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DOI . ORG {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Doi.org Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
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  14. CDN Services

We began analyzing https://link.springer.com/article/10.1007/s10555-024-10171-0, but it redirected us to https://link.springer.com/article/10.1007/s10555-024-10171-0. The analysis below is for the second page.

Title[redir]:
Dynamic interplay of nuclear receptors in tumor cell plasticity and drug resistance: Shifting gears in malignant transformations and applications in cancer therapeutics | Cancer and Metastasis Reviews
Description:
Recent advances have brought forth the complex interplay between tumor cell plasticity and its consequential impact on drug resistance and tumor recurrence, both of which are critical determinants of neoplastic progression and therapeutic efficacy. Various forms of tumor cell plasticity, instrumental in facilitating neoplastic cells to develop drug resistance, include epithelial-mesenchymal transition (EMT) alternatively termed epithelial-mesenchymal plasticity, the acquisition of cancer stem cell (CSC) attributes, and transdifferentiation into diverse cell lineages. Nuclear receptors (NRs) are a superfamily of transcription factors (TFs) that play an essential role in regulating a multitude of cellular processes, including cell proliferation, differentiation, and apoptosis. NRs have been implicated to play a critical role in modulating gene expression associated with tumor cell plasticity and drug resistance. This review aims to provide a comprehensive overview of the current understanding of how NRs regulate these key aspects of cancer biology. We discuss the diverse mechanisms through which NRs influence tumor cell plasticity, including EMT, stemness, and metastasis. Further, we explore the intricate relationship between NRs and drug resistance, highlighting the impact of NR signaling on chemotherapy, radiotherapy and targeted therapies. We also discuss the emerging therapeutic strategies targeting NRs to overcome tumor cell plasticity and drug resistance. This review also provides valuable insights into the current clinical trials that involve agonists or antagonists of NRs modulating various aspects of tumor cell plasticity, thereby delineating the potential of NRs as therapeutic targets for improved cancer treatment outcomes. Graphical Abstract

Matching Content Categories {📚}

  • Education
  • Science
  • Health & Fitness

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org 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.

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How Does Doi.org Make Money? {💸}

We're unsure how the site profits.

Some websites aren't about earning revenue; they're built to connect communities or raise awareness. There are numerous motivations behind creating websites. This might be one of them. Doi.org might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

pubmed, article, google, scholar, cas, cancer, central, cell, receptor, cells, stem, journal, breast, nuclear, receptors, molecular, signaling, resistance, httpsdoiorgs, nature, clinical, research, biology, wang, expression, tumor, transition, therapy, plasticity, prostate, reviews, vitamin, oncology, trial, epithelialmesenchymal, human, chen, drug, liu, acid, orphan, zhang, estrogen, retinoic, httpsdoiorg, patients, metastasis, androgen, emt, gene,

Topics {✒️}

bt/556/ne/u-excel/2016 grant awarded lnctcfl5-2-ybx1-sox2 signaling axis mir-18a-downregulated rora inhibits phosphatidylinositol 3-kinase/akt-mediated activation e-cadherin invasion-suppressor gene signal-transduction-pathway-specific desensitization month download article/chapter /mir-520f-3p/sox9 signaling beta-catenin/lef-1 signaling pathway restored tgf-β-smad4 signaling targeting hsa-mir-485-5p/rxralpha t-cell receptor-mediated apoptosis estrogen-related receptor alpha mitogen-activated protein kinase shrna-mediated pparalpha knockdown twist1-induced epithelial-mesenchymal transition pi3k/akt signaling pathways retinoic acid-induced differentiation cutaneous t-cell lymphoma phospholipase a2-dependent manner antagonizing p53-mediated apoptosis egfr/her2 signaling pathway e-cadherin germline mutations retinoic-acid-induced reprogramming repressing e-cadherin expression hormone-sensitive prostate cancer niclosamide induces mir-148a e-cadherin gene expression retinoid-related orphan receptors wnt/beta-catenin pathway inhibiting beta-catenin signaling tetrachlorodibenzo-p-dioxin bpa triple-negative breast cancer slug regulates e-cadherin androgen receptor-targeted therapy wnt/β-catenin signaling induced epithelial-mesenchymal transition estrogen receptor alpha estrogen receptor-alpha therapy-induced lineage plasticity her2-negative breast cancer tumor-targeted nanoparticles deliver kdm6b/jmjd3 histone demethylase open-label pilot study thyrotropin-beta promoter activity include epithelial-mesenchymal transition oral cancer-emerging players targeted therapy-induced resistance common tumor-suppressor phenotype emt-inducing transcription factors

Questions {❓}

  • Targeting Wnt signaling: Can we safely eradicate cancer stem cells?
  • Targeting minimal residual disease: A path to cure?
  • The cancer stem cell niche: How essential is the niche in regulating stemness of tumor cells?

Schema {🗺️}

WebPage:
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         headline:Dynamic interplay of nuclear receptors in tumor cell plasticity and drug resistance: Shifting gears in malignant transformations and applications in cancer therapeutics
         description:Recent advances have brought forth the complex interplay between tumor cell plasticity and its consequential impact on drug resistance and tumor recurrence, both of which are critical determinants of neoplastic progression and therapeutic efficacy. Various forms of tumor cell plasticity, instrumental in facilitating neoplastic cells to develop drug resistance, include epithelial-mesenchymal transition (EMT) alternatively termed epithelial-mesenchymal plasticity, the acquisition of cancer stem cell (CSC) attributes, and transdifferentiation into diverse cell lineages. Nuclear receptors (NRs) are a superfamily of transcription factors (TFs) that play an essential role in regulating a multitude of cellular processes, including cell proliferation, differentiation, and apoptosis. NRs have been implicated to play a critical role in modulating gene expression associated with tumor cell plasticity and drug resistance. This review aims to provide a comprehensive overview of the current understanding of how NRs regulate these key aspects of cancer biology. We discuss the diverse mechanisms through which NRs influence tumor cell plasticity, including EMT, stemness, and metastasis. Further, we explore the intricate relationship between NRs and drug resistance, highlighting the impact of NR signaling on chemotherapy, radiotherapy and targeted therapies. We also discuss the emerging therapeutic strategies targeting NRs to overcome tumor cell plasticity and drug resistance. This review also provides valuable insights into the current clinical trials that involve agonists or antagonists of NRs modulating various aspects of tumor cell plasticity, thereby delineating the potential of NRs as therapeutic targets for improved cancer treatment outcomes.
         datePublished:2024-03-22T00:00:00Z
         dateModified:2024-03-22T00:00:00Z
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            Cancer
            Cancer cell plasticity
            Cancer stem cells
            EMT
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            Nuclear receptors
            Cancer therapy
            Cancer Research
            Oncology
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      headline:Dynamic interplay of nuclear receptors in tumor cell plasticity and drug resistance: Shifting gears in malignant transformations and applications in cancer therapeutics
      description:Recent advances have brought forth the complex interplay between tumor cell plasticity and its consequential impact on drug resistance and tumor recurrence, both of which are critical determinants of neoplastic progression and therapeutic efficacy. Various forms of tumor cell plasticity, instrumental in facilitating neoplastic cells to develop drug resistance, include epithelial-mesenchymal transition (EMT) alternatively termed epithelial-mesenchymal plasticity, the acquisition of cancer stem cell (CSC) attributes, and transdifferentiation into diverse cell lineages. Nuclear receptors (NRs) are a superfamily of transcription factors (TFs) that play an essential role in regulating a multitude of cellular processes, including cell proliferation, differentiation, and apoptosis. NRs have been implicated to play a critical role in modulating gene expression associated with tumor cell plasticity and drug resistance. This review aims to provide a comprehensive overview of the current understanding of how NRs regulate these key aspects of cancer biology. We discuss the diverse mechanisms through which NRs influence tumor cell plasticity, including EMT, stemness, and metastasis. Further, we explore the intricate relationship between NRs and drug resistance, highlighting the impact of NR signaling on chemotherapy, radiotherapy and targeted therapies. We also discuss the emerging therapeutic strategies targeting NRs to overcome tumor cell plasticity and drug resistance. This review also provides valuable insights into the current clinical trials that involve agonists or antagonists of NRs modulating various aspects of tumor cell plasticity, thereby delineating the potential of NRs as therapeutic targets for improved cancer treatment outcomes.
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      pageStart:321
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         Cancer
         Cancer cell plasticity
         Cancer stem cells
         EMT
         Chemoresistance
         Nuclear receptors
         Cancer therapy
         Cancer Research
         Oncology
         Biomedicine
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                     type:PostalAddress
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            name:Mohamed Abbas
            affiliation:
                  name:King Khalid University
                  address:
                     name:Electrical Engineering Department, College of Engineering, King Khalid University, Abha, Saudi Arabia
                     type:PostalAddress
                  type:Organization
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            name:Ajaikumar B. Kunnumakkara
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               type:PostalAddress
            type:Organization
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            address:
               name:Radiological Sciences Department, College of Applied Medical Sciences, King Khalid University, Abha, Saudi Arabia
               type:PostalAddress
            type:Organization
      name:Mohamed Abbas
      affiliation:
            name:King Khalid University
            address:
               name:Electrical Engineering Department, College of Engineering, King Khalid University, Abha, Saudi Arabia
               type:PostalAddress
            type:Organization
      name:Ajaikumar B. Kunnumakkara
      affiliation:
            name:Indian Institute of Technology Guwahati (IITG)
            address:
               name:Cancer Biology Laboratory, Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati (IITG), Guwahati, India
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      name:Radiological Sciences Department, College of Applied Medical Sciences, King Khalid University, Abha, Saudi Arabia
      name:Electrical Engineering Department, College of Engineering, King Khalid University, Abha, Saudi Arabia
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External Links {🔗}(1095)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

Emails and Hosting {✉️}

Mail Servers:

  • mx.zoho.eu
  • mx2.zoho.eu
  • mx3.zoho.eu

Name Servers:

  • josh.ns.cloudflare.com
  • zita.ns.cloudflare.com

CDN Services {📦}

  • Crossref

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