We are analyzing https://link.springer.com/article/10.1186/s13045-017-0462-7.

Title:
Posttranslationally modified progesterone receptors direct ligand-specific expression of breast cancer stem cell-associated gene programs | Journal of Hematology & Oncology
Description:
Background Estrogen and progesterone are potent breast mitogens. In addition to steroid hormones, multiple signaling pathways input to estrogen receptor (ER) and progesterone receptor (PR) actions via posttranslational events. Protein kinases commonly activated in breast cancers phosphorylate steroid hormone receptors (SRs) and profoundly impact their activities. Methods To better understand the role of modified PRs in breast cancer, we measured total and phospho-Ser294 PRs in 209 human breast tumors represented on 2754 individual tissue spots within a tissue microarray and assayed the regulation of this site in human tumor explants cultured ex vivo. To complement this analysis, we assayed PR target gene regulation in T47D luminal breast cancer models following treatment with progestin (promegestone; R5020) and antiprogestins (mifepristone, onapristone, or aglepristone) in conditions under which the receptor is regulated by Lys388 SUMOylation (K388 intact) or is SUMO-deficient (via K388R mutation to mimic persistent Ser294 phosphorylation). Selected phospho-PR-driven target genes were validated by qRT-PCR and following RUNX2 shRNA knockdown in breast cancer cell lines. Primary and secondary mammosphere assays were performed to implicate phospho-Ser294 PRs, epidermal growth factor signaling, and RUNX2 in breast cancer stem cell biology. Results Phospho-Ser294 PR species were abundant in a majority (54%) of luminal breast tumors, and PR promoter selectivity was exquisitely sensitive to posttranslational modifications. Phospho-PR expression and target gene programs were significantly associated with invasive lobular carcinoma (ILC). Consistent with our finding that activated phospho-PRs undergo rapid ligand-dependent turnover, unique phospho-PR gene signatures were most prevalent in breast tumors clinically designated as PR-low to PR-null (luminal B) and included gene sets associated with cancer stem cell biology (HER2, PAX2, AHR, AR, RUNX). Validation studies demonstrated a requirement for RUNX2 in the regulation of selected phospho-PR target genes (SLC37A2). In vitro mammosphere formation assays support a role for phospho-Ser294-PRs via growth factor (EGF) signaling as well as RUNX2 as potent drivers of breast cancer stem cell fate. Conclusions We conclude that PR Ser294 phosphorylation is a common event in breast cancer progression that is required to maintain breast cancer stem cell fate, in part via cooperation with growth factor-initiated signaling pathways and key phospho-PR target genes including SLC37A2 and RUNX2. Clinical measurement of phosphorylated PRs should be considered a useful marker of breast tumor stem cell potential. Alternatively, unique phospho-PR target gene sets may provide useful tools with which to identify patients likely to respond to selective PR modulators that block PR Ser294 phosphorylation as part of rational combination (i.e., with antiestrogens) endocrine therapies designed to durably block breast cancer recurrence.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Science
Education
Health & Fitness

Content Management System {📝}

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 {📈}

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.
However, some sources were not loaded, we suggest to reload the page to get complete results.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Link.springer.com Make Money? {💸}

We're unsure how the site profits.

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 might have a hidden revenue stream, but it's not something we can detect.

Keywords {🔍}

breast, cells, cancer, pubmed, expression, gene, article, progesterone, google, scholar, cell, genes, cas, receptor, fig, phosphorylation, tumor, runx, ser, tumors, target, expressing, phosphoser, prs, tissue, data, central, total, stem, onapristone, analysis, estrogen, luminal, treatment, levels, mammospheres, progestin, transcriptional, prb, receptors, signaling, mifepristone, mammary, treated, samples, human, activated, primary, multiple, regulated,

Topics {✒️}

pgc-1alpha-responsive genes involved gov/docs/publications/brca_2012/brca phospho-ser294-pr-driven gene set progesterone-stimulated lateral side-branching sumo-deficient phospho-pr regulates full size image phospho-pr/sumo-deficient pr phospho-ser294-specific pr antibodies phospho-ser294 pr h-scores mitogen-activated protein kinases differential hormone-dependent phosphorylation subtype-specific breast cancer ligand-dependent pr downregulation cells expressing sumo-deficient rapid proteasome-mediated turnover cell-specific transcriptional outcomes custom phospho-ser294-pr ser294/sumo-deficient pr cyclin-dependent kinase activity activated cyclin-dependent kinases steroid hormone signalling kr-specific target genes implicate phospho-ser294 prs undergoing ligand-induced sumoylation progesterone-dependent mammary growth sumo-deficient/phosphorylated receptors phosphorylation erk/map kinase article download pdf pr-dependent transcriptional programs long-term serial passage progestin-mediated gene expression superinduce selected sumo-sensitive diaz flaque mc ligand-independent pathways primarily phospho-pr target genes aml1/runx binding motifs bel-art sp scienceware activated phospho-pr species eralpha-positive breast cancer progestin-driven mammary cancer estrogen-induced target gene pr-driven cell biology ligand-dependent transcription factors e-cadherin-positive spheres phospho-pr gene set target gene selectivity activated phospho-ser294 prs phospho-ser294 pr expression pr-driven breast cancers anti-estrogen/er-based therapies

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Posttranslationally modified progesterone receptors direct ligand-specific expression of breast cancer stem cell-associated gene programs
         description:Estrogen and progesterone are potent breast mitogens. In addition to steroid hormones, multiple signaling pathways input to estrogen receptor (ER) and progesterone receptor (PR) actions via posttranslational events. Protein kinases commonly activated in breast cancers phosphorylate steroid hormone receptors (SRs) and profoundly impact their activities. To better understand the role of modified PRs in breast cancer, we measured total and phospho-Ser294 PRs in 209 human breast tumors represented on 2754 individual tissue spots within a tissue microarray and assayed the regulation of this site in human tumor explants cultured ex vivo. To complement this analysis, we assayed PR target gene regulation in T47D luminal breast cancer models following treatment with progestin (promegestone; R5020) and antiprogestins (mifepristone, onapristone, or aglepristone) in conditions under which the receptor is regulated by Lys388 SUMOylation (K388 intact) or is SUMO-deficient (via K388R mutation to mimic persistent Ser294 phosphorylation). Selected phospho-PR-driven target genes were validated by qRT-PCR and following RUNX2 shRNA knockdown in breast cancer cell lines. Primary and secondary mammosphere assays were performed to implicate phospho-Ser294 PRs, epidermal growth factor signaling, and RUNX2 in breast cancer stem cell biology. Phospho-Ser294 PR species were abundant in a majority (54%) of luminal breast tumors, and PR promoter selectivity was exquisitely sensitive to posttranslational modifications. Phospho-PR expression and target gene programs were significantly associated with invasive lobular carcinoma (ILC). Consistent with our finding that activated phospho-PRs undergo rapid ligand-dependent turnover, unique phospho-PR gene signatures were most prevalent in breast tumors clinically designated as PR-low to PR-null (luminal B) and included gene sets associated with cancer stem cell biology (HER2, PAX2, AHR, AR, RUNX). Validation studies demonstrated a requirement for RUNX2 in the regulation of selected phospho-PR target genes (SLC37A2). In vitro mammosphere formation assays support a role for phospho-Ser294-PRs via growth factor (EGF) signaling as well as RUNX2 as potent drivers of breast cancer stem cell fate. We conclude that PR Ser294 phosphorylation is a common event in breast cancer progression that is required to maintain breast cancer stem cell fate, in part via cooperation with growth factor-initiated signaling pathways and key phospho-PR target genes including SLC37A2 and RUNX2. Clinical measurement of phosphorylated PRs should be considered a useful marker of breast tumor stem cell potential. Alternatively, unique phospho-PR target gene sets may provide useful tools with which to identify patients likely to respond to selective PR modulators that block PR Ser294 phosphorylation as part of rational combination (i.e., with antiestrogens) endocrine therapies designed to durably block breast cancer recurrence.
         datePublished:2017-04-17T00:00:00Z
         dateModified:2017-04-17T00:00:00Z
         pageStart:1
         pageEnd:24
         license:http://creativecommons.org/publicdomain/zero/1.0/
         sameAs:https://doi.org/10.1186/s13045-017-0462-7
         keywords:
            Progesterone receptor (PR)
            Phosphorylation
            ERK/MAP kinase (MAPK)
            SUMOylation
            Antiprogestin
            Onapristone
            Estrogen receptor (ER)
            Breast cancer
            RUNX2
            Cancer stem cells
            Oncology
            Hematology
            Cancer Research
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13045-017-0462-7/MediaObjects/13045_2017_462_Fig1_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13045-017-0462-7/MediaObjects/13045_2017_462_Fig2_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13045-017-0462-7/MediaObjects/13045_2017_462_Fig3_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13045-017-0462-7/MediaObjects/13045_2017_462_Fig4_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13045-017-0462-7/MediaObjects/13045_2017_462_Fig5_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13045-017-0462-7/MediaObjects/13045_2017_462_Fig6_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13045-017-0462-7/MediaObjects/13045_2017_462_Fig7_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13045-017-0462-7/MediaObjects/13045_2017_462_Fig8_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13045-017-0462-7/MediaObjects/13045_2017_462_Fig9_HTML.gif
         isPartOf:
            name:Journal of Hematology & Oncology
            issn:
               1756-8722
            volumeNumber:10
            type:
               Periodical
               PublicationVolume
         publisher:
            name:BioMed Central
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Todd P. Knutson
               affiliation:
                     name:University of Minnesota
                     address:
                        name:Departments of Medicine (Division of Hematology, Oncology, and Transplantation) and Pharmacology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Thu H. Truong
               affiliation:
                     name:University of Minnesota
                     address:
                        name:Departments of Medicine (Division of Hematology, Oncology, and Transplantation) and Pharmacology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Shihong Ma
               affiliation:
                     name:UT Southwestern Medical Center at Dallas
                     address:
                        name:Department of Urology, UT Southwestern Medical Center at Dallas, Dallas, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Nicholas J. Brady
               affiliation:
                     name:University of Minnesota
                     address:
                        name:Microbiology, Immunology, and Cancer Biology Graduate Program, University of Minnesota, Minneapolis, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Megan E. Sullivan
               affiliation:
                     name:NorthShore University HealthSystem
                     address:
                        name:Department of Pathology, Evanston Hospital, University of Chicago, NorthShore University HealthSystem, Evanston, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Ganesh Raj
               affiliation:
                     name:UT Southwestern Medical Center at Dallas
                     address:
                        name:Department of Urology, UT Southwestern Medical Center at Dallas, Dallas, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Kathryn L. Schwertfeger
               affiliation:
                     name:University of Minnesota
                     address:
                        name:Department of Laboratory Medicine and Pathology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Carol A. Lange
               affiliation:
                     name:University of Minnesota
                     address:
                        name:Departments of Medicine (Division of Hematology, Oncology, and Transplantation) and Pharmacology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Posttranslationally modified progesterone receptors direct ligand-specific expression of breast cancer stem cell-associated gene programs
      description:Estrogen and progesterone are potent breast mitogens. In addition to steroid hormones, multiple signaling pathways input to estrogen receptor (ER) and progesterone receptor (PR) actions via posttranslational events. Protein kinases commonly activated in breast cancers phosphorylate steroid hormone receptors (SRs) and profoundly impact their activities. To better understand the role of modified PRs in breast cancer, we measured total and phospho-Ser294 PRs in 209 human breast tumors represented on 2754 individual tissue spots within a tissue microarray and assayed the regulation of this site in human tumor explants cultured ex vivo. To complement this analysis, we assayed PR target gene regulation in T47D luminal breast cancer models following treatment with progestin (promegestone; R5020) and antiprogestins (mifepristone, onapristone, or aglepristone) in conditions under which the receptor is regulated by Lys388 SUMOylation (K388 intact) or is SUMO-deficient (via K388R mutation to mimic persistent Ser294 phosphorylation). Selected phospho-PR-driven target genes were validated by qRT-PCR and following RUNX2 shRNA knockdown in breast cancer cell lines. Primary and secondary mammosphere assays were performed to implicate phospho-Ser294 PRs, epidermal growth factor signaling, and RUNX2 in breast cancer stem cell biology. Phospho-Ser294 PR species were abundant in a majority (54%) of luminal breast tumors, and PR promoter selectivity was exquisitely sensitive to posttranslational modifications. Phospho-PR expression and target gene programs were significantly associated with invasive lobular carcinoma (ILC). Consistent with our finding that activated phospho-PRs undergo rapid ligand-dependent turnover, unique phospho-PR gene signatures were most prevalent in breast tumors clinically designated as PR-low to PR-null (luminal B) and included gene sets associated with cancer stem cell biology (HER2, PAX2, AHR, AR, RUNX). Validation studies demonstrated a requirement for RUNX2 in the regulation of selected phospho-PR target genes (SLC37A2). In vitro mammosphere formation assays support a role for phospho-Ser294-PRs via growth factor (EGF) signaling as well as RUNX2 as potent drivers of breast cancer stem cell fate. We conclude that PR Ser294 phosphorylation is a common event in breast cancer progression that is required to maintain breast cancer stem cell fate, in part via cooperation with growth factor-initiated signaling pathways and key phospho-PR target genes including SLC37A2 and RUNX2. Clinical measurement of phosphorylated PRs should be considered a useful marker of breast tumor stem cell potential. Alternatively, unique phospho-PR target gene sets may provide useful tools with which to identify patients likely to respond to selective PR modulators that block PR Ser294 phosphorylation as part of rational combination (i.e., with antiestrogens) endocrine therapies designed to durably block breast cancer recurrence.
      datePublished:2017-04-17T00:00:00Z
      dateModified:2017-04-17T00:00:00Z
      pageStart:1
      pageEnd:24
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s13045-017-0462-7
      keywords:
         Progesterone receptor (PR)
         Phosphorylation
         ERK/MAP kinase (MAPK)
         SUMOylation
         Antiprogestin
         Onapristone
         Estrogen receptor (ER)
         Breast cancer
         RUNX2
         Cancer stem cells
         Oncology
         Hematology
         Cancer Research
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13045-017-0462-7/MediaObjects/13045_2017_462_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13045-017-0462-7/MediaObjects/13045_2017_462_Fig2_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13045-017-0462-7/MediaObjects/13045_2017_462_Fig3_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13045-017-0462-7/MediaObjects/13045_2017_462_Fig4_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13045-017-0462-7/MediaObjects/13045_2017_462_Fig5_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13045-017-0462-7/MediaObjects/13045_2017_462_Fig6_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13045-017-0462-7/MediaObjects/13045_2017_462_Fig7_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13045-017-0462-7/MediaObjects/13045_2017_462_Fig8_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13045-017-0462-7/MediaObjects/13045_2017_462_Fig9_HTML.gif
      isPartOf:
         name:Journal of Hematology & Oncology
         issn:
            1756-8722
         volumeNumber:10
         type:
            Periodical
            PublicationVolume
      publisher:
         name:BioMed Central
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Todd P. Knutson
            affiliation:
                  name:University of Minnesota
                  address:
                     name:Departments of Medicine (Division of Hematology, Oncology, and Transplantation) and Pharmacology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Thu H. Truong
            affiliation:
                  name:University of Minnesota
                  address:
                     name:Departments of Medicine (Division of Hematology, Oncology, and Transplantation) and Pharmacology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Shihong Ma
            affiliation:
                  name:UT Southwestern Medical Center at Dallas
                  address:
                     name:Department of Urology, UT Southwestern Medical Center at Dallas, Dallas, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Nicholas J. Brady
            affiliation:
                  name:University of Minnesota
                  address:
                     name:Microbiology, Immunology, and Cancer Biology Graduate Program, University of Minnesota, Minneapolis, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Megan E. Sullivan
            affiliation:
                  name:NorthShore University HealthSystem
                  address:
                     name:Department of Pathology, Evanston Hospital, University of Chicago, NorthShore University HealthSystem, Evanston, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Ganesh Raj
            affiliation:
                  name:UT Southwestern Medical Center at Dallas
                  address:
                     name:Department of Urology, UT Southwestern Medical Center at Dallas, Dallas, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Kathryn L. Schwertfeger
            affiliation:
                  name:University of Minnesota
                  address:
                     name:Department of Laboratory Medicine and Pathology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Carol A. Lange
            affiliation:
                  name:University of Minnesota
                  address:
                     name:Departments of Medicine (Division of Hematology, Oncology, and Transplantation) and Pharmacology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Journal of Hematology & Oncology
      issn:
         1756-8722
      volumeNumber:10
Organization:
      name:BioMed Central
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University of Minnesota
      address:
         name:Departments of Medicine (Division of Hematology, Oncology, and Transplantation) and Pharmacology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
         type:PostalAddress
      name:University of Minnesota
      address:
         name:Departments of Medicine (Division of Hematology, Oncology, and Transplantation) and Pharmacology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
         type:PostalAddress
      name:UT Southwestern Medical Center at Dallas
      address:
         name:Department of Urology, UT Southwestern Medical Center at Dallas, Dallas, USA
         type:PostalAddress
      name:University of Minnesota
      address:
         name:Microbiology, Immunology, and Cancer Biology Graduate Program, University of Minnesota, Minneapolis, USA
         type:PostalAddress
      name:NorthShore University HealthSystem
      address:
         name:Department of Pathology, Evanston Hospital, University of Chicago, NorthShore University HealthSystem, Evanston, USA
         type:PostalAddress
      name:UT Southwestern Medical Center at Dallas
      address:
         name:Department of Urology, UT Southwestern Medical Center at Dallas, Dallas, USA
         type:PostalAddress
      name:University of Minnesota
      address:
         name:Department of Laboratory Medicine and Pathology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
         type:PostalAddress
      name:University of Minnesota
      address:
         name:Departments of Medicine (Division of Hematology, Oncology, and Transplantation) and Pharmacology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Todd P. Knutson
      affiliation:
            name:University of Minnesota
            address:
               name:Departments of Medicine (Division of Hematology, Oncology, and Transplantation) and Pharmacology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
               type:PostalAddress
            type:Organization
      name:Thu H. Truong
      affiliation:
            name:University of Minnesota
            address:
               name:Departments of Medicine (Division of Hematology, Oncology, and Transplantation) and Pharmacology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
               type:PostalAddress
            type:Organization
      name:Shihong Ma
      affiliation:
            name:UT Southwestern Medical Center at Dallas
            address:
               name:Department of Urology, UT Southwestern Medical Center at Dallas, Dallas, USA
               type:PostalAddress
            type:Organization
      name:Nicholas J. Brady
      affiliation:
            name:University of Minnesota
            address:
               name:Microbiology, Immunology, and Cancer Biology Graduate Program, University of Minnesota, Minneapolis, USA
               type:PostalAddress
            type:Organization
      name:Megan E. Sullivan
      affiliation:
            name:NorthShore University HealthSystem
            address:
               name:Department of Pathology, Evanston Hospital, University of Chicago, NorthShore University HealthSystem, Evanston, USA
               type:PostalAddress
            type:Organization
      name:Ganesh Raj
      affiliation:
            name:UT Southwestern Medical Center at Dallas
            address:
               name:Department of Urology, UT Southwestern Medical Center at Dallas, Dallas, USA
               type:PostalAddress
            type:Organization
      name:Kathryn L. Schwertfeger
      affiliation:
            name:University of Minnesota
            address:
               name:Department of Laboratory Medicine and Pathology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
               type:PostalAddress
            type:Organization
      name:Carol A. Lange
      affiliation:
            name:University of Minnesota
            address:
               name:Departments of Medicine (Division of Hematology, Oncology, and Transplantation) and Pharmacology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Departments of Medicine (Division of Hematology, Oncology, and Transplantation) and Pharmacology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
      name:Departments of Medicine (Division of Hematology, Oncology, and Transplantation) and Pharmacology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
      name:Department of Urology, UT Southwestern Medical Center at Dallas, Dallas, USA
      name:Microbiology, Immunology, and Cancer Biology Graduate Program, University of Minnesota, Minneapolis, USA
      name:Department of Pathology, Evanston Hospital, University of Chicago, NorthShore University HealthSystem, Evanston, USA
      name:Department of Urology, UT Southwestern Medical Center at Dallas, Dallas, USA
      name:Department of Laboratory Medicine and Pathology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
      name:Departments of Medicine (Division of Hematology, Oncology, and Transplantation) and Pharmacology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA

External Links {🔗}(338)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

5.5s.

LINK . SPRINGER . COM {}