ETV6-NTRK3 Fusion Oncogene Initiates Breast Cancer from Committed Mammary Progenitors via Activation of AP1 Complex

To better understand the cellular origin of breast cancer, we developed a mouse model that recapitulates expression of the ETV6-NTRK3 (EN) fusion oncoprotein, the product of the t(12;15)(p13;q25) translocation characteristic of human secretory breast carcinoma. Activation of EN expression in mammary...

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Published inCancer cell Vol. 12; no. 6; pp. 542 - 558
Main Authors Li, Zhe, Tognon, Cristina E., Godinho, Frank J., Yasaitis, Laura, Hock, Hanno, Herschkowitz, Jason I., Lannon, Chris L., Cho, Eunah, Kim, Seong-Jin, Bronson, Roderick T., Perou, Charles M., Sorensen, Poul H., Orkin, Stuart H.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.12.2007
Subjects
Alleles
Animals
Breast Neoplasms - genetics
Breast Neoplasms - pathology
CD24 Antigen - metabolism
Cell Transformation, Neoplastic
CELLCYCLE
Epithelial Cells - metabolism
Epithelial Cells - pathology
ETS Translocation Variant 6 Protein
Female
Genes, Dominant
Humans
Integrases - metabolism
Mammary Glands, Animal - pathology
Mammary Neoplasms, Animal - pathology
Mice
Multigene Family
Neoplastic Stem Cells - pathology
Oncogene Proteins, Fusion - metabolism
Parity
Penetrance
Pregnancy
Proto-Oncogene Proteins c-ets - metabolism
Proto-Oncogene Proteins c-jun - metabolism
Repressor Proteins - metabolism
STEMCELL
Transcription Factor AP-1 - metabolism
STEMCELL
CELLCYCLE
Online AccessGet full text
ISSN1535-6108
1878-3686
DOI10.1016/j.ccr.2007.11.012

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Abstract To better understand the cellular origin of breast cancer, we developed a mouse model that recapitulates expression of the ETV6-NTRK3 (EN) fusion oncoprotein, the product of the t(12;15)(p13;q25) translocation characteristic of human secretory breast carcinoma. Activation of EN expression in mammary tissues by Wap-Cre leads to fully penetrant, multifocal malignant breast cancer with short latency. We provide genetic evidence that, in nulliparous Wap-Cre;EN females, committed alveolar bipotent or CD61+ luminal progenitors are targets of tumorigenesis. Furthermore, EN transforms these otherwise transient progenitors through activation of the AP1 complex. Given the increasing relevance of chromosomal translocations in epithelial cancers, such mice serve as a paradigm for the study of their genetic pathogenesis and cellular origins, and generation of preclinical models.
AbstractList To better understand the cellular origin of breast cancer, we developed a mouse model that recapitulates expression of the ETV6-NTRK3 (EN) fusion oncoprotein, the product of the t(12;15)(p13;q25) translocation characteristic of human secretory breast carcinoma. Activation of EN expression in mammary tissues by Wap-Cre leads to fully penetrant, multifocal malignant breast cancer with short latency. We provide genetic evidence that, in nulliparous Wap-Cre;EN females, committed alveolar bipotent or CD61(+) luminal progenitors are targets of tumorigenesis. Furthermore, EN transforms these otherwise transient progenitors through activation of the AP1 complex. Given the increasing relevance of chromosomal translocations in epithelial cancers, such mice serve as a paradigm for the study of their genetic pathogenesis and cellular origins, and generation of preclinical models.To better understand the cellular origin of breast cancer, we developed a mouse model that recapitulates expression of the ETV6-NTRK3 (EN) fusion oncoprotein, the product of the t(12;15)(p13;q25) translocation characteristic of human secretory breast carcinoma. Activation of EN expression in mammary tissues by Wap-Cre leads to fully penetrant, multifocal malignant breast cancer with short latency. We provide genetic evidence that, in nulliparous Wap-Cre;EN females, committed alveolar bipotent or CD61(+) luminal progenitors are targets of tumorigenesis. Furthermore, EN transforms these otherwise transient progenitors through activation of the AP1 complex. Given the increasing relevance of chromosomal translocations in epithelial cancers, such mice serve as a paradigm for the study of their genetic pathogenesis and cellular origins, and generation of preclinical models.
To better understand the cellular origin of breast cancer, we developed a mouse model that recapitulates expression of the ETV6-NTRK3 (EN) fusion oncoprotein, the product of the t(12;15)(p13;q25) translocation characteristic of human secretory breast carcinoma. Activation of EN expression in mammary tissues by Wap-Cre leads to fully penetrant, multifocal malignant breast cancer with short latency. We provide genetic evidence that, in nulliparous Wap-Cre;EN females, committed alveolar bipotent or CD61+ luminal progenitors are targets of tumorigenesis. Furthermore, EN transforms these otherwise transient progenitors through activation of the AP1 complex. Given the increasing relevance of chromosomal translocations in epithelial cancers, such mice serve as a paradigm for the study of their genetic pathogenesis and cellular origins, and generation of preclinical models.
To better understand the cellular origin of breast cancer, we developed a mouse model that recapitulates expression of the ETV6-NTRK3 (EN) fusion oncoprotein, the product of the t(12;15)(p13;q25) translocation characteristic of human secretory breast carcinoma. Activation of EN expression in mammary tissues by Wap-Cre leads to fully penetrant, multifocal malignant breast cancer with short latency. We provide genetic evidence that in nulliparous Wap-Cre;EN females, committed alveolar bipotent or CD61 + luminal progenitors, are targets of tumorigenesis. Furthermore, EN transforms these otherwise transient progenitors through activation of the AP1 complex. Given increasing relevance of chromosomal translocations in epithelial cancers, such mice serve as a paradigm for the study of their genetic pathogenesis and cellular origins, and generation of novel preclinical models.
To better understand the cellular origin of breast cancer, we developed a mouse model that recapitulates expression of the ETV6-NTRK3 (EN) fusion oncoprotein, the product of the t(12; 15)(p13; q25) translocation characteristic of human secretory breast carcinoma. Activation of EN expression in mammary tissues by Wap-Cre leads to fully penetrant, multifocal malignant breast cancer with short latency. We provide genetic evidence that, in nulliparous Wap-Cre; EN females, committed alveolar bipotent or CD61 super(+) luminal progenitors are targets of tumorigenesis. Furthermore, EN transforms these otherwise transient progenitors through activation of the AP1 complex. Given the increasing relevance of chromosomal translocations in epithelial cancers, such mice serve as a paradigm for the study of their genetic pathogenesis and cellular origins, and generation of preclinical models.
Author Hock, Hanno
Li, Zhe
Yasaitis, Laura
Tognon, Cristina E.
Herschkowitz, Jason I.
Lannon, Chris L.
Bronson, Roderick T.
Sorensen, Poul H.
Orkin, Stuart H.
Godinho, Frank J.
Perou, Charles M.
Kim, Seong-Jin
Cho, Eunah
AuthorAffiliation 1 Division of Hematology/Oncology, Children’s Hospital Boston
6 Department of Molecular Oncology, British Columbia Cancer Research Centre, Vancouver, British Columbia V5Z 1L3, Canada
2 Department of Pediatric Oncology, Dana Farber Cancer Institute
7 Departments of Genetics and Pathology, Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
4 Harvard Medical School
8 Laboratory of Cell Regulation and Carcinogenesis, National Cancer Institute, Bethesda, MD 20892, USA
5 Harvard Stem Cell Institute Boston, MA 02115, USA
3 Howard Hughes Medical Institute
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/18068631$$D View this record in MEDLINE/PubMed
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content type line 23
Present address: Center for Cancer Research, Massachusetts General Hospital, Boston, MA 02414, USA
Present address: Lee Gil Ya Cancer and Diabetes Institute, Gachon University of Medicine and Science, Songdo, Incheon 406-840, Korea
These two authors contributed equally
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  day: 01
PublicationDecade 2000
PublicationPlace United States
PublicationPlace_xml – name: United States
PublicationTitle Cancer cell
PublicationTitleAlternate Cancer Cell
PublicationYear 2007
Publisher Elsevier Inc
Publisher_xml – name: Elsevier Inc
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Snippet To better understand the cellular origin of breast cancer, we developed a mouse model that recapitulates expression of the ETV6-NTRK3 (EN) fusion oncoprotein,...
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SubjectTerms Alleles
Animals
Breast Neoplasms - genetics
Breast Neoplasms - pathology
CD24 Antigen - metabolism
Cell Transformation, Neoplastic
CELLCYCLE
Epithelial Cells - metabolism
Epithelial Cells - pathology
ETS Translocation Variant 6 Protein
Female
Genes, Dominant
Humans
Integrases - metabolism
Mammary Glands, Animal - pathology
Mammary Neoplasms, Animal - pathology
Mice
Multigene Family
Neoplastic Stem Cells - pathology
Oncogene Proteins, Fusion - metabolism
Parity
Penetrance
Pregnancy
Proto-Oncogene Proteins c-ets - metabolism
Proto-Oncogene Proteins c-jun - metabolism
Repressor Proteins - metabolism
STEMCELL
Transcription Factor AP-1 - metabolism
Title ETV6-NTRK3 Fusion Oncogene Initiates Breast Cancer from Committed Mammary Progenitors via Activation of AP1 Complex
URI https://dx.doi.org/10.1016/j.ccr.2007.11.012
https://www.ncbi.nlm.nih.gov/pubmed/18068631
https://www.proquest.com/docview/20620864
https://www.proquest.com/docview/69048472
https://pubmed.ncbi.nlm.nih.gov/PMC2175032
Volume 12
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