Tumor Necrosis Factor Production in B Cell Chronic Lymphocytic Leukemia

Hahn, Talia; Kusminsky, Gustavo; Bassous, Lucette; Berrébi, Alain

doi:10.3109/10428199109068054

Cited by 16 publications

(5 citation statements)

References 17 publications

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“…Higher TNFα levels are associated with more aggressive disease [ 12 , 13 ], although CLL cells with aggressive clinical behavior make less TNFα than cells from patients with indolent disease. [ 13 , 18 , 22 ]. TNFα in the plasma of an additional 43 patients was found to correlate inversely with IgG level at the same time-point.…”

Section: Resultsmentioning

confidence: 99%

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Association of blood IgG with tumor necrosis factor-alpha and clinical course of chronic lymphocytic leukemia

et al. 2018

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The intrinsic humoral immunodeficiency of chronic lymphocytic leukemia (CLL) is often managed with immunoglobulin replacement therapy (IgRT) to maintain IgG levels in the low-normal range (6–8 g/L) but optimal targets for IgG and timing to commence IgRT are unclear. IgG levels fell near 6 g/L at rates of −0.85±0.14 g/L/year in 51 patients who required treatment for CLL within 4.5±0.4 years from initial diagnosis and − 0.27±0.04 g/L/year in 40 patients with progressive disease who remained untreated after 8.5±0.5 years. In contrast, endogenous IgG levels remained above 8 g/L in patients with highly indolent disease (n = 25) and TNFα and beta-2-microglobulin (β2M) in blood decreased when IgRT was used to increase IgG levels over 9 g/L. At 15 g/L but not 5 g/L, the IgRT product Hizentra® inhibited B cell receptor (BCR)-activation, TNFα production, and survival in vitro , particularly of CLL cells that spontaneously made little TNFα. These findings suggest deterioration of the humoral immune system is associated with progressive CLL and altering the dosing of IgRT to achieve higher than conventional IgG target levels may have therapeutic activity.

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Section: Resultsmentioning

confidence: 99%

“…3 B,C) were not obviously different in terms of these factors. Although it has been reported that lack of spontaneous production of TNFα by CLL cells is associated with clinically aggressive behavior [ 13 , 18 , 22 ], there are no obvious clinical characteristics that distinguish group 1 and group 2 patients ( Fig. 5 , Fig.…”

Section: Discussionmentioning

confidence: 99%

Association of blood IgG with tumor necrosis factor-alpha and clinical course of chronic lymphocytic leukemia

et al. 2018

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“…Among different tumor-cell products, certain cytokines are known for their ability to induce procoagulant activity on endothelial cells or macrophages (72). Evidence for production of cytokines with these properties has been demonstrated in benign and malignant (83)(84)(85)(86)(87) lymphoid disorders; in short term cultures of acute (72); and in cultured melanoma (88,89), squamous carcinoma (90), and fibrosarcoma cell lines (73).…”

Section: B Mechanisms Of Extrgvascular Activation Of Coagulation Patmentioning

confidence: 99%

Fibrin and Cancer

Costantini

Zacharski

1993

Thromb Haemost

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An extensive biomedical literature attests to the controversy regarding the significance of coagulation activation in cancer. It has been known for over a century that thromboembolism may complicate the course of malignancy (1) and that fibrin may occur in association with intravascular tumor deposits in humans (2). That peripheral blood coagulation changes, indicative of disseminated intravascular coagulation (DIC), occur regularly in cancer is common knowledge (3). However, the biological significance of such activation of blood coagulation is still not completely clear. Some investigators claim that it is only an insignificant epiphenomenon in a disease that often involves multiple organ systems and that uses the bloodstream for metastatic dissemination. However, other investigators, on the basis of recent clinical and experimental data, including therapeutic intervention studies with antithrombotic drugs, have argued that such activation of the coagulation mechanism might be capable of contributing to progression of malignancy (4-11). The purpose of this review is to evaluate critically the evidence that addresses the significance of blood coagulation activation in malignancy by analyzing the extent, pattern, and possible role of fibrin deposition in situ in tumor tissues. Particular emphasis will be placed on defining the evident heterogeneity that exists between tumor types in an attempt to interpret the existing literature on the coagulation-cancer interaction that is both intriguing and confusing. Fibrin Deposition in Solid Tumors O'Meara (12) first called attention to the possibility of fibrin deposition in solid tumors. However, more convincing evidence that fibrinogen-related proteins were localized in solid tumors came from the work of investigators who showed that systemic administration of fibrinogen together with antifibrinogen antibody leads to their sequestration in animal and human tumors (13, I4).Laki and Yancey (15) reviewed their earlier work that showed direct conversion of fibrinogen to fibrin by cultured malignant cells that were placed in a fibrinogen solution. Fibrin was observed by electron microscopy adjacent to these tumor cells following their innoculation into mice. Other investigators demonstrated fibrinogen-related proteins by immunofluorescence in several experimental and human neoplasms (15, 16). The conclusions derived from these early reports, the results of which Supported in part by the Italian Association for Cancer Research (A.I.R.C.), Milan, Italy (V.C.

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“…The production of IL-1 and TNF in cancer patients has been reported to be defective in some cancers [11,15,31] as well as comparable or increased in others [1,13,28,29]. According to our results (Table 1), unstimulated monocytes from patients of both the groups showed a slightly higher level of IL-1 activity than normal donors which was not found to be significant.…”

Section: Inhibition Of Monocyte Cytotoxicity By Monoclonal Antibody Tmentioning

confidence: 40%

Production of interleukin-1 and tumour necrosis factor in non-Hodgkin's lymphoma patients

Jhaver

Advani

et al. 1991

Cancer Immunol Immunother

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Peripheral blood monocytes from non-Hodgkin's lymphoma (NHL) patients were assessed for the monocyte functions with respect to their ability to secrete interleukin-1 and tumour necrosis factor (TNF) and their cytotoxic potential to tumour target WEHI 164 clone 13. Our results indicate comparable levels of interleukin-1 and TNF production by NHL patients. The cytotoxic potential by monocytes was also not depressed in these patients. The data obtained suggest normal monocyte functions in NHL patients.

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Tumor Necrosis Factor Production in B Cell Chronic Lymphocytic Leukemia

Cited by 16 publications

References 17 publications

Association of blood IgG with tumor necrosis factor-alpha and clinical course of chronic lymphocytic leukemia

Association of blood IgG with tumor necrosis factor-alpha and clinical course of chronic lymphocytic leukemia

Fibrin and Cancer

Production of interleukin-1 and tumour necrosis factor in non-Hodgkin's lymphoma patients

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