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Benign Melanocytic Lesions
Published in Ashfaq A Marghoob, Ralph Braun, Natalia Jaimes, Atlas of Dermoscopy, 2023
Natalia Jaimes, Ashfaq A. Marghoob
Congenital melanocytic nevi (CMN) develop as a result of mutations acquired during embryogenesis (8), and these nevi are clinically visible on the skin of 1% to 2% of newborns (1). However, at least 6% of the population harbor melanocytic nevi displaying the characteristic morphologic features associated with CMN. While some of these so-called congenital nevus–like nevi (CNLN) may result from postnatally acquired mutations, some may be tardive CMN (6). These tardive CMN are presumed to be due to mutations that are determined in utero, but for unknown reasons, the nevi do not become clinically manifest until months to years after birth. It is possible that some of these tardive CMN may initially be present as small incipient nevus nests in the skin, and these nevus clusters may proliferate at some point in life and grow large enough to become clinically apparent (14). Another hypothesis is that some tardive CMN may initially lack the ability to form melanin, and only after the induction of melanogenesis do they become visible on the skin.
Benign Neoplasms
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Abdullah Demirbaş, Ömer Faruk Elmas, Necmettin Akdeniz
Definition: Congenital nevi appear at birth and are caused by benign melanocyte proliferation in the dermis, epidermis, or both. Occasionally, nevi that are not present at birth but are histologically similar to congenital nevi may develop within the first 2 years of life. Tardive congenital nevus is the term for this condition.
Genetics and optical coherence tomography features in a child with an achromatic retinal patch
Published in Ophthalmic Genetics, 2022
Noy Ashkenazy, Nicolas A. Yannuzzi, Audina M. Berrocal
The differential diagnosis for a flat, hypopigmented retinal lesion in a pediatric patient includes congenital hypertrophy of the retinal pigment epithelium (CHRPE), amelanotic congenital nevus, astrocytic hamartoma, and an achromatic, or achromic, retinal patch. A CHRPE would generally be hyperpigmented, and a congenital nevus would be confined to the choroid (4). Linear RPE and outer retinal abnormalities in pediatric patients with hypotony have been described after glaucoma drainage implantation, but do not fit the current clinical scenario (8). The seizure history raised concern for a retinal manifestation of a systemic disorder, such as TS. An astrocytic hamartoma generally arises from the nerve fiber layer (NFL), which was not seen in this case (9). Findings were most consistent with an achromatic retinal patch, which has a known association with tuberous sclerosis and has not been described in any other diseases (2–4,6,10,11).
Novel insights into the pathogenesis and treatment of NRAS mutant melanoma
Published in Expert Review of Precision Medicine and Drug Development, 2021
Jeffrey Zhao, Carlos Galvez, Kathryn Eby Beckermann, Douglas B. Johnson, Jeffrey A Sosman
Though canonical driver [44] mutations in NRAS are causally related to tumor formation in model systems, the development of human cutaneous melanoma from normal skin and precursor lesions is multifactorial. Human melanomas featuring these mutations arise in a complex series of steps at the intersection of environmental risk factors including UV exposure as well as germline genetic variants. Sun exposure (from chronic intermittent environmental sources) has been shown to be the major environmental risk factor for WHO pathway I–III melanomas (including superficial spreading, lentigo maligna, desmoplastic histologic subtypes) and nodular melanomas [45]. The role of UV radiation in NRAS-mutant melanoma pathogenesis is complex, as sun damage does not appear to be a requirement for the development of genetic alterations at the NRAS locus as demonstrated by the presence of these mutations in acral and mucosal subtypes as well as melanomas arising in a congenital nevus (WHO V, VI, and VII). Non-sun exposed melanomas – including acral lentiginous melanomas – also harbor NRAS mutations but less frequently than sun-associated melanomas [46]. For UV-associated melanomas, irradiation appears to mediate base pair mutagenesis in-vitro and in-vivo within the confines of the NRAS gene. UV exposure produces signature cyclobutane pyrimidine dimers at codons 12, 13, and 61. Compared to the heterogeneity of UV signature mutations seen at other loci including TP53, CDKN2A (p16INK4A) and PTEN/MMAC1, UV-associated lesions that fall within NRAS are positioned in a highly stereotypical manner at just a few genomic hot spots [1]. Interactions between UV exposure and tumor genetic background appear to be codon-specific, with transgenic NRASQ61R but not NRASG12D mice developing increased rates of tumor formation after UV treatment [47].
Efficacy of 1064-nm Nd:YAG picosecond laser in lichen amyloidosis treatment: clinical and dermoscopic evaluation
Published in Journal of Cosmetic and Laser Therapy, 2021
Suparuj Lueangarun, Therdpong Tempark
Rather than using biophysical evaluation, our study evaluated the efficacies of 1,064 nm ps-Nd:YAG laser in the treatment of LA from clinical, patient satisfaction, itching score, and dermoscopic evaluation. To our knowledge, there has been no study of LA treated with 1,064 nm ps-Nd:YAG laser. Nonetheless, Picosecond lasers (ps-lasers) are used for treatment of various pigmented lesions, such as nevus of Ito, congenital nevus, nevus spilus, nevus of Ota, Hori’s macules, café-au-lait patches, lentigines, and Becker nevus, with promising results (14).