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We are analyzing https://link.springer.com/article/10.1007/s12672-013-0131-4.

Title:
Interplay Between Genomic Alterations and Androgen Receptor Signaling During Prostate Cancer Development and Progression | Discover Oncology
Description:
Advanced prostate cancer (PCa) treated with androgen deprivation therapy (ADT) eventually relapses to an ADT-resistant disease referred to as castration-resistant PCa (CRPC). Recent integrative analyses of PCa genomes have led to the elucidation of potential subtypes that are revelatory to the development of PCa as well as the mechanisms of resistance to ADT and CRPC progression. These studies have confirmed that alterations in the androgen receptor (AR) signaling axis are central to CRPC progression, and have uncovered complex mechanisms by which AR and other components of the AR signaling axis affect, and are affected by, genomic changes and epigenetic transformations. Among the most frequent alterations in CRPC are direct alterations in the AR gene. These AR gene alterations include AR amplification, point mutations, and more recently AR gene rearrangements leading to expression of truncated, constitutively active AR splice variants that are impervious to ADT. In this review, we will highlight genomic alterations that are important for development and progression of PCa, with a focus on how these alterations affect, and are affected by, activity of the AR signaling axis.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Science
  • Education
  • Health & Fitness

Content Management System {πŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {πŸ’Έ}

We can't see how the site brings in money.

Many websites are intended to earn money, but some serve to share ideas or build connections. Websites exist for all kinds of purposes. This might be one of them. Link.springer.com has a secret sauce for making money, but we can't detect it yet.

Keywords {πŸ”}

cancer, pca, article, google, scholar, pubmed, variants, androgen, prostate, cas, gene, truncated, crpc, cell, receptor, expression, alterations, genomic, cells, signaling, progression, rearrangements, fulllength, splice, resistance, activity, binding, exons, studies, splicing, variant, mutations, occur, genes, ets, copy, number, role, line, nuclear, levels, subtypes, transcriptional, events, genome, erg, res, therapy, adt, mechanisms,

Topics {βœ’οΈ}

drive androgen-independent growth enhancer-driven lineage-specific transcription require dht/ar-mediated recruitment androgen-independent prostate cancer androgen-dependent subline derived castration-resistant prostate cancer tmprss2–erg rearrangement-positive cancers castration-recurrent prostate cancer dna-directed enzymatic activities require full-length ar androgen-independent growth tmprss2-erg gene fusions speckle-type poz protein androgen deprivation therapy irradiation-induced dna damage h3k4-specific histone methyltransferase androgen/ar signaling axis ar-driven enhancer element castrate-recurrent prostate cancer spink1-positive prostate cancer late-passage lncap cells activation-induced cytidine deaminase cwr-r1 cell line cul3-based ubiquitin ligase ar-v7 variant encoded hormone-dependent cancer full-length ar expression full-length ar activity duplication-positive cells coincided cwr-r1 xenografts grown genome-wide copy number ar-v7 overexpression arises cwr-r1 cell lines androgen receptor signaling signal-dependent proteolysis human androgen receptor adt-resistant disease referred median ar-v7 expression ets family fusions viable therapeutic target androgen-independent function active transcription driven line ar-targeted therapies androgen receptor mutations create chromatin environments androgen receptor mutation constitutively active forms metastatic prostate cancer therapeutic targets downstream activate oncogenic signaling

Questions {❓}

  • These integrative and whole-genome sequencing studies have raised an intriguing question: why is there a propensity towards structural alteration in the PCa genome?

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:Interplay Between Genomic Alterations and Androgen Receptor Signaling During Prostate Cancer Development and Progression
         description:Advanced prostate cancer (PCa) treated with androgen deprivation therapy (ADT) eventually relapses to an ADT-resistant disease referred to as castration-resistant PCa (CRPC). Recent integrative analyses of PCa genomes have led to the elucidation of potential subtypes that are revelatory to the development of PCa as well as the mechanisms of resistance to ADT and CRPC progression. These studies have confirmed that alterations in the androgen receptor (AR) signaling axis are central to CRPC progression, and have uncovered complex mechanisms by which AR and other components of the AR signaling axis affect, and are affected by, genomic changes and epigenetic transformations. Among the most frequent alterations in CRPC are direct alterations in the AR gene. These AR gene alterations include AR amplification, point mutations, and more recently AR gene rearrangements leading to expression of truncated, constitutively active AR splice variants that are impervious to ADT. In this review, we will highlight genomic alterations that are important for development and progression of PCa, with a focus on how these alterations affect, and are affected by, activity of the AR signaling axis.
         datePublished:2013-01-10T00:00:00Z
         dateModified:2013-01-10T00:00:00Z
         pageStart:61
         pageEnd:69
         sameAs:https://doi.org/10.1007/s12672-013-0131-4
         keywords:
            Androgen Receptor
            Androgen Deprivation Therapy
            Abiraterone
            Enzalutamide
            Androgen Receptor Gene
            Oncology
            Cancer Research
            Surgical Oncology
            Molecular Medicine
            Radiotherapy
            Internal Medicine
         image:
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         isPartOf:
            name:Hormones and Cancer
            issn:
               1868-8500
               1868-8497
            volumeNumber:4
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               Periodical
               PublicationVolume
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            name:Springer-Verlag
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               type:ImageObject
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         author:
               name:Michael D. Nyquist
               affiliation:
                     name:University of Minnesota, Twin Cities
                     address:
                        name:Masonic Cancer Center, University of Minnesota, Twin Cities, Minneapolis, USA
                        type:PostalAddress
                     type:Organization
                     name:University of Minnesota, Twin Cities
                     address:
                        name:Graduate Program in Molecular, Cellular, Developmental Biology and Genetics, University of Minnesota, Twin Cities, Minneapolis, USA
                        type:PostalAddress
                     type:Organization
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               name:Scott M. Dehm
               affiliation:
                     name:University of Minnesota, Twin Cities
                     address:
                        name:Masonic Cancer Center, University of Minnesota, Twin Cities, Minneapolis, USA
                        type:PostalAddress
                     type:Organization
                     name:University of Minnesota, Twin Cities
                     address:
                        name:Department of Laboratory Medicine and Pathology, University of Minnesota, Twin Cities, Minneapolis, USA
                        type:PostalAddress
                     type:Organization
               email:[email protected]
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ScholarlyArticle:
      headline:Interplay Between Genomic Alterations and Androgen Receptor Signaling During Prostate Cancer Development and Progression
      description:Advanced prostate cancer (PCa) treated with androgen deprivation therapy (ADT) eventually relapses to an ADT-resistant disease referred to as castration-resistant PCa (CRPC). Recent integrative analyses of PCa genomes have led to the elucidation of potential subtypes that are revelatory to the development of PCa as well as the mechanisms of resistance to ADT and CRPC progression. These studies have confirmed that alterations in the androgen receptor (AR) signaling axis are central to CRPC progression, and have uncovered complex mechanisms by which AR and other components of the AR signaling axis affect, and are affected by, genomic changes and epigenetic transformations. Among the most frequent alterations in CRPC are direct alterations in the AR gene. These AR gene alterations include AR amplification, point mutations, and more recently AR gene rearrangements leading to expression of truncated, constitutively active AR splice variants that are impervious to ADT. In this review, we will highlight genomic alterations that are important for development and progression of PCa, with a focus on how these alterations affect, and are affected by, activity of the AR signaling axis.
      datePublished:2013-01-10T00:00:00Z
      dateModified:2013-01-10T00:00:00Z
      pageStart:61
      pageEnd:69
      sameAs:https://doi.org/10.1007/s12672-013-0131-4
      keywords:
         Androgen Receptor
         Androgen Deprivation Therapy
         Abiraterone
         Enzalutamide
         Androgen Receptor Gene
         Oncology
         Cancer Research
         Surgical Oncology
         Molecular Medicine
         Radiotherapy
         Internal Medicine
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12672-013-0131-4/MediaObjects/12672_2013_131_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12672-013-0131-4/MediaObjects/12672_2013_131_Fig2_HTML.gif
      isPartOf:
         name:Hormones and Cancer
         issn:
            1868-8500
            1868-8497
         volumeNumber:4
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer-Verlag
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Michael D. Nyquist
            affiliation:
                  name:University of Minnesota, Twin Cities
                  address:
                     name:Masonic Cancer Center, University of Minnesota, Twin Cities, Minneapolis, USA
                     type:PostalAddress
                  type:Organization
                  name:University of Minnesota, Twin Cities
                  address:
                     name:Graduate Program in Molecular, Cellular, Developmental Biology and Genetics, University of Minnesota, Twin Cities, Minneapolis, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Scott M. Dehm
            affiliation:
                  name:University of Minnesota, Twin Cities
                  address:
                     name:Masonic Cancer Center, University of Minnesota, Twin Cities, Minneapolis, USA
                     type:PostalAddress
                  type:Organization
                  name:University of Minnesota, Twin Cities
                  address:
                     name:Department of Laboratory Medicine and Pathology, University of Minnesota, Twin Cities, Minneapolis, USA
                     type:PostalAddress
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      name:Hormones and Cancer
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      name:University of Minnesota, Twin Cities
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         name:Masonic Cancer Center, University of Minnesota, Twin Cities, Minneapolis, USA
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      name:University of Minnesota, Twin Cities
      address:
         name:Graduate Program in Molecular, Cellular, Developmental Biology and Genetics, University of Minnesota, Twin Cities, Minneapolis, USA
         type:PostalAddress
      name:University of Minnesota, Twin Cities
      address:
         name:Masonic Cancer Center, University of Minnesota, Twin Cities, Minneapolis, USA
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      name:University of Minnesota, Twin Cities
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      name:Michael D. Nyquist
      affiliation:
            name:University of Minnesota, Twin Cities
            address:
               name:Masonic Cancer Center, University of Minnesota, Twin Cities, Minneapolis, USA
               type:PostalAddress
            type:Organization
            name:University of Minnesota, Twin Cities
            address:
               name:Graduate Program in Molecular, Cellular, Developmental Biology and Genetics, University of Minnesota, Twin Cities, Minneapolis, USA
               type:PostalAddress
            type:Organization
      name:Scott M. Dehm
      affiliation:
            name:University of Minnesota, Twin Cities
            address:
               name:Masonic Cancer Center, University of Minnesota, Twin Cities, Minneapolis, USA
               type:PostalAddress
            type:Organization
            name:University of Minnesota, Twin Cities
            address:
               name:Department of Laboratory Medicine and Pathology, University of Minnesota, Twin Cities, Minneapolis, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Masonic Cancer Center, University of Minnesota, Twin Cities, Minneapolis, USA
      name:Graduate Program in Molecular, Cellular, Developmental Biology and Genetics, University of Minnesota, Twin Cities, Minneapolis, USA
      name:Masonic Cancer Center, University of Minnesota, Twin Cities, Minneapolis, USA
      name:Department of Laboratory Medicine and Pathology, University of Minnesota, Twin Cities, Minneapolis, USA

External Links {πŸ”—}(196)

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