Ultraviolet-radiation-caused skin cancer development and immune system response

Research output: Contribution to journalReview articlepeer-review


Ultraviolet (UV) radiation is an important environmental carcinogen. Apoptosis, or programmed cell death, is a major cellular homeostatic mechanism in normal skin and plays an important role in the defence against damaged or transformed cells. As a response to UV light-mediated DNA damage, the tumour suppressor protein p53 is upregulated and "sunburn cells" are removed by apoptosis. UV-induced mutations in the p53 tumour suppressor gene play an essential role in skin cancer development. The loss of p53 function by mechanisms such as UV-induced mutations reduces the capacity of p53 to trigger cell death, leading to increased proliferation or tumourigenesis of the cells. UV radiation causes unique mutations in the p53 gene, which have been found in most of the human skin cancers, for example, in squamous cell carcinoma, in basal cell carcinoma, and in actinic keratoses. There are two important adverse consequences when UV radioation strikes the skin: direct damage to tissues and cells, and local and systemic immunosuppression. Consequences of long-term UV exposure include photoageing, mutations, and carcinogenesis.
Original languageEnglish
Pages (from-to)93-102
JournalProceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences.
Issue number3
Publication statusPublished - 2002


  • ultraviolet radiation
  • apoptosis
  • skin cancer

Field of Science*

  • 3.2 Clinical medicine

Publication Type*

  • 1.1. Scientific article indexed in Web of Science and/or Scopus database


Dive into the research topics of 'Ultraviolet-radiation-caused skin cancer development and immune system response'. Together they form a unique fingerprint.

Cite this