Polymorphismes du MC1R et photovieillissement du visage

Latreille, Julie; Ezzedine, Khaled; Elfakir, Anissa; Ambroisine, Laurence; Jdid, Randa; Galán, Pilar; Herçberg, Serge; Грубер, Флориан; Malvy, Denis; Tschachler, Erwin; Guinot, Christiane

doi:10.1016/j.annder.2011.02.026

Cited by 4 publications

(2 citation statements)

References 15 publications

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“…The increased risk associated with MC1R variants spans all histological subtypes and it occurs on both chronically and intermittently sun-exposed skin [ 44 ]. MC1R genetic variants are determinant also in the acquisition of skin aging-related features [ 45 , 46 ] including specific dermal variation during photoaging [ 47 , 48 ]. Since properties referred to functional aging of the skin have been associated with the potential pro-tumorigenic phenotype of fibroblast [ 49 , 50 ], impaired functionality of the (α-melanocyte stimulating hormone) α-MSH/MC1R axis might contribute to creating a favorable milieu for hyperproliferative diseases in photo-exposed bodies’ area.…”

Section: Introductionmentioning

confidence: 99%

The Keratinocyte in the Picture Cutaneous Melanoma Microenvironment

Marrapodi,

Bellei

2024

Cancers

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Melanoma progression is a multistep evolution from a common melanocytic nevus through a radial superficial growth phase, the invasive vertical growth phase finally leading to metastatic dissemination into distant organs. Melanoma aggressiveness largely depends on the propensity to metastasize, which means the capacity to escape from the physiological microenvironment since tissue damage due to primary melanoma lesions is generally modest. Physiologically, epidermal melanocytes are attached to the basement membrane, and their adhesion/migration is under the control of surrounding keratinocytes. Thus, the epidermal compartment represents the first microenvironment responsible for melanoma spread. This complex process involves cell–cell contact and a broad range of secreted bioactive molecules. Invasion, or at the beginning of the microinvasion, implies the breakdown of the dermo-epidermal basement membrane followed by the migration of neoplastic melanocytic cells in the superficial papillary dermis. Correspondingly, several experimental evidences documented the structural and functional rearrangement of the entire tissue surrounding neoplasm that in some way reflects the atypia of tumor cells. Lastly, the microenvironment must support the proliferation and survival of melanocytes outside the normal epidermal–melanin units. This task presumably is mostly delegated to fibroblasts and ultimately to the self-autonomous capacity of melanoma cells. This review will discuss remodeling that occurs in the epidermis during melanoma formation as well as skin changes that occur independently of melanocytic hyperproliferation having possible pro-tumoral features.

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Section: Introductionmentioning

confidence: 99%

The Keratinocyte in the Picture Cutaneous Melanoma Microenvironment

Marrapodi,

Bellei

2024

Cancers

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“…Both chronological aging and extrinsic aging are affected by the specific genetic background that includes gender. Of interest, polymorphic variants of the MC1R gene, one of the most important pigmentary-related genes, negatively impact both photoaging and skin cancer risk [ 49 , 50 , 51 , 52 ]. Protection against cancer is not a simple secondary event related to melanin synthesis and distribution since activation of this membrane receptor by its ligand α-melanocyte-stimulating hormone (α-MSH) exerts pleiotropic effects such as stimulation of intracellular antioxidant machinery, antagonization of inflammation, and modulation of collagen metabolism [ 53 , 54 ].…”

Section: Introductionmentioning

confidence: 99%

Skin Cancer Microenvironment: What We Can Learn from Skin Aging?

D’Arino,

Caputo,

Eibenschutz

et al. 2023

IJMS

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Aging is a natural intrinsic process associated with the loss of fibrous tissue, a slower cell turnover, and a reduction in immune system competence. In the skin, the continuous exposition of environmental factors superimposes extrinsic damage, mainly due to ultraviolet radiation causing photoaging. Although not usually considered a pathogenic event, photoaging affects cutaneous biology, increasing the risk of skin carcinogenesis. At the cellular level, aging is typified by the rise of senescence cells a condition characterized by reduced or absent capacity to proliferate and aberrant hyper-secretory activity. Senescence has a double-edged sword in cancer biology given that senescence prevents the uncontrolled proliferation of damaged cells and favors their clearance by paracrine secretion. Nevertheless, the cumulative insults and the poor clearance of injured cells in the elderly increase cancer incidence. However, there are not conclusive data proving that aged skin represents a permissive milieu for tumor onset. On the other hand, tumor cells are capable of activating resident fibroblasts onto a pro-tumorigenic phenotype resembling those of senescent fibroblasts suggesting that aged fibroblasts might facilitate cancer progression. This review discusses changes that occur during aging that can prime neoplasm or increase the aggressiveness of melanoma and non-melanoma skin cancer.

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