Immunoprophylactic and immunotherapeutic control of hormone receptor-positive breast cancer

Hormone receptor (HR) + breast cancer (BC) causes most BC-related deaths, calling for improved therapeutic approaches. Despite expectations, immune checkpoint blockers (ICBs) are poorly active in patients with HR + BC, in part reflecting the lack of preclinical models that recapitulate disease progr...

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Published inNature communications Vol. 11; no. 1; pp. 3819 - 18
Main Authors Buqué, Aitziber, Bloy, Norma, Perez-Lanzón, Maria, Iribarren, Kristina, Humeau, Juliette, Pol, Jonathan G., Levesque, Sarah, Mondragon, Laura, Yamazaki, Takahiro, Sato, Ai, Aranda, Fernando, Durand, Sylvère, Boissonnas, Alexandre, Fucikova, Jitka, Senovilla, Laura, Enot, David, Hensler, Michal, Kremer, Margerie, Stoll, Gautier, Hu, Yang, Massa, Chiara, Formenti, Silvia C., Seliger, Barbara, Elemento, Olivier, Spisek, Radek, André, Fabrice, Zitvogel, Laurence, Delaloge, Suzette, Kroemer, Guido, Galluzzi, Lorenzo
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 30.07.2020
Nature Publishing Group
Nature Portfolio
Subjects
13/31
14/19
38/91
49
59
631/67/1059
631/67/1347
631/67/2195
631/67/580
64/110
64/60
9,10-Dimethyl-1,2-benzanthracene
Acetic acid
Animals
Anthracene
Breast cancer
Breast Neoplasms - immunology
Breast Neoplasms - metabolism
Breast Neoplasms - therapy
Carcinogenesis - drug effects
Carcinogenesis - immunology
Carcinogens
Dietary supplements
Disease Progression
Effector cells
ErbB-2 protein
Female
Humanities and Social Sciences
Humans
Immune checkpoint
Immunology
Immunosurveillance
Immunotherapy
Immunotherapy - methods
In vivo methods and tests
Interferon
Interferon Type I - immunology
Interferon Type I - metabolism
Life Sciences
Mammary Neoplasms, Experimental - chemically induced
Mammary Neoplasms, Experimental - immunology
Mammary Neoplasms, Experimental - prevention & control
Medroxyprogesterone Acetate
Metastases
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
multidisciplinary
Niacinamide - administration & dosage
Nicotinamide
Progestin
Receptor, ErbB-2 - immunology
Receptor, ErbB-2 - metabolism
Receptors
Science
Science (multidisciplinary)
Survival Analysis
Tumorigenesis
Tumors
Online AccessGet full text
ISSN2041-1723
2041-1723
DOI10.1038/s41467-020-17644-0

Cover

Abstract Hormone receptor (HR) + breast cancer (BC) causes most BC-related deaths, calling for improved therapeutic approaches. Despite expectations, immune checkpoint blockers (ICBs) are poorly active in patients with HR + BC, in part reflecting the lack of preclinical models that recapitulate disease progression in immunocompetent hosts. We demonstrate that mammary tumors driven by medroxyprogesterone acetate (M) and 7,12-dimethylbenz[a]anthracene (D) recapitulate several key features of human luminal B HR + HER2 − BC, including limited immune infiltration and poor sensitivity to ICBs. M/D-driven oncogenesis is accelerated by immune defects, demonstrating that M/D-driven tumors are under immunosurveillance. Safe nutritional measures including nicotinamide (NAM) supplementation efficiently delay M/D-driven oncogenesis by reactivating immunosurveillance. NAM also mediates immunotherapeutic effects against established M/D-driven and transplantable BC, largely reflecting increased type I interferon secretion by malignant cells and direct stimulation of immune effector cells. Our findings identify NAM as a potential strategy for the prevention and treatment of HR + BC. Current preclinical models to investigate human HR + breast cancer progression and response to immunotherapy in vivo are limited. Here, the authors demonstrate that mammary tumours driven by a synthetic progestin combined with an oral carcinogen recapitulate several immunobiological features of human HR + breast cancers.
AbstractList Hormone receptor (HR) + breast cancer (BC) causes most BC-related deaths, calling for improved therapeutic approaches. Despite expectations, immune checkpoint blockers (ICBs) are poorly active in patients with HR + BC, in part reflecting the lack of preclinical models that recapitulate disease progression in immunocompetent hosts. We demonstrate that mammary tumors driven by medroxyprogesterone acetate (M) and 7,12-dimethylbenz[a]anthracene (D) recapitulate several key features of human luminal B HR + HER2 − BC, including limited immune infiltration and poor sensitivity to ICBs. M/D-driven oncogenesis is accelerated by immune defects, demonstrating that M/D-driven tumors are under immunosurveillance. Safe nutritional measures including nicotinamide (NAM) supplementation efficiently delay M/D-driven oncogenesis by reactivating immunosurveillance. NAM also mediates immunotherapeutic effects against established M/D-driven and transplantable BC, largely reflecting increased type I interferon secretion by malignant cells and direct stimulation of immune effector cells. Our findings identify NAM as a potential strategy for the prevention and treatment of HR + BC. Current preclinical models to investigate human HR + breast cancer progression and response to immunotherapy in vivo are limited. Here, the authors demonstrate that mammary tumours driven by a synthetic progestin combined with an oral carcinogen recapitulate several immunobiological features of human HR + breast cancers.
Hormone receptor (HR)+ breast cancer (BC) causes most BC-related deaths, calling for improved therapeutic approaches. Despite expectations, immune checkpoint blockers (ICBs) are poorly active in patients with HR+ BC, in part reflecting the lack of preclinical models that recapitulate disease progression in immunocompetent hosts. We demonstrate that mammary tumors driven by medroxyprogesterone acetate (M) and 7,12-dimethylbenz[a]anthracene (D) recapitulate several key features of human luminal B HR+HER2− BC, including limited immune infiltration and poor sensitivity to ICBs. M/D-driven oncogenesis is accelerated by immune defects, demonstrating that M/D-driven tumors are under immunosurveillance. Safe nutritional measures including nicotinamide (NAM) supplementation efficiently delay M/D-driven oncogenesis by reactivating immunosurveillance. NAM also mediates immunotherapeutic effects against established M/D-driven and transplantable BC, largely reflecting increased type I interferon secretion by malignant cells and direct stimulation of immune effector cells. Our findings identify NAM as a potential strategy for the prevention and treatment of HR+ BC.Current preclinical models to investigate human HR + breast cancer progression and response to immunotherapy in vivo are limited. Here, the authors demonstrate that mammary tumours driven by a synthetic progestin combined with an oral carcinogen recapitulate several immunobiological features of human HR + breast cancers.
Hormone receptor (HR) breast cancer (BC) causes most BC-related deaths, calling for improved therapeutic approaches. Despite expectations, immune checkpoint blockers (ICBs) are poorly active in patients with HR BC, in part reflecting the lack of preclinical models that recapitulate disease progression in immunocompetent hosts. We demonstrate that mammary tumors driven by medroxyprogesterone acetate (M) and 7,12-dimethylbenz[a]anthracene (D) recapitulate several key features of human luminal B HR HER2 BC, including limited immune infiltration and poor sensitivity to ICBs. M/D-driven oncogenesis is accelerated by immune defects, demonstrating that M/D-driven tumors are under immunosurveillance. Safe nutritional measures including nicotinamide (NAM) supplementation efficiently delay M/D-driven oncogenesis by reactivating immunosurveillance. NAM also mediates immunotherapeutic effects against established M/D-driven and transplantable BC, largely reflecting increased type I interferon secretion by malignant cells and direct stimulation of immune effector cells. Our findings identify NAM as a potential strategy for the prevention and treatment of HR BC.
Abstract Hormone receptor (HR) + breast cancer (BC) causes most BC-related deaths, calling for improved therapeutic approaches. Despite expectations, immune checkpoint blockers (ICBs) are poorly active in patients with HR + BC, in part reflecting the lack of preclinical models that recapitulate disease progression in immunocompetent hosts. We demonstrate that mammary tumors driven by medroxyprogesterone acetate (M) and 7,12-dimethylbenz[a]anthracene (D) recapitulate several key features of human luminal B HR + HER2 − BC, including limited immune infiltration and poor sensitivity to ICBs. M/D-driven oncogenesis is accelerated by immune defects, demonstrating that M/D-driven tumors are under immunosurveillance. Safe nutritional measures including nicotinamide (NAM) supplementation efficiently delay M/D-driven oncogenesis by reactivating immunosurveillance. NAM also mediates immunotherapeutic effects against established M/D-driven and transplantable BC, largely reflecting increased type I interferon secretion by malignant cells and direct stimulation of immune effector cells. Our findings identify NAM as a potential strategy for the prevention and treatment of HR + BC.
Hormone receptor (HR) + breast cancer (BC) causes most BC-related deaths, calling for improved therapeutic approaches. Despite expectations, immune checkpoint blockers (ICBs) are poorly active in patients with HR + BC, in part reflecting the lack of preclinical models that recapitulate disease progression in immunocompetent hosts. We demonstrate that mammary tumors driven by medroxyprogesterone acetate (M) and 7,12-dimethylbenz[a]anthracene (D) recapitulate several key features of human luminal B HR + HER2 − BC, including limited immune infiltration and poor sensitivity to ICBs. M/D-driven oncogenesis is accelerated by immune defects, demonstrating that M/D-driven tumors are under immunosurveillance. Safe nutritional measures including nicotinamide (NAM) supplementation efficiently delay M/D-driven oncogenesis by reactivating immunosurveillance. NAM also mediates immunotherapeutic effects against established M/D-driven and transplantable BC, largely reflecting increased type I interferon secretion by malignant cells and direct stimulation of immune effector cells. Our findings identify NAM as a potential strategy for the prevention and treatment of HR + BC.
Current preclinical models to investigate human HR + breast cancer progression and response to immunotherapy in vivo are limited. Here, the authors demonstrate that mammary tumours driven by a synthetic progestin combined with an oral carcinogen recapitulate several immunobiological features of human HR + breast cancers.
Hormone receptor (HR)+ breast cancer (BC) causes most BC-related deaths, calling for improved therapeutic approaches. Despite expectations, immune checkpoint blockers (ICBs) are poorly active in patients with HR+ BC, in part reflecting the lack of preclinical models that recapitulate disease progression in immunocompetent hosts. We demonstrate that mammary tumors driven by medroxyprogesterone acetate (M) and 7,12-dimethylbenz[a]anthracene (D) recapitulate several key features of human luminal B HR+HER2- BC, including limited immune infiltration and poor sensitivity to ICBs. M/D-driven oncogenesis is accelerated by immune defects, demonstrating that M/D-driven tumors are under immunosurveillance. Safe nutritional measures including nicotinamide (NAM) supplementation efficiently delay M/D-driven oncogenesis by reactivating immunosurveillance. NAM also mediates immunotherapeutic effects against established M/D-driven and transplantable BC, largely reflecting increased type I interferon secretion by malignant cells and direct stimulation of immune effector cells. Our findings identify NAM as a potential strategy for the prevention and treatment of HR+ BC.Hormone receptor (HR)+ breast cancer (BC) causes most BC-related deaths, calling for improved therapeutic approaches. Despite expectations, immune checkpoint blockers (ICBs) are poorly active in patients with HR+ BC, in part reflecting the lack of preclinical models that recapitulate disease progression in immunocompetent hosts. We demonstrate that mammary tumors driven by medroxyprogesterone acetate (M) and 7,12-dimethylbenz[a]anthracene (D) recapitulate several key features of human luminal B HR+HER2- BC, including limited immune infiltration and poor sensitivity to ICBs. M/D-driven oncogenesis is accelerated by immune defects, demonstrating that M/D-driven tumors are under immunosurveillance. Safe nutritional measures including nicotinamide (NAM) supplementation efficiently delay M/D-driven oncogenesis by reactivating immunosurveillance. NAM also mediates immunotherapeutic effects against established M/D-driven and transplantable BC, largely reflecting increased type I interferon secretion by malignant cells and direct stimulation of immune effector cells. Our findings identify NAM as a potential strategy for the prevention and treatment of HR+ BC.
ArticleNumber 3819
Author Spisek, Radek
Buqué, Aitziber
Bloy, Norma
Sato, Ai
Zitvogel, Laurence
Galluzzi, Lorenzo
Pol, Jonathan G.
Hu, Yang
Boissonnas, Alexandre
Levesque, Sarah
Fucikova, Jitka
Elemento, Olivier
Massa, Chiara
Mondragon, Laura
Seliger, Barbara
Kroemer, Guido
Perez-Lanzón, Maria
Delaloge, Suzette
Hensler, Michal
Stoll, Gautier
André, Fabrice
Enot, David
Kremer, Margerie
Yamazaki, Takahiro
Humeau, Juliette
Durand, Sylvère
Formenti, Silvia C.
Aranda, Fernando
Iribarren, Kristina
Senovilla, Laura
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/32732875$$D View this record in MEDLINE/PubMed
https://hal.science/hal-03994636$$DView record in HAL
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Snippet Hormone receptor (HR) + breast cancer (BC) causes most BC-related deaths, calling for improved therapeutic approaches. Despite expectations, immune checkpoint...
Hormone receptor (HR) breast cancer (BC) causes most BC-related deaths, calling for improved therapeutic approaches. Despite expectations, immune checkpoint...
Hormone receptor (HR)+ breast cancer (BC) causes most BC-related deaths, calling for improved therapeutic approaches. Despite expectations, immune checkpoint...
Abstract Hormone receptor (HR) + breast cancer (BC) causes most BC-related deaths, calling for improved therapeutic approaches. Despite expectations, immune...
Current preclinical models to investigate human HR + breast cancer progression and response to immunotherapy in vivo are limited. Here, the authors demonstrate...
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9,10-Dimethyl-1,2-benzanthracene
Acetic acid
Animals
Anthracene
Breast cancer
Breast Neoplasms - immunology
Breast Neoplasms - metabolism
Breast Neoplasms - therapy
Carcinogenesis - drug effects
Carcinogenesis - immunology
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Dietary supplements
Disease Progression
Effector cells
ErbB-2 protein
Female
Humanities and Social Sciences
Humans
Immune checkpoint
Immunology
Immunosurveillance
Immunotherapy
Immunotherapy - methods
In vivo methods and tests
Interferon
Interferon Type I - immunology
Interferon Type I - metabolism
Life Sciences
Mammary Neoplasms, Experimental - chemically induced
Mammary Neoplasms, Experimental - immunology
Mammary Neoplasms, Experimental - prevention & control
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Metastases
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
multidisciplinary
Niacinamide - administration & dosage
Nicotinamide
Progestin
Receptor, ErbB-2 - immunology
Receptor, ErbB-2 - metabolism
Receptors
Science
Science (multidisciplinary)
Survival Analysis
Tumorigenesis
Tumors
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Title Immunoprophylactic and immunotherapeutic control of hormone receptor-positive breast cancer
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