We are analyzing https://link.springer.com/article/10.1007/s10555-010-9220-9.

Title:
Senescent cells as a source of inflammatory factors for tumor progression | Cancer and Metastasis Reviews
Description:
Cellular senescence, which is associated with aging, is a process by which cells enter a state of permanent cell cycle arrest, therefore constituting a potent tumor suppressive mechanism. Recent studies show that, despite the beneficial effects of cellular senescence, senescent cells can also exert harmful effects on the tissue microenvironment. The most significant of these effects is the acquisition of a senescent-associated secretory phenotype (SASP), which entails a striking increase in the secretion of pro-inflammatory cytokines. Here, we summarize our knowledge of the SASP and the impact it has on tissue microenvironments and ability to stimulate tumor progression.
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Keywords {🔍}

cells, google, scholar, cas, pubmed, article, senescent, senescence, cancer, cell, sasp, tumor, fibroblasts, human, cellular, factors, growth, epithelial, journal, hmgb, nature, research, expression, aging, effects, tissue, secretion, progression, dna, inflammatory, promote, damage, response, senescenceassociated, secreted, endothelial, biology, reviews, culture, activity, vivo, shown, levels, mechanisms, protein, molecular, phenotype, cytokines, proliferation, development,

Topics {✒️}

ras–raf–mek–erk signaling pathway pierre-yves desprez cell surface-bound il-1alpha constitutive nf-kappab activation doe contract ac03-76sf00098 hepatocyte growth factor nf-kappab-dependent induction interleukin-1a antisense oligomer article download pdf largely pro-angiogenic profile ink4a/arf gene locus p53 c-terminal domain nuclear factor-kappab tissue-type plasminogen activators sustained il-1r stimulation transcription factors nf-κb tumor-suppressor protein p53 rb-mediated heterochromatin formation senescence-enhanced oxidative stress pleiotropic pro-inflammatory cytokine growth-related oncogene alpha specific t-cell populations secrete pro-angiogenic factors small pro-inflammatory stimulus rare pre-malignant cells oncogene-induced senescence relayed recombinant hmgb1 protein surface-bound il-1α functional nf-kappa high-affinity binding important positive-feedback component rescue p21-induced senescence interleukin-dependent inflammatory network ets1 transcription factor p21-mediated ros accumulation privacy choices/manage cookies csfs including granulocyte-macrophage pathway involving atm versatile signalling orchestrator positive autoregulatory loop mammary epithelial microenvironment interleukin signaling pathway pivotal transcription factor experimental gerontology release nitric oxide extracellular protein levels jean-philippe coppe tobacco-driven senescence oncogene-induced senescence markers extracellular hmgb1 protein

Questions {❓}

Arterial aging: Is it an immutable cardiovascular risk factor?
Cancer and ageing: Rival demons?
Cellular senescence in the tumor with a bone niche microenvironment: friend or foe?
Chemokines: Agents for the immunotherapy of cancer?

Schema {🗺️}

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         description:Cellular senescence, which is associated with aging, is a process by which cells enter a state of permanent cell cycle arrest, therefore constituting a potent tumor suppressive mechanism. Recent studies show that, despite the beneficial effects of cellular senescence, senescent cells can also exert harmful effects on the tissue microenvironment. The most significant of these effects is the acquisition of a senescent-associated secretory phenotype (SASP), which entails a striking increase in the secretion of pro-inflammatory cytokines. Here, we summarize our knowledge of the SASP and the impact it has on tissue microenvironments and ability to stimulate tumor progression.
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      headline:Senescent cells as a source of inflammatory factors for tumor progression
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         Interleukins
         Proliferation
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         general
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