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Age-associated inflammation connects RAS-induced senescence to stem cell dysfunction and epidermal malignancy.

L Golomb1, A Sagiv1, I S Pateras2

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Aging accelerates skin cancer progression. Aged skin with H-Ras activation shows more dysplasia and immune cell infiltration, hindering regeneration compared to young skin, increasing cancer risk.

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Area of Science:

  • Oncology
  • Immunology
  • Dermatology
  • Aging Research

Background:

  • Aging is the primary risk factor for cancer development.
  • Non-melanoma skin cancers are common age-associated malignancies.
  • Mutant H-Ras activation is frequent in cutaneous squamous cell carcinoma (SCC).

Purpose of the Study:

  • To investigate the differential effects of H-Ras activation on young versus aged mouse skin.
  • To explore the role of aging, inflammation, immune response, and cell senescence in skin cancer progression.

Main Methods:

  • Induction of mutant H-Ras in mouse epidermis.
  • Comparative analysis of young and aged mouse skin responses.
  • Assessment of hyperplasia, dysplasia, inflammation, immune cell infiltration, cell senescence, and gene expression (IL4/IL10, Pdl1).
  • Evaluation of skin regeneration after oncogenic H-Ras inactivation.

Main Results:

  • H-Ras activation in aged skin led to more dysplasia and progression to in situ SCC compared to young skin (hyperplasia).
  • Aged skin showed increased inflammation, immune cell accumulation (T cells, macrophages, mast cells), and cell senescence.
  • An age-dependent increase in pro-inflammatory mediators, enhanced IL4/IL10 expression, and a Th2 immune skewing were observed.
  • Aged skin exhibited increased Pdl1 expression, promoting immune evasion.
  • Young skin regenerated upon H-Ras inactivation, while aged skin failed to repair, indicating aged epidermal stem cell dysfunction.

Conclusions:

  • Aging exacerbates H-Ras-driven skin carcinogenesis through increased inflammation, immune suppression, and senescence.
  • Aged epidermal stem cells show impaired regenerative capacity, contributing to failed tissue repair.
  • Findings highlight an age-dependent link between senescence, immune infiltration, and cancer progression, explaining increased cancer risk in the elderly.