancer

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“…On the basis of in vitro studies [9] it was proposed that the improvement in monocyte function might be a direct effect of cisplatin on the monocytes. Nevertheless, the evidence was indirect; Isra61 et al [6] strongly questioned this and found the decreased tumor burden that followed chemotherapy a more reasonable explanation.…”

Section: Discussionmentioning

confidence: 99%

Normalization of defective monocyte chemotaxis during chemotherapy in patients with small cell anaplastic carcinoma of the lung

Nielsen

Bennedsen

Dombernowsky

1982

Cancer Immunol Immunother

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Monocyte chemotactic responsiveness (MCR) in 14 patients with small cell anaplastic bronchogenic carcinoma was depressed before treatment compared with the MCR in 28 normal controls (P = 0.00004). MCR was subsequently monitored during combination chemotherapy and after 6 months the MCR had become normalized compared with pretreatment values (P = 0.00006). In addition, chemotactic factor inhibitor (CFI) activity in plasma was measured before treatment and after 6 months. When incubated with plasma before treatment casein had 62% of normal activity and when incubated with plasma after chemotherapy, 81% of normal activity (P = 0.0009). CFI activity decreased by greater amounts in patients in complete remission than in patients in partial remission or in non-responders (P = 0.01). This study supports the concept that cancer patients have depressed monocyte function. Chemotherapy seems to enhance monocyte chemotaxis in vitro and to decrease CFI activity in plasma.

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Monocyte chemotaxis in patients with nonseminomatous testicular carcinoma

Nielsen

Rørth²,

Bennedsen

1985

Cancer Immunol Immunother

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The chemotactic responsiveness of blood monocytes was tested in 16 patients with nonseminomatous testicular carcinoma before, during, and after chemotherapy. All the patients initially had monocyte chemotaxis within the normal range. No correlation with the histology of the tumor, the clinical stage, or the presence in serum of alpha-fetoprotein and human chorionic gonadotropin was observed. Plasma from the patients did not inhibit the chemotaxis of normal monocytes, and serum from the patients contained no chemotactic factor inhibitor. During intensive chemotherapy with cis-platinum, bleomycin, and vinblastine a reversible defect in chemotaxis occurred without correlation to the development of fever. Two months after the completion of chemotherapy the chemotactic responsiveness was unchanged compared with pretreatment values. In conclusion, this study shows normal monocyte chemotaxis in patients with testicular carcinoma, which is in contrast to reports on a variety of other solid tumors.

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Defective Monocyte Killing in Cancer Patients

Cited by 5 publications

References 4 publications

Lymphocyte subpopulations in patients with breast cancer after postoperative radiotherapy

Lymphocyte subpopulations in patients with breast cancer after postoperative radiotherapy

Normalization of defective monocyte chemotaxis during chemotherapy in patients with small cell anaplastic carcinoma of the lung

Monocyte chemotaxis in patients with nonseminomatous testicular carcinoma

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