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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries
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We are analyzing https://link.springer.com/article/10.1007/s10555-024-10221-7.

Title:
Vaping and tumor metastasis: current insights and progress | Cancer and Metastasis Reviews
Description:
Tumor metastasis is the primary cause of cancer-related mortality and remains a major hurdle in cancer treatment. Traditional cigarette smoking has been extensively studied for its role in promoting metastasis. However, the impact of e-cigarette (e-cig) on cancer metastasis is not well understood despite their increasing popularity as a supposedly safer alternative. This mini review synthesizes current literature on the effects of e-cig on cancer metastasis, focusing on the processes of dissemination, dormancy, and colonization. It also incorporates recent findings from our laboratory regarding the role of e-cig in tumor progression. E-cig exposure enhances metastatic potential through various mechanisms: it induces epithelial-mesenchymal transition (EMT), increasing cell migratory and invasive capabilities; promotes lymphangiogenesis, aiding tumor cell spread; and alters the pre-metastatic niche to support dormant tumor cells, enhancing their reactivation and colonization. Furthermore, e-cig induce significant epigenetic changes, such as DNA methylation and histone modifications, which regulate genes involved in metastasis. Our data suggest that e-cig upregulate histone demethylases like KDM6B in macrophages, impacting the TME and promoting metastasis. These findings underscore the need for further research to understand the long-term health implications of e-cig use and inform public health policies to reduce e-cig use. Graphical abstract
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

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

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How Does Link.springer.com Make Money? {πŸ’Έ}

We don’t know how the website earns 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 might have a hidden revenue stream, but it's not something we can detect.

Keywords {πŸ”}

pubmed, article, google, scholar, cancer, cas, central, metastasis, journal, cell, lung, ecigarette, tumor, research, electronic, httpsdoiorgs, wang, cigarette, cells, medicine, nature, transition, promotes, health, nicotine, cigarettes, liu, yang, ecig, oral, american, physiology, tobacco, science, smoking, epithelialmesenchymal, access, oncology, epithelial, vaping, review, effects, histone, chen, molecular, privacy, cookies, function, content, data,

Topics {βœ’οΈ}

month download article/chapter flavored e-cigarette e-liquids high-plasticity cell state induces epithelial-mesenchymal transition macrophage-tumor cells crosstalk aryl hydrocarbon receptor generating pre-metastatic niche flavored e-cigarette liquids ceramic wick-based technology e-cigarette flavoring chemicals onco-suppressor dab2ip expression kras-mutant lung cancer e-cigarette vaping surge mir-155-5p/ndfip1 axis epithelial-mesenchymal transition distinct immune microenvironment histone methyltransferase ezh2 nod-scid-gamma mice solid tumor microenvironment immunosuppressive tumor microenvironment high school students central neural control full article pdf bronchial epithelial cells squamous cell carcinoma pre-metastatic niche e-cigarette liquids long-term health implications jama network open post-translational modifications related subjects reduce e-cig cancer-related mortality lung cancer cells disseminated tumor cells immune-mediated pruning oral cavity cancer privacy choices/manage cookies human breast cancer nature cell biology breast cancer metastasis tumor-immune ecosystem cigarette smoke affects e-cigarette users nature reviews cancer high-income countries extensive electronic cigarette lung cancer metastasis nicotine vaping products reducing combustible cigarette

Questions {❓}

  • Are e-cigarette users at an increased risk of bladder and lung cancer?
  • The effect of hypoxia and hypoxia-associated pathways in the regulation of antitumor response: Friends or foes?
  • Tissue regeneration: Reserve or reverse?

Schema {πŸ—ΊοΈ}

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         description:Tumor metastasis is the primary cause of cancer-related mortality and remains a major hurdle in cancer treatment. Traditional cigarette smoking has been extensively studied for its role in promoting metastasis. However, the impact of e-cigarette (e-cig) on cancer metastasis is not well understood despite their increasing popularity as a supposedly safer alternative. This mini review synthesizes current literature on the effects of e-cig on cancer metastasis, focusing on the processes of dissemination, dormancy, and colonization. It also incorporates recent findings from our laboratory regarding the role of e-cig in tumor progression. E-cig exposure enhances metastatic potential through various mechanisms: it induces epithelial-mesenchymal transition (EMT), increasing cell migratory and invasive capabilities; promotes lymphangiogenesis, aiding tumor cell spread; and alters the pre-metastatic niche to support dormant tumor cells, enhancing their reactivation and colonization. Furthermore, e-cig induce significant epigenetic changes, such as DNA methylation and histone modifications, which regulate genes involved in metastasis. Our data suggest that e-cig upregulate histone demethylases like KDM6B in macrophages, impacting the TME and promoting metastasis. These findings underscore the need for further research to understand the long-term health implications of e-cig use and inform public health policies to reduce e-cig use.
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      description:Tumor metastasis is the primary cause of cancer-related mortality and remains a major hurdle in cancer treatment. Traditional cigarette smoking has been extensively studied for its role in promoting metastasis. However, the impact of e-cigarette (e-cig) on cancer metastasis is not well understood despite their increasing popularity as a supposedly safer alternative. This mini review synthesizes current literature on the effects of e-cig on cancer metastasis, focusing on the processes of dissemination, dormancy, and colonization. It also incorporates recent findings from our laboratory regarding the role of e-cig in tumor progression. E-cig exposure enhances metastatic potential through various mechanisms: it induces epithelial-mesenchymal transition (EMT), increasing cell migratory and invasive capabilities; promotes lymphangiogenesis, aiding tumor cell spread; and alters the pre-metastatic niche to support dormant tumor cells, enhancing their reactivation and colonization. Furthermore, e-cig induce significant epigenetic changes, such as DNA methylation and histone modifications, which regulate genes involved in metastasis. Our data suggest that e-cig upregulate histone demethylases like KDM6B in macrophages, impacting the TME and promoting metastasis. These findings underscore the need for further research to understand the long-term health implications of e-cig use and inform public health policies to reduce e-cig use.
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External Links {πŸ”—}(365)

Analytics and Tracking {πŸ“Š}

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