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Your search keyword '"Interferon Type I -- metabolism"' showing total 3 results
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3 results on '"Interferon Type I -- metabolism"'

1. Type I interferon/IRF7 axis instigates chemotherapy-induced immunological dormancy in breast cancer.

Author

Lan, Qiang, Peyvandi, Sanam, Duffey, Nathalie, Huang, Yu-Ting, Barras, David, Held, Werner, Richard, François, Delorenzi, Mauro, Sotiriou, Christos, Desmedt, Christine, Lorusso, Girieca, Rüegg, Curzio, Lan, Qiang, Peyvandi, Sanam, Duffey, Nathalie, Huang, Yu-Ting, Barras, David, Held, Werner, Richard, François, Delorenzi, Mauro, Sotiriou, Christos, Desmedt, Christine, Lorusso, Girieca, and Rüegg, Curzio

Abstract

Neoadjuvant and adjuvant chemotherapies provide survival benefits to breast cancer patients, in particular in estrogen receptor negative (ER-) cancers, by reducing rates of recurrences. It is assumed that the benefits of (neo)adjuvant chemotherapy are due to the killing of disseminated, residual cancer cells, however, there is no formal evidence for it. Here, we provide experimental evidence that ER- breast cancer cells that survived high-dose Doxorubicin and Methotrexate based chemotherapies elicit a state of immunological dormancy. Hallmark of this dormant phenotype is the sustained activation of the IRF7/IFN-β/IFNAR axis subsisting beyond chemotherapy treatment. Upregulation of IRF7 in treated cancer cells promoted resistance to chemotherapy, reduced cell growth and induced switching of the response from a myeloid derived suppressor cell-dominated immune response to a CD4+/CD8+ T cell-dependent anti-tumor response. IRF7 silencing in tumor cells or systemic blocking of IFNAR reversed the state of dormancy, while spontaneous escape from dormancy was associated with loss of IFN-β production. Presence of IFN-β in the circulation of ER- breast cancer patients treated with neoadjuvant Epirubicin chemotherapy correlated with a significantly longer distant metastasis-free survival. These findings establish chemotherapy-induced immunological dormancy in ER- breast cancer as a novel concept for (neo)adjuvant chemotherapy activity, and implicate sustained activation of the IRF7/IFN-β/IFNAR pathway in this effect. Further, IFN-β emerges as a potential predictive biomarker and therapeutic molecule to improve outcome of ER- breast cancer patients treated with (neo)adjuvant chemotherapy., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2018

2. Interleukin-12 family members and type I interferons in Th17-mediated inflammatory disorders.

Author

Goriely, Stanislas, Cavoy, Rani, Goldman, Michel, Goriely, Stanislas, Cavoy, Rani, and Goldman, Michel

Abstract

Cytokines produced by antigen-presenting cells govern the fate of helper T-cell responses. Herein, we review the impact of interleukin (IL)-23 and IL-27 on the outcome of T-helper (Th) 17 cell responses and discuss their impact in the pathogenesis of T-cell-mediated inflammatory disorders of autoimmune or allergic origin. We then discuss how type I interferons might influence the course of autoimmune diseases by tipping the balance between IL-12 family members., Journal Article, Research Support, Non-U.S. Gov't, Review, FLWIN, info:eu-repo/semantics/published

Published
2009

3. Type I interferon/IRF7 axis instigates chemotherapy-induced immunological dormancy in breast cancer

Author

Werner Held, Mauro Delorenzi, Curzio Rüegg, Nathalie Duffey, Christine Desmedt, Francois Richard, Qiang Lan, Yu-Ting Huang, Girieca Lorusso, David Barras, Sanam Peyvandi, Christos Sotiriou, and Institute of Biotechnology

Subjects
0301 basic medicine, Cancer Research, Receptor, ErbB-2, Interferon Regulatory Factor-7, medicine.medical_treatment, Mice, SCID, Breast Neoplasms -- drug therapy -- metabolism, Metastasis, PATHWAY, Chemotherapy, Adjuvant -- methods, Mice, Breast cancer, 0302 clinical medicine, Mice, Inbred NOD, Antineoplastic Combined Chemotherapy Protocols, immune-mediated dormancy, Receptor, ErbB-2 -- metabolism, site, TUMOR-INFILTRATING LYMPHOCYTES, Genetics & Heredity, Mice, Inbred BALB C, mechanisms, SITE, Neoadjuvant Therapy -- methods, Sciences bio-médicales et agricoles, Biomarkers, Tumor -- metabolism, Neoadjuvant Therapy, 3. Good health, Doxorubicin -- pharmacology, Oncology, Chemotherapy, Adjuvant, 030220 oncology & carcinogenesis, tumor-infiltrating lymphocytes, Interferon Type I, Female, Life Sciences & Biomedicine, Adjuvant, Antineoplastic Combined Chemotherapy Protocols -- pharmacology, Epirubicin, medicine.drug, EXPRESSION, Biochemistry & Molecular Biology, Interferon-beta -- metabolism, 3122 Cancers, Immunology, Methotrexate -- pharmacology, Mice, Nude, Breast Neoplasms, Biology, Article, MECHANISMS, resistance, 03 medical and health sciences, Interferon Regulatory Factor-7 -- metabolism, Cell Line, Tumor, expression, Biomarkers, Tumor, Animals, Antineoplastic Combined Chemotherapy Protocols/pharmacology, Biomarkers, Tumor/metabolism, Breast Neoplasms/drug therapy, Breast Neoplasms/metabolism, Chemotherapy, Adjuvant/methods, Doxorubicin/pharmacology, Epirubicin/pharmacology, Humans, Interferon Regulatory Factor-7/metabolism, Interferon Type I/metabolism, Interferon-beta/metabolism, Methotrexate/pharmacology, Neoadjuvant Therapy/methods, Neoplasm Recurrence, Local/metabolism, Receptor, ErbB-2/metabolism, Genetics, medicine, metastasis, Doxorubicin, Molecular Biology, Neoplasm Recurrence, Local -- metabolism, Chemotherapy, Science & Technology, IMMUNE-MEDIATED DORMANCY, Tumor-infiltrating lymphocytes, pathway, Médecine pathologie humaine, Interferon-beta, Cell Biology, medicine.disease, Epirubicin -- pharmacology, Interferon Type I -- metabolism, Cancérologie, Methotrexate, 030104 developmental biology, CELLS, METASTASIS, Cancer cell, Cancer research, cells, Neoplasm Recurrence, Local, RESISTANCE
Abstract

Neoadjuvant and adjuvant chemotherapies provide survival benefits to breast cancer patients, in particular in estrogen receptor negative (ER-) cancers, by reducing rates of recurrences. It is assumed that the benefits of (neo)adjuvant chemotherapy are due to the killing of disseminated, residual cancer cells, however, there is no formal evidence for it. Here, we provide experimental evidence that ER- breast cancer cells that survived high-dose Doxorubicin and Methotrexate based chemotherapies elicit a state of immunological dormancy. Hallmark of this dormant phenotype is the sustained activation of the IRF7/IFN-β/IFNAR axis subsisting beyond chemotherapy treatment. Upregulation of IRF7 in treated cancer cells promoted resistance to chemotherapy, reduced cell growth and induced switching of the response from a myeloid derived suppressor cell-dominated immune response to a CD4+/CD8+ T cell-dependent anti-tumor response. IRF7 silencing in tumor cells or systemic blocking of IFNAR reversed the state of dormancy, while spontaneous escape from dormancy was associated with loss of IFN-β production. Presence of IFN-β in the circulation of ER- breast cancer patients treated with neoadjuvant Epirubicin chemotherapy correlated with a significantly longer distant metastasis-free survival. These findings establish chemotherapy-induced immunological dormancy in ER- breast cancer as a novel concept for (neo)adjuvant chemotherapy activity, and implicate sustained activation of the IRF7/IFN-β/IFNAR pathway in this effect. Further, IFN-β emerges as a potential predictive biomarker and therapeutic molecule to improve outcome of ER- breast cancer patients treated with (neo)adjuvant chemotherapy., SCOPUS: ar.j, info:eu-repo/semantics/published

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