Prostate cancer originating in basal cells progresses to adenocarcinoma propagated by luminal-like cells

Tanya Stoyanova, Aaron R. Cooper, Xian Liu, Andrew J. Armstrong, Kenneth J. Pienta, Hong Zhang, Donald B. Kohn, Jiaoti Huang, Owen N. Witte, Andrew S. Goldstein

    Research output: Contribution to journalArticle

    78 Citations (Scopus)

    Abstract

    The relationship between the cells that initiate cancer and the cancer stem-like cells that propagate tumors has been poorly defined. In a human prostate tissue transformation model, basal cells expressing the oncogenes Myc and myristoylated AKT can initiate heterogeneous tumors. Tumors contain features of acinartype adenocarcinoma with elevated eIF4E-driven protein translation and squamous cell carcinoma marked by activated betacatenin. Lentiviral integration site analysis revealed that alternative histological phenotypes can be clonally derived from a common cell of origin. In advanced disease, adenocarcinoma can be propagated by self-renewing tumor cells with an androgen receptor-low immature luminal phenotype in the absence of basal-like cells. These data indicate that advanced prostate adenocarcinoma initiated in basal cells can be maintained by luminal-like tumor-propagating cells. Determining the cells that maintain human prostate adenocarcinoma and the signaling pathways characterizing these tumor-propagating cells is critical for developing effective therapeutic strategies against this population.

    Original languageEnglish (US)
    Pages (from-to)20111-20116
    Number of pages6
    JournalProceedings of the National Academy of Sciences of the United States of America
    Volume110
    Issue number50
    DOIs
    StatePublished - Dec 10 2013

    Fingerprint

    Prostatic Neoplasms
    Adenocarcinoma
    Neoplasms
    Prostate
    Phenotype
    myc Genes
    Neoplastic Stem Cells
    Androgen Receptors
    Protein Biosynthesis
    Squamous Cell Carcinoma
    Population

    All Science Journal Classification (ASJC) codes

    • General

    Cite this

    Stoyanova, Tanya ; Cooper, Aaron R. ; Liu, Xian ; Armstrong, Andrew J. ; Pienta, Kenneth J. ; Zhang, Hong ; Kohn, Donald B. ; Huang, Jiaoti ; Witte, Owen N. ; Goldstein, Andrew S. / Prostate cancer originating in basal cells progresses to adenocarcinoma propagated by luminal-like cells. In: Proceedings of the National Academy of Sciences of the United States of America. 2013 ; Vol. 110, No. 50. pp. 20111-20116.
    @article{7d13e3066742419489e324e23d5087c5,
    title = "Prostate cancer originating in basal cells progresses to adenocarcinoma propagated by luminal-like cells",
    abstract = "The relationship between the cells that initiate cancer and the cancer stem-like cells that propagate tumors has been poorly defined. In a human prostate tissue transformation model, basal cells expressing the oncogenes Myc and myristoylated AKT can initiate heterogeneous tumors. Tumors contain features of acinartype adenocarcinoma with elevated eIF4E-driven protein translation and squamous cell carcinoma marked by activated betacatenin. Lentiviral integration site analysis revealed that alternative histological phenotypes can be clonally derived from a common cell of origin. In advanced disease, adenocarcinoma can be propagated by self-renewing tumor cells with an androgen receptor-low immature luminal phenotype in the absence of basal-like cells. These data indicate that advanced prostate adenocarcinoma initiated in basal cells can be maintained by luminal-like tumor-propagating cells. Determining the cells that maintain human prostate adenocarcinoma and the signaling pathways characterizing these tumor-propagating cells is critical for developing effective therapeutic strategies against this population.",
    author = "Tanya Stoyanova and Cooper, {Aaron R.} and Xian Liu and Armstrong, {Andrew J.} and Pienta, {Kenneth J.} and Hong Zhang and Kohn, {Donald B.} and Jiaoti Huang and Witte, {Owen N.} and Goldstein, {Andrew S.}",
    year = "2013",
    month = "12",
    day = "10",
    doi = "https://doi.org/10.1073/pnas.1320565110",
    language = "English (US)",
    volume = "110",
    pages = "20111--20116",
    journal = "Proceedings of the National Academy of Sciences of the United States of America",
    issn = "0027-8424",
    number = "50",

    }

    Stoyanova, T, Cooper, AR, Liu, X, Armstrong, AJ, Pienta, KJ, Zhang, H, Kohn, DB, Huang, J, Witte, ON & Goldstein, AS 2013, 'Prostate cancer originating in basal cells progresses to adenocarcinoma propagated by luminal-like cells', Proceedings of the National Academy of Sciences of the United States of America, vol. 110, no. 50, pp. 20111-20116. https://doi.org/10.1073/pnas.1320565110

    Prostate cancer originating in basal cells progresses to adenocarcinoma propagated by luminal-like cells. / Stoyanova, Tanya; Cooper, Aaron R.; Liu, Xian; Armstrong, Andrew J.; Pienta, Kenneth J.; Zhang, Hong; Kohn, Donald B.; Huang, Jiaoti; Witte, Owen N.; Goldstein, Andrew S.

    In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 110, No. 50, 10.12.2013, p. 20111-20116.

    Research output: Contribution to journalArticle

    TY - JOUR

    T1 - Prostate cancer originating in basal cells progresses to adenocarcinoma propagated by luminal-like cells

    AU - Stoyanova, Tanya

    AU - Cooper, Aaron R.

    AU - Liu, Xian

    AU - Armstrong, Andrew J.

    AU - Pienta, Kenneth J.

    AU - Zhang, Hong

    AU - Kohn, Donald B.

    AU - Huang, Jiaoti

    AU - Witte, Owen N.

    AU - Goldstein, Andrew S.

    PY - 2013/12/10

    Y1 - 2013/12/10

    N2 - The relationship between the cells that initiate cancer and the cancer stem-like cells that propagate tumors has been poorly defined. In a human prostate tissue transformation model, basal cells expressing the oncogenes Myc and myristoylated AKT can initiate heterogeneous tumors. Tumors contain features of acinartype adenocarcinoma with elevated eIF4E-driven protein translation and squamous cell carcinoma marked by activated betacatenin. Lentiviral integration site analysis revealed that alternative histological phenotypes can be clonally derived from a common cell of origin. In advanced disease, adenocarcinoma can be propagated by self-renewing tumor cells with an androgen receptor-low immature luminal phenotype in the absence of basal-like cells. These data indicate that advanced prostate adenocarcinoma initiated in basal cells can be maintained by luminal-like tumor-propagating cells. Determining the cells that maintain human prostate adenocarcinoma and the signaling pathways characterizing these tumor-propagating cells is critical for developing effective therapeutic strategies against this population.

    AB - The relationship between the cells that initiate cancer and the cancer stem-like cells that propagate tumors has been poorly defined. In a human prostate tissue transformation model, basal cells expressing the oncogenes Myc and myristoylated AKT can initiate heterogeneous tumors. Tumors contain features of acinartype adenocarcinoma with elevated eIF4E-driven protein translation and squamous cell carcinoma marked by activated betacatenin. Lentiviral integration site analysis revealed that alternative histological phenotypes can be clonally derived from a common cell of origin. In advanced disease, adenocarcinoma can be propagated by self-renewing tumor cells with an androgen receptor-low immature luminal phenotype in the absence of basal-like cells. These data indicate that advanced prostate adenocarcinoma initiated in basal cells can be maintained by luminal-like tumor-propagating cells. Determining the cells that maintain human prostate adenocarcinoma and the signaling pathways characterizing these tumor-propagating cells is critical for developing effective therapeutic strategies against this population.

    UR - http://www.scopus.com/inward/record.url?scp=84890275857&partnerID=8YFLogxK

    UR - http://www.scopus.com/inward/citedby.url?scp=84890275857&partnerID=8YFLogxK

    U2 - https://doi.org/10.1073/pnas.1320565110

    DO - https://doi.org/10.1073/pnas.1320565110

    M3 - Article

    VL - 110

    SP - 20111

    EP - 20116

    JO - Proceedings of the National Academy of Sciences of the United States of America

    JF - Proceedings of the National Academy of Sciences of the United States of America

    SN - 0027-8424

    IS - 50

    ER -