Differential effects of 5‐aminolaevulinic acid photodynamic therapy and psoralen + ultraviolet A therapy on p53 phosphorylation in normal human skin in vivo

  title={Differential effects of 5‐aminolaevulinic acid photodynamic therapy and psoralen + ultraviolet A therapy on p53 phosphorylation in normal human skin in vivo},
  author={Lee E. Finlan and N M Kernohan and G Thomson and Paula E. Beattie and Ted R. Hupp and Sally Helen Ibbotson},
  journal={British Journal of Dermatology},
Background  Phosphorylation of the tumour suppressor p53 by the CK2/FACT pathway plays a central role in suppressing ultraviolet (UV)‐induced skin cancer in animal models. Although p53 protein stabilization is induced after solar‐simulated irradiation of human skin in vivo, p53 phosphorylation has not been defined. 

Adverse effects of topical photodynamic therapy

  • S. Ibbotson
  • Medicine
    Photodermatology, photoimmunology & photomedicine
  • 2011
A review explores the adverse effects of topical PDT, particularly for the treatment of superficial non‐melanoma skin cancer and dysplasia.

Adverse effects of topical photodynamic therapy: a consensus review and approach to management

Topical photodynamic therapy (PDT) is widely used to treat superficial nonmelanoma skin cancer and dysplasia, and is generally well tolerated. However, as with all treatments, adverse effects may

Photodynamic therapy.

Enoxacin with UVA Irradiation Induces Apoptosis in the AsPC1 Human Pancreatic Cancer Cell Line Through ROS Generation.

It is suggested that UVA irradiation activates enoxacin, after which activated en oxacin induces apoptosis of AsPC1 cells through generation of reactive oxygen species, which may be a useful method for treating pancreatic cancer.

CK2-site Phosphorylation of p53 is Induced in ΔNp63 Expressing Basal Stem Cells in UVB Irradiated Human Skin

A selective induction of p53 phosphorylation at the CK2-site in the basal cells of UV irradiated human skin is found and this data identify a physiological model with which to identify signalling pathways that mediate cross-talk between p63αΔΝ and activating p53 kinase pathways after DNA damage in basal cell populations.

Down-regulation of heat-shock protein 27-induced resistance to photodynamic therapy in oral cancer cells.

  • Jisun KimHyun-Chul Jung Okjoon Kim
  • Biology
    Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
  • 2013
Down-regulation of HSP27 restored cell survival in HP-PDT-induced apoptotic KB cells and confers resistance to PDT through interruption of apoptotic protein activity in PDT-induced cell death.

Psoralen reverses docetaxel-induced multidrug resistance in A549/D16 human lung cancer cells lines.

Guidelines for topical photodynamic therapy: update

Multicentre randomized controlled studies now demonstrate high efficacy of topical photodynamic therapy (PDT) for actinic keratoses, Bowen’s disease (BD) and superficial basal cell carcinoma (BCC),



The effect of ultraviolet (UV) A1, UVB and solar‐simulated radiation on p53 activation and p21Waf1/Cip1

High‐dose ultraviolet A1 therapy is effective for atopic dermatitis and scleroderma and UVA1 has been shown to induce a dose‐dependent increase in p53 expression in keratinocytes.


The incidence of skin cancer is reported to have increased and is predicted to increase further largely due to an increase in "recreational" exposure to sunlight as well as a result of the depletion of the stratospheric ozone layer.

Role of p53 and ATM in photodynamic therapy‐induced apoptosis

Photodynamic therapy (PDT) induces cell death through a laser light‐activated photosensitizer and is a treatment option for tumors resistant to radio‐ and chemo‐therapy.

Guidelines for topical photodynamic therapy: report of a workshop of the British Photodermatology Group

Current evidence indicates topical PDT to be effective in actinic keratoses on the face and scalp, Bowen's disease and superficial basal cell carcinomas, and several non‐coherent and coherent light sources are effective in PDT.

The expression of p53, p21, Bax and induction of apoptosis in normal volunteers in response to different doses of ultraviolet radiation

Summary Background Ultraviolet radiation (UVR) damages keratinocytes. Direct DNA damage may undergo enzymatic repair followed by resumption of the normal cell cycle. Cells may also be eliminated

Photodynamic therapy sensitivity is not altered in human tumor cells after abrogation of p53 function.

Results indicate that p53 expression does not directly modulate tumor cell sensitivity to PDT in either apoptosis-responsive (LS513) or nonresponsive (MCF-7) cells.

Photodynamic therapy in dermatology: history and horizons.

  • A. Taub
  • Medicine, Biology
    Journal of drugs in dermatology : JDD
  • 2004
The introduction of aminolevulinic acid, which does not make patients susceptible to phototoxicity for extended periods, has reduced morbidity associated with PDT and led to new interest in PDT not only for nonmelanoma skin cancer and premalignant lesions but also in the treatment of acne and as an adjuvant to photorejuvenation procedures.

Increased Sensitivity to UV Radiation in Mice with a p53 Point Mutation at Ser389

P53.S389A mice show increased sensitivity to UV-induced skin tumor development, signifying the importance of serine 389 phosphorylation for the tumor-suppressive function of p53.

Sunburn and p53 in the onset of skin cancer

Skin appears to possess a p53-dependent 'guardian-of-the-tissue' response to DNA damage which aborts precancerous cells, and if this response is reduced in a single cell by a prior p53 mutation, sunburn can select for clonal expansion of the p 53-mutated cell into the AK.