p53 in Dermatology

Gasparro, Francis P.

doi:10.1001/archderm.134.8.1029

Cited by 10 publications

(17 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It is more likely to be related to the chronic inflammatory status of plaquetype psoriasis because p53 expression was noted to increase with chronic inflammation. 9,12,24 It was supposed that autoimmunity induced by antigenic cross-reactivity between the keratin proteins and virally-or bacterially-derived antigens might induce Table 4. Comparisons of the mean values of the p53 positive cell numbers among the different groups…”

Section: Discussionmentioning

confidence: 99%

“…Up to now, the cutaneous expression of p53 protein has been demonstrated in malignant (basal and squamous cell carcinomas, malignant melanoma, sebaceous carcinoma of the vulva), premalignant (Bowen's disease, solar keratoses, keratoacanthoma) and benign (e.g. rheumatoid arthritis, pleomorphic adenoma, lichen planus, verruca vulgaris, lichen simplex chronicus, condyloma acuminata, lupus erythematosus) diseases including psoriasis 1,9,12–18 …”

Section: Introductionmentioning

confidence: 99%

“…rheumatoid arthritis, pleomorphic adenoma, lichen planus, verruca vulgaris, lichen simplex chronicus, condyloma acuminata, lupus erythematosus) diseases including psoriasis. 1,9,[12][13][14][15][16][17][18] It was shown that epidermis expresses p53 and the gene may regulate epidermal keratinocyte growth and carcinogenesis. 19 This suggests the possible role of p53 in the pathogenesis of psoriasis as first mentioned by Tadini et al 1 In the present study, we examined the expression of p53 protein by immunohistochemical analysis in the skin samples obtained from patients with plaque-type or guttate-type psoriasis.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Expression of p53 in lesions and unaffected skin of patients with plaque‐type and guttate psoriasis: A quantitative comparative study

Yazıcı

Karabulut

Özen

et al. 2007

The Journal of Dermatology

View full text Add to dashboard Cite

Psoriasis is a common inflammatory and hyperproliferative skin disease characterized by hyperproliferation of keratinocytes. The pathogenesis of psoriasis has yet to be determined. The control of cell growth is a delicately balanced process, regulated by external signals or the internal genetic program of an individual cell. In psoriasis, these processes are disturbed and some candidate genes like p53 are suspected of being involved in the pathogenesis of the disease. The p53 protein is essential for the regulation of cell proliferation. The study was performed on 32 patients with psoriasis (24 plaque type, eight guttate type). Biopsy specimens for immunohistochemical determination of p53 protein expression were collected from both the lesional and the nonlesional skin sites that were not exposed to sun in all of the patients (n = 32). Taking the ultraviolet (UV) exposure of the skin into consideration, a third skin sample was taken from each patient (n = 7) who had lesions on the sun-exposed areas. Immunohistochemical assessment of p53 expression in skin was determined as p53 protein expression per 1000 cells (keratinocytes). The statistical analysis revealed that the expressions of p53 per 1000 cells were higher in non-sun-exposed lesional skin than the non-sun-exposed nonlesional skin, also in plaque-type psoriasis than guttate-type psoriasis (P = 0.000, P = 0.046, P = 0.037, respectively). There was a positive correlation between the p53 expression in non-sun-exposed lesional skin versus expression in sun-exposed lesional skin (cubic centimeters = 0.811, P = 0.027). Our results show a stronger association of elevated p53 expression with chronic rather than acute inflammatory psoriasis. This may indicate a mechanistic difference between plaque-type and guttate psoriasis. Alternatively, this could reflect a chronological course as the disease transitions from an acute to a chronic phase.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Expression of p53 in lesions and unaffected skin of patients with plaque‐type and guttate psoriasis: A quantitative comparative study

Yazıcı

Karabulut

Özen

et al. 2007

The Journal of Dermatology

View full text Add to dashboard Cite

show abstract

“…Therefore, several skin disorders are treated with a combination of 8-methoxypsoralen (8-MOP) with broadband UVA irradiation (PUVA). Long-term PUVA therapy results in premature skin ageing and an enhanced skin tumor incidence (8,9). A single PUVA exposure of primary human dermal fibroblasts induces morphological and functional changes reminiscent of cellular senescence (10).…”

Section: Introductionmentioning

confidence: 99%

Differential roles for Chk1 and FANCD2 in ATR-mediated signalling for psoralen photoactivation-induced senescence

Hovest

Krieg

Herrmann

2011

Experimental Dermatology

View full text Add to dashboard Cite

Cellular senescence is a stress-inducible, naturally irreversible cell cycle arrest, which is likely linked with ageing. Premature ageing of the skin is a prominent side effect of psoralen photoactivation, which is used for the treatment of various skin disorders. Previously, we have shown that DNA interstrand crosslink formation by photoactivated psoralens induces a senescent phenotype in primary fibroblasts that is mediated by Ataxia telangiectasia-mutated and Rad3-related (ATR) kinase. Checkpoint kinase 1 (Chk1) initiates cell cycle checkpoints, and FANCD2 is known to be involved in DNA damage-induced S-phase arrest and crosslink repair. In this study, we examined a role for Chk1 and FANCD2 as downstream effectors of ATR in senescence signalling. We demonstrate that Chk1 and FANCD2 are long-lastingly activated after psoralen photoactivation. Separate and combined reduction in Chk1 and FANCD2 expression by small interfering RNA (siRNA) preceding irradiation partly prevented the initiation of the senescence-like phenotype, whereas siRNA (Chk1 and FANCD2) transfection of senesced fibroblasts released cells from growth arrest. We observed that Chk1 and FANCD2 signal equally and additively for senescence induction, while Chk1 is predominantly responsible for maintaining persistent cell cycle arrest. In conclusion, Chk1 and FANCD2 function downstream of ATR in a non-redundant manner for the establishment and maintenance of psoralen photoactivation-induced senescence.

show abstract

“…p53 is frequently targeted for dermatological treatments. For example, psoriasis treatment by psoralin-UV-A (PUVA) induces intended genotoxic damage, activating p53; but DNA damage may also have the negative result of inducing p53 mutation, possibly leading to squamous cell carcinoma (SCC) [5]. Introducing wild type p53 back into a variety of human cancer cell lines stops their growth or induces apoptosis (programmed cell death).…”

Section: Introductionmentioning

confidence: 99%

P53 Family Activities in Development and Cancer: Relationship to Melanocyte and Keratinocyte Carcinogenesis

Johnson

Lagowski

Sundberg

et al. 2005

Journal of Investigative Dermatology

View full text Add to dashboard Cite

p53 in Dermatology

Cited by 10 publications

References 34 publications

Expression of p53 in lesions and unaffected skin of patients with plaque‐type and guttate psoriasis: A quantitative comparative study

Expression of p53 in lesions and unaffected skin of patients with plaque‐type and guttate psoriasis: A quantitative comparative study

Differential roles for Chk1 and FANCD2 in ATR-mediated signalling for psoralen photoactivation-induced senescence

P53 Family Activities in Development and Cancer: Relationship to Melanocyte and Keratinocyte Carcinogenesis

Contact Info

Product

Resources

About