Why vitiligo is associated with fewer risk of skin cancer? Providing a molecular mechanism

Feily, Amir; Pazyar, Nader

doi:10.1007/s00403-011-1165-5

Cited by 21 publications

(22 citation statements)

References 21 publications

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“…Moreover, it has recently been suggested that increased levels of glutathione peroxidase and superoxide dismutase, the important roles of interleukin 1 and tumor necrosis factor-alfa in superoxide dismutase induction, and decreased levels of transforming growth factor-b and interleukin 10 seen in vitiligo may explain the negative association between vitiligo and skin cancer. 23 In our study patients with vitiligo treated with phototherapy had a markedly higher risk of both melanoma and NMSC compared with those who had not received it (6.0& vs 0.8& and 14.1& vs 3.2&, respectively). The photoaging effect of PUVA and narrowband UVB is generally thought to increase the risk of skin cancer.…”

Section: Discussionmentioning

confidence: 88%

Markedly reduced incidence of melanoma and nonmelanoma skin cancer in a nonconcurrent cohort of 10,040 patients with vitiligo

Paradisi

Tabolli

Didona

et al. 2014

Journal of the American Academy of Dermatology

122

121

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Section: Discussionmentioning

confidence: 88%

Markedly reduced incidence of melanoma and nonmelanoma skin cancer in a nonconcurrent cohort of 10,040 patients with vitiligo

Paradisi

Tabolli

Didona

et al. 2014

Journal of the American Academy of Dermatology

122

121

View full text Add to dashboard Cite

“…The acquisition of senescence-associated secretory phenotypes, combing the effect of intracellular signaling pathway deregulation with extracellular environments perturbation, could affect the behavior of neighboring cells and also systemic homeostasis since melanocytes could release into circulation melanocyte signaling molecules and neurotransmitter-like factors [56]. The senescent-prone phenotype could also provide a molecular explanation to the observation that vitiligo is associated with fewer risks of skin cancer [57]–[58] since premalignant human nevi contain cells that express senescence markers [59].…”

Section: Discussionmentioning

confidence: 99%

Vitiligo: A Possible Model of Degenerative Diseases

et al. 2013

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Vitiligo is characterized by the progressive disappearance of pigment cells from skin and hair follicle. Several in vitro and in vivo studies show evidence of an altered redox status, suggesting that loss of cellular redox equilibrium might be the pathogenic mechanism in vitiligo. However, despite the numerous data supporting a pathogenic role of oxidative stress, there is still no consensus explanation underlying the oxidative stress-driven disappear of melanocytes from the epidermis. In this study, in vitro characterization of melanocytes cultures from non-lesional vitiligo skin revealed at the cellular level aberrant function of signal transduction pathways common with neurodegenerative diseases including modification of lipid metabolism, hyperactivation of mitogen-activated protein kinase (MAPK) and cAMP response element-binding protein (CREB), constitutive p53-dependent stress signal transduction cascades, and enhanced sensibility to pro-apoptotic stimuli. Notably, these long-term effects of subcytotoxic oxidative stress are also biomarkers of pre-senescent cellular phenotype. Consistent with this, vitiligo cells showed a significant increase in p16 that did not correlate with the chronological age of the donor. Moreover, vitiligo melanocytes produced many biologically active proteins among the senescence-associated secretory phenotype (SAPS), such as interleukin-6 (IL-6), matrix metallo proteinase-3 (MMP3), cyclooxygenase-2 (Cox-2), insulin-like growth factor-binding protein-3 and 7 (IGFBP3, IGFBP7). Together, these data argue for a complicated pathophysiologic puzzle underlying melanocytes degeneration resembling, from the biological point of view, neurodegenerative diseases. Our results suggest new possible targets for intervention that in combination with current therapies could correct melanocytes intrinsic defects.

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“…[29] The vitiligo pathogenesis is linked to cellular immunity. MIF is a powerful activator of macrophages and possesses a pivotal role in cell-mediated immunity.…”

Section: Resultsmentioning

confidence: 99%

Macrophage migration inhibitory factor as an incriminating agent in dermatological disorders

2013

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Macrophage migration inhibitory factor (MIF) is a critical immunoregulatory pluripotent cytokine. It has been re-evaluated as a proinflammatory cytokine, pituitary hormone and glucocorticoid-induced immunoregulatory protein. MIF exists in human epidermis, especially in the basal layer and also is expressed constitutively by monocytes/macrophages, T cells, B cells, endocrine, and epithelial cells. In the field of dermatology, MIF is believed to be a detrimental factor in inflammatory dermatological diseases including atopic dermatitis (AD), psoriasis, vitiligo, pemphigus vulgaris, bullous pemphigoid (BP), alopecia areata (AA) as well as other conditions such as photoaging, and photocarcinigenesis. The objective of this review is to gather and summarize MIF related disorders in dermatology and present valuable information for readers and researchers.

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Why vitiligo is associated with fewer risk of skin cancer? Providing a molecular mechanism

Cited by 21 publications

References 21 publications

Markedly reduced incidence of melanoma and nonmelanoma skin cancer in a nonconcurrent cohort of 10,040 patients with vitiligo

Markedly reduced incidence of melanoma and nonmelanoma skin cancer in a nonconcurrent cohort of 10,040 patients with vitiligo

Vitiligo: A Possible Model of Degenerative Diseases

Macrophage migration inhibitory factor as an incriminating agent in dermatological disorders

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