Molecular pathways and targets in prostate cancer

Emma Shtivelman, Tomasz (Tom) Beer, Christopher P. Evans

    Research output: Contribution to journalArticle

    46 Citations (Scopus)

    Abstract

    Prostate cancer co-opts a unique set of cellular pathways in its initiation and progression. The heterogeneity of prostate cancers is evident at earlier stages, and has led to rigorous efforts to stratify the localized prostate cancers, so that progression to advanced stages could be predicted based upon salient features of the early disease. The deregulated androgen receptor signaling is undeniably most important in the progression of the majority of prostate tumors. It is perhaps because of the primacy of the androgen receptor governed transcriptional program in prostate epithelium cells that once this program is corrupted, the consequences of the ensuing changes in activity are pleotropic and could contribute to malignancy in multiple ways. Following localized surgical and radiation therapies, 20-40% of patients will relapse and progress, and will be treated with androgen deprivation therapies. The successful development of the new agents that inhibit androgen signaling has changed the progression free survival in hormone resistant disease, but this has not changed the almost ubiquitous development of truly resistant phenotypes in advanced prostate cancer. This review summarizes the current understanding of the molecular pathways involved in localized and metastatic prostate cancer, with an emphasis on the clinical implications of the new knowledge.

    Original languageEnglish (US)
    Pages (from-to)7217-7259
    Number of pages43
    JournalOncotarget
    Volume5
    Issue number17
    StatePublished - 2014

    Fingerprint

    Prostatic Neoplasms
    Androgen Receptors
    Androgens
    Prostate
    Disease-Free Survival
    Neoplasms
    Radiotherapy
    Epithelium
    Hormones
    Phenotype
    Recurrence
    Therapeutics

    Keywords

    • CRPC
    • Localized prostate cance
    • Molecular targets
    • Prostate cancer

    ASJC Scopus subject areas

    • Oncology
    • Medicine(all)

    Cite this

    Shtivelman, E., Beer, T. T., & Evans, C. P. (2014). Molecular pathways and targets in prostate cancer. Oncotarget, 5(17), 7217-7259.

    Molecular pathways and targets in prostate cancer. / Shtivelman, Emma; Beer, Tomasz (Tom); Evans, Christopher P.

    In: Oncotarget, Vol. 5, No. 17, 2014, p. 7217-7259.

    Research output: Contribution to journalArticle

    Shtivelman, E, Beer, TT & Evans, CP 2014, 'Molecular pathways and targets in prostate cancer', Oncotarget, vol. 5, no. 17, pp. 7217-7259.
    Shtivelman E, Beer TT, Evans CP. Molecular pathways and targets in prostate cancer. Oncotarget. 2014;5(17):7217-7259.
    Shtivelman, Emma ; Beer, Tomasz (Tom) ; Evans, Christopher P. / Molecular pathways and targets in prostate cancer. In: Oncotarget. 2014 ; Vol. 5, No. 17. pp. 7217-7259.
    @article{9b7111dbe5d744b9b517458632217af5,
    title = "Molecular pathways and targets in prostate cancer",
    abstract = "Prostate cancer co-opts a unique set of cellular pathways in its initiation and progression. The heterogeneity of prostate cancers is evident at earlier stages, and has led to rigorous efforts to stratify the localized prostate cancers, so that progression to advanced stages could be predicted based upon salient features of the early disease. The deregulated androgen receptor signaling is undeniably most important in the progression of the majority of prostate tumors. It is perhaps because of the primacy of the androgen receptor governed transcriptional program in prostate epithelium cells that once this program is corrupted, the consequences of the ensuing changes in activity are pleotropic and could contribute to malignancy in multiple ways. Following localized surgical and radiation therapies, 20-40{\%} of patients will relapse and progress, and will be treated with androgen deprivation therapies. The successful development of the new agents that inhibit androgen signaling has changed the progression free survival in hormone resistant disease, but this has not changed the almost ubiquitous development of truly resistant phenotypes in advanced prostate cancer. This review summarizes the current understanding of the molecular pathways involved in localized and metastatic prostate cancer, with an emphasis on the clinical implications of the new knowledge.",
    keywords = "CRPC, Localized prostate cance, Molecular targets, Prostate cancer",
    author = "Emma Shtivelman and Beer, {Tomasz (Tom)} and Evans, {Christopher P.}",
    year = "2014",
    language = "English (US)",
    volume = "5",
    pages = "7217--7259",
    journal = "Oncotarget",
    issn = "1949-2553",
    publisher = "Impact Journals",
    number = "17",

    }

    TY - JOUR

    T1 - Molecular pathways and targets in prostate cancer

    AU - Shtivelman, Emma

    AU - Beer, Tomasz (Tom)

    AU - Evans, Christopher P.

    PY - 2014

    Y1 - 2014

    N2 - Prostate cancer co-opts a unique set of cellular pathways in its initiation and progression. The heterogeneity of prostate cancers is evident at earlier stages, and has led to rigorous efforts to stratify the localized prostate cancers, so that progression to advanced stages could be predicted based upon salient features of the early disease. The deregulated androgen receptor signaling is undeniably most important in the progression of the majority of prostate tumors. It is perhaps because of the primacy of the androgen receptor governed transcriptional program in prostate epithelium cells that once this program is corrupted, the consequences of the ensuing changes in activity are pleotropic and could contribute to malignancy in multiple ways. Following localized surgical and radiation therapies, 20-40% of patients will relapse and progress, and will be treated with androgen deprivation therapies. The successful development of the new agents that inhibit androgen signaling has changed the progression free survival in hormone resistant disease, but this has not changed the almost ubiquitous development of truly resistant phenotypes in advanced prostate cancer. This review summarizes the current understanding of the molecular pathways involved in localized and metastatic prostate cancer, with an emphasis on the clinical implications of the new knowledge.

    AB - Prostate cancer co-opts a unique set of cellular pathways in its initiation and progression. The heterogeneity of prostate cancers is evident at earlier stages, and has led to rigorous efforts to stratify the localized prostate cancers, so that progression to advanced stages could be predicted based upon salient features of the early disease. The deregulated androgen receptor signaling is undeniably most important in the progression of the majority of prostate tumors. It is perhaps because of the primacy of the androgen receptor governed transcriptional program in prostate epithelium cells that once this program is corrupted, the consequences of the ensuing changes in activity are pleotropic and could contribute to malignancy in multiple ways. Following localized surgical and radiation therapies, 20-40% of patients will relapse and progress, and will be treated with androgen deprivation therapies. The successful development of the new agents that inhibit androgen signaling has changed the progression free survival in hormone resistant disease, but this has not changed the almost ubiquitous development of truly resistant phenotypes in advanced prostate cancer. This review summarizes the current understanding of the molecular pathways involved in localized and metastatic prostate cancer, with an emphasis on the clinical implications of the new knowledge.

    KW - CRPC

    KW - Localized prostate cance

    KW - Molecular targets

    KW - Prostate cancer

    UR - http://www.scopus.com/inward/record.url?scp=84907536832&partnerID=8YFLogxK

    UR - http://www.scopus.com/inward/citedby.url?scp=84907536832&partnerID=8YFLogxK

    M3 - Article

    C2 - 25277175

    AN - SCOPUS:84907536832

    VL - 5

    SP - 7217

    EP - 7259

    JO - Oncotarget

    JF - Oncotarget

    SN - 1949-2553

    IS - 17

    ER -