Disease relevance of Lentigo

• Carney complex is an autosomal dominant syndrome characterized by multiple neoplasias, including myxomas at various sites and endocrine tumors, and lentiginosis [1].
• We found frequent amplification of CD1 in AM (44.4%) and occasional amplification in lentigo maligna melanoma (10.5%) and superficial spreading melanoma (5.6%) [2].
• Carney complex shares skin abnormalities and some nonendocrine tumors with the lentiginoses and certain of the hamartomatoses, particularly Peutz-Jeghers syndrome, with which it shares mucosal lentiginosis and an unusual gonadal tumor, large-cell calcifying Sertoli cell tumor [3].
• Carney complex (CNC) is a familial multiple neoplasia and lentiginosis syndrome with features overlapping those of McCune-Albright syndrome (MAS) and other multiple endocrine neoplasia (MEN) syndromes, MEN type 1 (MEN 1), in particular [4].
• The role of the epidermal endothelin cascade in the hyperpigmentation mechanism of lentigo senilis [5].

High impact information on Lentigo

• The most prevalent clinical manifestation in patients with Carney complex was spotty skin pigmentation, similar to that observed in Peutz-Jeghers and other lentiginosis syndromes [1].
• The majority of the XP melanomas were of the lentigo maligna melanoma (LMM) type, as found in the elderly. p53 point mutations were found in 60% of XP-C melanomas and in only 10% of XPV melanomas, this latter frequency being similar to what has been reported in the general population [6].
• The lack of both gelatinase B and EMMPRIN in lentigo maligna may contribute to the indolent behavior of this type of pigment cell lesion [7].
• Carney complex (CNC) is a familial multiple neoplasia and lentiginosis syndrome (OMIM 160980, http://www.ncbi.nlm.nih.gov/omim) with features overlapping those of other multiple endocrine neoplasias and hamartomatoses, Peutz-Jeghers syndrome (PJS) in particular [8].
• Prevalence of exon 15 BRAF mutations in primary melanoma of the superficial spreading, nodular, acral, and lentigo maligna subtypes [9].

Chemical compound and disease context of Lentigo

• Azelaic acid was successfully used in the clinical treatment of 7 cases of lentigo maligna in that remission of the lesions was observed in all our patients [10].
• Several reports have been published over the last two decades describing the successful removal of benign cutaneous pigmented lesions such as lentigines, café au lait macules' nevi, nevus of Ota, and lentigo maligna by a variety of lasers such as the excimer (351 nm), argon (488,514 nm), ruby (694 nm), Nd:YAG (1060 nm), and CO2 (10,600 nm) [11].
• Treatment of lentigo maligna with tazarotene 0.1% gel [12].
• Oestrogen and progesterone receptors in lentigo maligna [13].
• No effect of topical tretinoin on lentigo maligna [14].

Biological context of Lentigo

• Genetics of Peutz-Jeghers syndrome, Carney complex and other familial lentiginoses [15].
• Ionically separated epidermal sheets from pigmentations of two patients with lentiginosis profusa were incubated in dopa (3,4 dihydroxyphenylalanine) and slide-mounted [16].

Anatomical context of Lentigo

• Carney complex is a multiple neoplasia and lentiginosis syndrome that affects endocrine glands, including the pituitary, adrenals, and testes; thyroid gland involvement has not been unequivocally demonstrated [17].
• Eight percent of the lentigo maligna samples were positive for keratinocyte expression of bcl-2, 24% were positive for p53, and 76% were positive for bax; respective findings for solar keratoses were 35%, 85%, and 90% [18].
• This combined finding may be one of pure coincidence, but hypertrophic cardiomyopathy like changes of the myocardium are known to occur in Friedreich's ataxia and lentiginosis . The occurrence may, therefore, indicate some fundamental interrelation [19].

Gene context of Lentigo

• Comparison of DNA ploidy-related parameters between lentigos with and without exonic deletions in MSH2 and MLH1 did not show any significant differences [20].
• Relationship between DNA ploidy-related parameters and the deletions in mismatch repair genes MLH1 and MSH2 in lentigo maligna and malignant melanomas [20].
• Carney complex (CNC) is an autosomal dominant multiple endocrine neoplasia and lentiginosis syndrome characterised by spotty skin pigmentation, cardiac, skin, and breast myxomas, and a variety of endocrine and other tumours [21].
• Peutz-Jeghers syndrome (PJS, #175200) and Carney complex (CNC, OMIM#160980) are the two most common multiple neoplasia syndromes associated with lentiginosis [15].
• Further identification of HLA-G antigen expression in inflammatory infiltrating cells results in an overall frequency of HLA-G expressing cells that is higher in melanoma (28/79, 35.5%) than in naevi (5/60, 8.3%) or lentigo (2/23, 8.7%) [22].

Analytical, diagnostic and therapeutic context of Lentigo

• Immunohistochemical staining of lentigo maligna during Mohs micrographic surgery using MART-1 [23].
• The familial lentiginoses, as these syndromes are collectively known, include Carney complex, the LEOPARD and Peutz-Jeghers syndromes, and the newly described 'syndrome of arterial dissections with lentiginosis'; isolated, familial lentiginosis has also been described [24].

References