Protective specific immunity induced by doxorubicin plus TNF-α combination treatment of EL4 lymphoma-bearing C57BL/6 mice

Ehrke, M. Jane; Verstovšek, Srđan; Maccubbin, Darbie; Ujházy, Peter; Zaleskis, Gintaras; Berleth, Erica S.; Mihich, Enrico

doi:10.1002/1097-0215(20000701)87:1<101::aid-ijc15>3.0.co;2-b

Cited by 29 publications

(19 citation statements)

References 23 publications

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“…Surprisingly, groups treated with TNF␣ 10 + either PTX or ADM showed apoptotic indices exactly similar to the apoptotic indices of the PTX + ADM groups. The therapeutic efficacy of the ADM + TNF␣ combination treatment in vivo has been reported and correlated with an increase in specific long-term immune memory [55].…”

Section: Discussionmentioning

confidence: 99%

In vivo and in vitro sensitization of leukemic cells to adriamycin-induced apoptosis by pentoxifyllineInvolvement of caspase cascades and IκBα phosphorylation

Lerma-Díaz¹,

Hernández‐Flores²,

Domínguez-Rodríguez³

et al. 2006

Immunology Letters

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Section: Discussionmentioning

confidence: 99%

In vivo and in vitro sensitization of leukemic cells to adriamycin-induced apoptosis by pentoxifyllineInvolvement of caspase cascades and IκBα phosphorylation

Lerma-Díaz¹,

Hernández‐Flores²,

Domínguez-Rodríguez³

et al. 2006

Immunology Letters

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“…Combinations of doxorubicin with various therapeutic proteins, such as IL-2, tumor necrosis factor-a, and CNGRCtumor necrosis factor-a, or therapeutic genes, such as TRAIL, for treating tumors were tested previously (37 -41), but only a few reports examined the robust antitumor efficacy by coadministration of doxorubicin and IL-12 recombinant protein (18,19,42). Coadministration of doxorubicin and the IL-12 gene has not been explored previously.…”

Section: Discussionmentioning

confidence: 99%

Doxorubicin Directs the Accumulation of Interleukin-12–Induced IFNγ into Tumors for Enhancing STAT1–Dependent Antitumor Effect

Zhu

Waguespack

Barker

et al. 2007

Clinical Cancer Research

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Purpose: To examine the mechanism by which doxorubicin plus interleukin-12 (IL-12) gene transfer induces enhanced therapeutic efficacy against tumors. Experimental Design: Tumor-bearing mice were treated with doxorubicin, IL-12^encoding plasmid DNA, doxorubicin plus IL-12^encoding plasmid DNA, or plasmid DNA control. Doxorubicin was systemically given via i.p. injection, and IL-12 was systemically expressed via i.m. injection.To show that doxorubicin enhances the accumulation of IL-12^induced IFNg into tumors and the signal transducer and activator of transcription 1 (Stat1)^dependent antitumor efficacy, the distribution of IFNg and the therapeutic end points, such asT-cell infiltration, inhibition of tumor vessel density, tumor growth inhibition, and inhibition of spontaneous tumor metastasis in wildtype and Stat1 -/-host and tumors were determined after the treatment at the indicated time points. Results: In this study, a novel mechanism was unveiled. We discovered that doxorubicin enhances the accumulation of IL-

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“…The chemotherapy-cytokine treatments included cyclophosphamide plus TNF-α [15,16] [18] and doxorubicin plus IL-2 [17]. Treatment with doxorubicin plus TNF-α, which results in prolonged survival but no cure, also gave rise to T cell-mediated immunity [19,20], including rejection of implants of doxorubicin-resistant EL4 cells [19]. This immunity was correlated with the presence of anti-EL4 CD8 + CD44 + CTLs [16][17][18]20], but no adoptive transfer experiments were reported.…”

Section: Discussionmentioning

confidence: 99%

“…Treatment with doxorubicin plus TNF-α, which results in prolonged survival but no cure, also gave rise to T cell-mediated immunity [19,20], including rejection of implants of doxorubicin-resistant EL4 cells [19]. This immunity was correlated with the presence of anti-EL4 CD8 + CD44 + CTLs [16][17][18]20], but no adoptive transfer experiments were reported. Interestingly, it was noted that in C57BL/6 mice that received a curative cyclophosphamide plus TNF-α combination, there was initially thymic involution followed by regrowth [15,18].…”

Section: Discussionmentioning

confidence: 99%

Antibody treatment of human tumor xenografts elicits active anti-tumor immunity in nude mice

et al. 2007

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Athymic nude mice bearing subcutaneous tumor xenografts of the human anti-colorectal cancer cell line SW480 were used as a preclinical model to explore anti-tumor immunotherapies. Intratumor or systemic treatment of the mice with murine anti-SW480 serum, recombinant anti-SW480 polyclonal antibodies, or the anti-colorectal cancer monoclonal antibody CO17-1A, caused retardation or regression of SW480 tumor xenografts. Interestingly, when mice that had regressed their tumors were re-challenged with SW480 cells, these mice regressed the new tumors without further antibody treatment. Adoptive transfer of spleen cells from mice that had regressed their tumors conferred antitumor immunity to naïve nude mice. Pilot experiments suggest that the transferred anti-tumor immunity is mediated by T cells of both γδ and αβ lineages. These results demonstrate that passive anti-tumor immunotherapy can elicit active immunity and support a role for extra-thymic γδ and αβ T cells in tumor rejection. Implications for potential immunotherapies include injection of tumor nodules in cancer patients with anti-tumor antibodies to induce anti-tumor T cell immunity.

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Protective specific immunity induced by doxorubicin plus TNF-α combination treatment of EL4 lymphoma-bearing C57BL/6 mice

Cited by 29 publications

References 23 publications

In vivo and in vitro sensitization of leukemic cells to adriamycin-induced apoptosis by pentoxifyllineInvolvement of caspase cascades and IκBα phosphorylation

In vivo and in vitro sensitization of leukemic cells to adriamycin-induced apoptosis by pentoxifyllineInvolvement of caspase cascades and IκBα phosphorylation

Doxorubicin Directs the Accumulation of Interleukin-12–Induced IFNγ into Tumors for Enhancing STAT1–Dependent Antitumor Effect

Antibody treatment of human tumor xenografts elicits active anti-tumor immunity in nude mice

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