Development of metastatic HER2+ breast cancer is independent of the adaptive immune system
The tumour‐modulating effects of the endogenous adaptive immune system are rather paradoxical. Whereas some clinical and experimental observations offer compelling evidence for the existence of immunosurveillance, other studies have revealed promoting effects of the adaptive immune system on primary...
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| Vydané v: | The Journal of pathology Ročník 224; číslo 1; s. 56 - 66 |
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| Hlavní autori: | , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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Chichester, UK
John Wiley & Sons, Ltd
01.05.2011
Wiley |
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| ISSN: | 0022-3417, 1096-9896, 1096-9896 |
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| Abstract | The tumour‐modulating effects of the endogenous adaptive immune system are rather paradoxical. Whereas some clinical and experimental observations offer compelling evidence for the existence of immunosurveillance, other studies have revealed promoting effects of the adaptive immune system on primary cancer development and metastatic disease. We examined the functional significance of the adaptive immune system as a regulator of spontaneous HER2+ breast tumourigenesis and pulmonary metastasis formation, using the MMTV–NeuT mouse model in which mammary carcinogenesis is induced by transgenic expression of the activated HER2/neu oncogene. Although T and B lymphocytes infiltrate human and experimental HER2+ breast tumours, genetic elimination of the adaptive immune system does not affect development of premalignant hyperplasias or primary breast cancers. In addition, we demonstrate that pulmonary metastasis formation in MMTV–NeuT mice is not dependent on the adaptive immune system. Thus, our findings reveal that spontaneous HER2‐driven mammary tumourigenesis and metastasis formation are neither suppressed, nor altered by immunosurveillance mechanisms, nor promoted by the adaptive immune system. Copyright © 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. |
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| AbstractList | The tumour-modulating effects of the endogenous adaptive immune system are rather paradoxical. Whereas some clinical and experimental observations offer compelling evidence for the existence of immunosurveillance, other studies have revealed promoting effects of the adaptive immune system on primary cancer development and metastatic disease. We examined the functional significance of the adaptive immune system as a regulator of spontaneous HER2(+) breast tumourigenesis and pulmonary metastasis formation, using the MMTV-NeuT mouse model in which mammary carcinogenesis is induced by transgenic expression of the activated HER2/neu oncogene. Although T and B lymphocytes infiltrate human and experimental HER2(+) breast tumours, genetic elimination of the adaptive immune system does not affect development of premalignant hyperplasias or primary breast cancers. In addition, we demonstrate that pulmonary metastasis formation in MMTV-NeuT mice is not dependent on the adaptive immune system. Thus, our findings reveal that spontaneous HER2-driven mammary tumourigenesis and metastasis formation are neither suppressed, nor altered by immunosurveillance mechanisms, nor promoted by the adaptive immune system.The tumour-modulating effects of the endogenous adaptive immune system are rather paradoxical. Whereas some clinical and experimental observations offer compelling evidence for the existence of immunosurveillance, other studies have revealed promoting effects of the adaptive immune system on primary cancer development and metastatic disease. We examined the functional significance of the adaptive immune system as a regulator of spontaneous HER2(+) breast tumourigenesis and pulmonary metastasis formation, using the MMTV-NeuT mouse model in which mammary carcinogenesis is induced by transgenic expression of the activated HER2/neu oncogene. Although T and B lymphocytes infiltrate human and experimental HER2(+) breast tumours, genetic elimination of the adaptive immune system does not affect development of premalignant hyperplasias or primary breast cancers. In addition, we demonstrate that pulmonary metastasis formation in MMTV-NeuT mice is not dependent on the adaptive immune system. Thus, our findings reveal that spontaneous HER2-driven mammary tumourigenesis and metastasis formation are neither suppressed, nor altered by immunosurveillance mechanisms, nor promoted by the adaptive immune system. The tumour-modulating effects of the endogenous adaptive immune system are rather paradoxical. Whereas some clinical and experimental observations offer compelling evidence for the existence of immunosurveillance, other studies have revealed promoting effects of the adaptive immune system on primary cancer development and metastatic disease. We examined the functional significance of the adaptive immune system as a regulator of spontaneous HER2+ breast tumourigenesis and pulmonary metastasis formation, using the MMTV-NeuT mouse model in which mammary carcinogenesis is induced by transgenic expression of the activated HER2/neu oncogene. Although T and B lymphocytes infiltrate human and experimental HER2+ breast tumours, genetic elimination of the adaptive immune system does not affect development of premalignant hyperplasias or primary breast cancers. In addition, we demonstrate that pulmonary metastasis formation in MMTV-NeuT mice is not dependent on the adaptive immune system. Thus, our findings reveal that spontaneous HER2-driven mammary tumourigenesis and metastasis formation are neither suppressed, nor altered by immunosurveillance mechanisms, nor promoted by the adaptive immune system. The tumour‐modulating effects of the endogenous adaptive immune system are rather paradoxical. Whereas some clinical and experimental observations offer compelling evidence for the existence of immunosurveillance, other studies have revealed promoting effects of the adaptive immune system on primary cancer development and metastatic disease. We examined the functional significance of the adaptive immune system as a regulator of spontaneous HER2+ breast tumourigenesis and pulmonary metastasis formation, using the MMTV–NeuT mouse model in which mammary carcinogenesis is induced by transgenic expression of the activated HER2/neu oncogene. Although T and B lymphocytes infiltrate human and experimental HER2+ breast tumours, genetic elimination of the adaptive immune system does not affect development of premalignant hyperplasias or primary breast cancers. In addition, we demonstrate that pulmonary metastasis formation in MMTV–NeuT mice is not dependent on the adaptive immune system. Thus, our findings reveal that spontaneous HER2‐driven mammary tumourigenesis and metastasis formation are neither suppressed, nor altered by immunosurveillance mechanisms, nor promoted by the adaptive immune system. Copyright © 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. |
| Author | Speksnijder, Ewoud N Ciampricotti, Metamia Jonkers, Jos Vrijland, Kim Hau, Cheei-Sing Wartha, Katharina Doornebal, Chris W Pemovska, Tea de Visser, Karin E |
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| Keywords | Breast disease Her2/neu erbB2 Gene Natural immunity Breast cancer Malignant tumor Metastasis adaptive immune system immunosurveillance innate immune system Mammary gland diseases Immunological surveillance Anatomic pathology Development Advanced stage Metastatic Cancer Immune system |
| Language | English |
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| Notes | ArticleID:PATH2837 istex:86CEE8F2F34138D6B121F1B376618F2A5E4B48CF Supporting Information: Figure S1. Increased infiltration of immune cells in human and mouse HER2+ breast cancer.Supporting Information: Figure S2. Absence of CD4+ and CD8+ T cells and CD20+/CD19+ B cells in NeuT/Rag-2−/− mice.Supporting Information: Figure S3. The adaptive immune system does not modulate proliferation of breast cancer cells in MMTV-NeuT mice.Supporting Information: Figure S4. Influx of Gr1+ CD11b+ granulocytes in the tumour microenvironment and spleen is not altered by the absence of the adaptive immune system.Supporting Information: Figure S5. Size-categories of pulmonary metastases.Supporting Information: Table S1. Detailed information about antibodies used for (a) immunohistochemistry and (b) flow cytometry.Supporting Information: Legends to Figure S1 to S5 ark:/67375/WNG-BDTNV5XF-7 ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
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| SubjectTerms | adaptive immune system Adaptive Immunity - immunology Animal models Animals Biological and medical sciences Breast cancer Carcinogenesis Cell Transformation, Neoplastic - immunology ErbB-2 protein Female Gynecology. Andrology. Obstetrics Her2/neu Humans Hyperplasia Immune system Immune Tolerance - immunology Immunologic Surveillance - immunology Immunosurveillance innate immune system Investigative techniques, diagnostic techniques (general aspects) Lung Lung Neoplasms - immunology Lung Neoplasms - secondary Lymphocyte Subsets - immunology Lymphocytes B Mammary gland diseases Mammary Neoplasms, Experimental - immunology Mammary Neoplasms, Experimental - metabolism Medical sciences Metastases metastasis Mice Mice, Transgenic Neoplasm Transplantation Oncogenes Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques Receptor, ErbB-2 - metabolism Tumor Microenvironment - immunology Tumorigenesis Tumors |
| Title | Development of metastatic HER2+ breast cancer is independent of the adaptive immune system |
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