Correlation of immunomodulatory and therapeutic activities of interferon and interferon inducers in metastatic disease

Black, Paul L.; Phillips, Hamblin; Tribble, Henry R.; Pennington, Robin; Schneider, Mark; Talmadge, James E.

doi:10.1002/jcb.240360407

Cited by 9 publications

(2 citation statements)

References 54 publications

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“…Increased CTL activity in the lung has previously been reported to be associated with decreased metastasis in mice treated with IFN-y and challenged i.v. with B16-BL6 tumor cells (Black et al, 1988), increased CTL activity in the lung strongly correlating with the therapeutic efficacy of IFN-y in the treatment of lung metastasis.…”

Section: Discussionmentioning

confidence: 84%

Neoadjuvant immunotherapy with interferon of the spontaneously metastasizing murine B16F10L melanoma

Markovic

Murasko

1990

Intl Journal of Cancer

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We have previously demonstrated that administration of interferon a/b (IFN) for 4-5 days after challenge with a transplantable Moloney sarcoma virus-induced tumor completely inhibited tumor development. In the present study, we examined the therapeutic effects of IFN on mortality induced by metastatic dissemination of the B16F10L murine melanoma. IFN was administered at various times in relation to the surgical removal of primary tumor: days -5 to -1 prior to tumor excision (neo-adjuvant protocol), or for 5 days after tumor excision, beginning on days 1, 6 or 11 after excision of the primary tumor (adjuvant protocols). The neo-adjuvant protocol was superior to all other protocols, significantly increasing percentage survival (56% vs. 0%) and median survival time (greater than 84 days vs. 33 days) compared to untreated controls, as well as to all adjuvant protocols. In contrast, IFN treatment on days 1 to 5 after excision of the primary tumor decreased median survival time of cases compared to untreated controls (20 days vs. 33 days). Both IFN-induced inhibition and enhancement of metastatic dissemination were dose-dependent, with higher amounts of IFN producing greater inhibition or enhancement. The superior therapeutic efficacy of the neo-adjuvant IFN treatment was associated with increased spleen and lung-derived natural killer cell cytolytic activity (on days -4, 0 and 2) followed by a later (day 13) increase in lung-associated cytolytic T-cell responses.

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Section: Discussionmentioning

confidence: 84%

Neoadjuvant immunotherapy with interferon of the spontaneously metastasizing murine B16F10L melanoma

Markovic

Murasko

1990

Intl Journal of Cancer

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“…IFN-γ has immunomodulatory activities such as the augmentation of Th1 cells activity, macrophage tumoricidal activity, and natural killer cell cytotoxicity and can exert a suppression of tumor growth and pulmonary metastasis (3,4,7,26,37). The adoption of transferred tumor-specific T cells, demonstrated that secretion of IFN-γ, plays an essential role in tumor rejection (2,11,28,45).…”

Section: Discussionmentioning

confidence: 99%

Anti‐Tumor Mechanism of Z‐100, an Immunomodulatory Arabinomannan Extracted from Mycobacterium tuberculosis Strain Aoyama B, on Pulmonary Metastases of B16F10 Melanoma: Restoration of Helper T Cell Responses via Suppression of Glucocorticoid‐Genesis

oka

Emori

Sasaki

et al. 2002

Microbiology and Immunology

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In the present study, the anti‐tumor mechanism of Z‐100 was investigated with the use of pulmonary metastasis of B16F10 melanoma. In B16F10 mice, Th1 cytokine production (IL‐2, IFN‐γ) was suppressed in comparison with normal mice. On the other hand, Th2 cytokine production (IL‐4, IL‐10) was increased in the B16F10 mice. The administration of Z‐100 to B16F10 mice restored the balance of Th1/Th2 cell responses from the Th2 dominant state to the normal state. Z‐100 significantly suppressed the pulmonary metastasis of B16F10 melanoma in a dose‐dependent manner. These results suggest that Z‐100 restored the breakdown of Th1 cell responses, resulting in the suppression of pulmonary metastasis of B16F10 melanoma. Moreover, Z‐100 decreased the corticosterone levels, which is known to suppress the Th1 cell responses, in both serum specimens and splenic tissue, and the steroidogenic CYP11A1 mRNA expression in CD4+ T cells. These results suggest that a suppression of pulmonary metastasis and restoration of Th1/Th2 cell responses by Z‐100 may be due to the decrease in the corticosterone levels and the steroidogenic CYP11A1 mRNA expression of CD4+ T cells in B16F10 mice. Further, the role of Th1 cytokine, IFN‐γ, on these activities of Z‐100 was examined. The suppressive effects of Z‐100 on pulmonary metastasis and restoration of Th1/Th2 cell responses were eliminated by the administration of anti‐IFN‐γ mAb. Moreover, the suppressive effects of Z‐100 on glucocorticoid‐genesis were eliminated by the administration of anti‐IFN‐γ mAb. These results suggest that Z‐100 restores the balance of Th1/Th2 cell responses via the suppression of glucocorticoid‐genesis by Z‐100‐induced IFN‐γ. IFN‐γ acts as a key cytokine in anti‐tumor activities of Z‐100.

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Evaluation of Immunomodulatory and Therapeutic Properties of Biological Response Modifiers: A Comparison of Preclinical and Clinical Studies

Talmadge

Pinsky²,

Herberman

et al. 1987

Anticarcinogenesis and Radiation Protection

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Correlation of immunomodulatory and therapeutic activities of interferon and interferon inducers in metastatic disease

Cited by 9 publications

References 54 publications

Neoadjuvant immunotherapy with interferon of the spontaneously metastasizing murine B16F10L melanoma

Neoadjuvant immunotherapy with interferon of the spontaneously metastasizing murine B16F10L melanoma

Anti‐Tumor Mechanism of Z‐100, an Immunomodulatory Arabinomannan Extracted from Mycobacterium tuberculosis Strain Aoyama B, on Pulmonary Metastases of B16F10 Melanoma: Restoration of Helper T Cell Responses via Suppression of Glucocorticoid‐Genesis

Evaluation of Immunomodulatory and Therapeutic Properties of Biological Response Modifiers: A Comparison of Preclinical and Clinical Studies

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