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  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
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We are analyzing https://link.springer.com/article/10.1186/s13045-020-00986-z.

Title:
Immunosenescence: a key player in cancer development | Journal of Hematology & Oncology
Description:
Immunosenescence is a process of immune dysfunction that occurs with age and includes remodeling of lymphoid organs, leading to changes in the immune function of the elderly, which is closely related to the development of infections, autoimmune diseases, and malignant tumors. T cell–output decline is an important feature of immunosenescence as well as the production of senescence-associated secretory phenotype, increased glycolysis, and reactive oxygen species. Senescent T cells exhibit abnormal phenotypes, including downregulation of CD27, CD28, and upregulation of CD57, killer cell lectin-like receptor subfamily G, Tim-3, Tight, and cytotoxic T-lymphocyte-associated protein 4, which are tightly related to malignant tumors. The role of immunosenescence in tumors is sophisticated: the many factors involved include cAMP, glucose competition, and oncogenic stress in the tumor microenvironment, which can induce the senescence of T cells, macrophages, natural killer cells, and dendritic cells. Accordingly, these senescent immune cells could also affect tumor progression. In addition, the effect of immunosenescence on the response to immune checkpoint blocking antibody therapy so far is ambiguous due to the low participation of elderly cancer patients in clinical trials. Furthermore, many other senescence-related interventions could be possible with genetic and pharmacological methods, including mTOR inhibition, interleukin-7 recombination, and NAD+ activation. Overall, this review aims to highlight the characteristics of immunosenescence and its impact on malignant tumors and immunotherapy, especially the future directions of tumor treatment through senescence-focused strategies.
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.
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How Does Link.springer.com Make Money? {💸}

We find it hard to spot revenue streams.

While many websites aim to make money, others are created to share knowledge or showcase creativity. People build websites for various reasons. This could be one of them. Link.springer.com might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

pubmed, article, google, scholar, cells, cas, cell, central, aging, cancer, immunosenescence, immune, senescence, patients, age, elderly, mice, tumor, function, agerelated, immunol, studies, expression, tumors, increased, system, senescent, nat, zhang, progression, process, thymus, role, ageing, microenvironment, immunotherapy, aged, lifespan, oncol, nad, memory, therapy, human, signaling, thymic, cart, diseases, development, factors, study,

Topics {✒️}

pi3k-akt-mtor signaling pathway mek-extracellular signal-regulated kinase beta cell-specific sirt1-overexpressing pd-1/pd-l1 blocking antibodies article download pdf hyper-long telomeres show cooh-terminal src kinase high-dimensional longitudinal monitoring macrophage-derived ccl22 promotes n-terminal extracellular domain glucose-stimulated insulin secretion urh1/pnp1/meu1 pathways triple-negative breast cancer intra-tumoral niche maintains engelbreth-holm-swarm cancer age-modified tissue-specific macrophages wnt/β-catenin signaling myeloid-derived suppressor cells wnt/β-catenin pathway macrophage-mediated immunosuppressive disorders anti-pd-l1 antibodies kinase p38 activated anti-pd-l1 treatment berlin base-ii study cgas-sting signaling pathway tumor-bearing aged mice short-lived mouse models tumor-derived γδ regulatory wild-type mice fed b-cell lymphoblastic leukemia immune checkpoint-related molecules future immunosenescence-based interventions regulatory t-cell populations pka-creb signaling pathway long-lived c57bl/6 mice english language editing tumor-intrinsic signaling pathways age-related thymic involution central memory cd8+ central memory cd8 anti-pd-1 treatment showed senescent hiv-1-specific cytotoxic reflecting age-related differences cyclin-dependent kinase immune-related adverse events dna damage induced inhibiting tumor-specific effector existing immunological techniques cd4 t-cell compartment trigger age-related diseases

Questions {❓}

  • Age and immunity: What is “immunosenescence”?
  • Are senescence and exhaustion intertwined or unrelated processes that compromise immunity?
  • Can people with type 2 diabetes live longer than those without?
  • Cellular senescence: the sought or the unwanted?
  • Educational initiatives in geriatric oncology - Who, why, and how?
  • Hallmarks of human “immunosenescence”: adaptation or dysregulation?
  • Immunosenescence and immunecheckpoint inhibitors in non-small cell lung cancer patients: does age really matter?
  • Immunosenescence: a product of the environment?
  • Is immunosenescence influenced by our lifetime “dose” of exercise?
  • Mechanisms shaping the naïve T cell repertoire in the elderly - thymic involution or peripheral homeostatic proliferation?
  • Metformin: do we finally have an anti-aging drug?
  • Natural killer cell immunosenescence in acute myeloid leukaemia patients: new targets for immunotherapeutic strategies?
  • Sex, gender and immunosenescence: a key to understand the different lifespan between men and women?

Schema {🗺️}

WebPage:
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         headline:Immunosenescence: a key player in cancer development
         description:Immunosenescence is a process of immune dysfunction that occurs with age and includes remodeling of lymphoid organs, leading to changes in the immune function of the elderly, which is closely related to the development of infections, autoimmune diseases, and malignant tumors. T cell–output decline is an important feature of immunosenescence as well as the production of senescence-associated secretory phenotype, increased glycolysis, and reactive oxygen species. Senescent T cells exhibit abnormal phenotypes, including downregulation of CD27, CD28, and upregulation of CD57, killer cell lectin-like receptor subfamily G, Tim-3, Tight, and cytotoxic T-lymphocyte-associated protein 4, which are tightly related to malignant tumors. The role of immunosenescence in tumors is sophisticated: the many factors involved include cAMP, glucose competition, and oncogenic stress in the tumor microenvironment, which can induce the senescence of T cells, macrophages, natural killer cells, and dendritic cells. Accordingly, these senescent immune cells could also affect tumor progression. In addition, the effect of immunosenescence on the response to immune checkpoint blocking antibody therapy so far is ambiguous due to the low participation of elderly cancer patients in clinical trials. Furthermore, many other senescence-related interventions could be possible with genetic and pharmacological methods, including mTOR inhibition, interleukin-7 recombination, and NAD+ activation. Overall, this review aims to highlight the characteristics of immunosenescence and its impact on malignant tumors and immunotherapy, especially the future directions of tumor treatment through senescence-focused strategies.
         datePublished:2020-11-10T00:00:00Z
         dateModified:2025-03-05T00:00:00Z
         pageStart:1
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            Aging
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            Oncology
            Hematology
            Cancer Research
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      headline:Immunosenescence: a key player in cancer development
      description:Immunosenescence is a process of immune dysfunction that occurs with age and includes remodeling of lymphoid organs, leading to changes in the immune function of the elderly, which is closely related to the development of infections, autoimmune diseases, and malignant tumors. T cell–output decline is an important feature of immunosenescence as well as the production of senescence-associated secretory phenotype, increased glycolysis, and reactive oxygen species. Senescent T cells exhibit abnormal phenotypes, including downregulation of CD27, CD28, and upregulation of CD57, killer cell lectin-like receptor subfamily G, Tim-3, Tight, and cytotoxic T-lymphocyte-associated protein 4, which are tightly related to malignant tumors. The role of immunosenescence in tumors is sophisticated: the many factors involved include cAMP, glucose competition, and oncogenic stress in the tumor microenvironment, which can induce the senescence of T cells, macrophages, natural killer cells, and dendritic cells. Accordingly, these senescent immune cells could also affect tumor progression. In addition, the effect of immunosenescence on the response to immune checkpoint blocking antibody therapy so far is ambiguous due to the low participation of elderly cancer patients in clinical trials. Furthermore, many other senescence-related interventions could be possible with genetic and pharmacological methods, including mTOR inhibition, interleukin-7 recombination, and NAD+ activation. Overall, this review aims to highlight the characteristics of immunosenescence and its impact on malignant tumors and immunotherapy, especially the future directions of tumor treatment through senescence-focused strategies.
      datePublished:2020-11-10T00:00:00Z
      dateModified:2025-03-05T00:00:00Z
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         Immunosenescence
         Tumor progression
         Aging
         Tumor microenvironment
         Cancer immunotherapy
         Oncology
         Hematology
         Cancer Research
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            name:The First Affiliated Hospital of Zhengzhou University
            address:
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               type:PostalAddress
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      name:Yi Zhang
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      affiliation:
            name:The First Affiliated Hospital of Zhengzhou University
            address:
               name:Biotherapy Center and Cancer Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
               type:PostalAddress
            type:Organization
            name:State Key Laboratory of Esophageal Cancer Prevention and Treatment
            address:
               name:State Key Laboratory of Esophageal Cancer Prevention and Treatment, Zhengzhou, China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Biotherapy Center and Cancer Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
      name:State Key Laboratory of Esophageal Cancer Prevention and Treatment, Zhengzhou, China
      name:Biotherapy Center and Cancer Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
      name:State Key Laboratory of Esophageal Cancer Prevention and Treatment, Zhengzhou, China
      name:Clinical Laboratory, Henan Medical College Hospital Workers, Zhengzhou, China
      name:Biotherapy Center and Cancer Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
      name:State Key Laboratory of Esophageal Cancer Prevention and Treatment, Zhengzhou, China
      name:Biotherapy Center and Cancer Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
      name:State Key Laboratory of Esophageal Cancer Prevention and Treatment, Zhengzhou, China

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