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Melanocytic nevus

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qurrat-ul-ain Abid, M.D.[2] Martin I. Newman, M.D., F.A.C.S. [3]; Michel C. Samson, M.D., FRCSC, FACS [4]; Faizan Sheraz, M.D. [5] Roukoz A. Karam, M.D.[6]

Synonyms and keywords: Pigmented nevus, benign nevi, melanocytic nevus, moles, dysplastic nevus, dysplastic atypical nevus, atypical nevus, acquired melanocytic nevus.

Overview

Overview

Editors-In-Chief: Martin I. Newman, M.D., FACS, Cleveland Clinic Florida, [1]; Michel C. Samson, M.D., FRCSC, FACS [2]

Overview

A mole, technically known as a melanocytic nevus, is a small, dark spot on human skin. According to the American Academy of Dermatology, the majority of moles appear during the first two decades of a person’s life while about one in every 100 babies are born with moles. Acquired moles are a form of benign neoplasm, while congenitalmoles are considered a minor malformation, or hamartoma. A mole can be either subdermal (composed of melanin), or a pigmented growth on the skin, formed mostly of a type of cell known as melanocytes. The high concentration of the body’s pigmenting agent, melanin, is responsible for their dark color. Moles are a member of the family of skin lesions known as nevi.

Historical Perspective

At one time in the 1950s and 60s, (and, to lesser extent, currently) a mole was known as a “beauty mark” when it appeared in certain spots on a woman’s face. Examples include Marilyn Monroe, model Cindy Crawford and singer Madonna. Madonna’s facial mole — below her right nostril — has been surgically removed.

Classification

Melanocytic nevus is a type of melanocytic lesion. Depending on the degree of cytologic atypia it can be classified into mild, moderate or severe.

Pathophysiology

Melanocytic nevus is a benign growth on the skin (usually tan, brown, or flesh-colored) that contains a cluster of melanocytes and surrounding supportive tissue.

Causes

Scientists suspect that overexposure to ultraviolet light, including excessive sunlight, may play a role in the formation of acquired moles.[1] However, more research is needed in this area.

Differentiating Melanocytic Nevus from Other Diseases

Melanocytic nevus must be differentiate from dysplastic nevus, melanoma and epidermal nevus.

Epidemiology and Demographics

Darker skin shades tend to have fewer moles compared to fair complexion.

Risk Factors

Most important risk factor for melanocytic nevus is sunlight however, genetic predisposition is an important factor as well.

Natural History, Complications, and Prognosis

Vast majority of moles are benign. Nonetheless, the National (U.S.) Cancer Institute reported 59,940 new cases of melanoma by June, 2007, with 8,110 deaths.[2]

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Medical Therapy

Surgery

If a mole is highly suspicious of being a melanoma, then it might need to be removed and biopsied (microscopic evaluation by a pathologist). Other reasons for removal may be cosmetic, or because a raised mole interferes with daily living (e.g. shaving).

Moles can be removed by laser, surgery or electrocautery. They leave a red mark on the site which morphs back to the patient’s usual skin color in about two weeks. However, there might still be a risk of spread of the melanoma, so the methods of Melanoma diagnosis, including e.g. excitional biopsy.


References

  1. ↑ Arne van Schanke, Gemma M.C.A.L. van Venrooij, Marjan J. Jongsma, H. Alexander Banus, Leon H.F. Mullenders, Henk J. van Kranen and Frank R. de Gruijl. Induction of Nevi and Skin Tumors in Ink4a/ArfXpa Knockout Mice by Neonatial, Intermittent, or Chronic UVB Exposures. Cancer Res 2006; 66 (5), 2608-15.
  2. ↑ http://www.nci.nih.gov/cancertopics/types/melanoma


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Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: : Qurrat-ul-ain Abid, M.D.[2]; Roukoz A. Karam, M.D.[3]

Overview

Dysplastic nevus was first discovered by Clark and his colleagues in 1978.

Historical Perspective

  • Dysplastic nevus was first discovered by Clark and his colleagues in 1978.[1]
  • The name ‘dysplastic nevus’ was proposed since they are benign melanocytic nevi that include cytologic atypia, similar to dysplastic lesions of other organs, such as the cervix.[2]
  • At one time in the 1950s and 60s, (and, to lesser extent, currently) a mole was known as a “beauty mark” when it appeared in certain spots on a woman’s face. Examples include Marilyn Monroe, model Cindy Crawford and singer Madonna. Madonna’s facial mole — below her right nostril — has been surgically removed.

References

  1. ↑ Clark WH, Reimer RR, Greene M, Ainsworth AM, Mastrangelo MJ (1978). “Origin of familial malignant melanomas from heritable melanocytic lesions. ‘The B-K mole syndrome‘“. Arch Dermatol. 114 (5): 732–8. PMID 646394.
  2. ↑ Elder DE, Goldman LI, Goldman SC, Greene MH, Clark WH (1980). “Dysplastic nevus syndrome: a phenotypic association of sporadic cutaneous melanoma”. Cancer. 46 (8): 1787–94. doi:10.1002/1097-0142(19801015)46:8<1787::aid-cncr2820460816>3.0.co;2-s. PMID 7427881.


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Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: ; Roukoz A. Karam, M.D.[2]

Overview

Melanocytic nevus is a type of melanocytic lesion. Depending on the degree of cytologic atypia it can be classified into mild, moderate or severe.

Classification

Most dermatologists and dermatopathologists use a system devised by the National Institutes of Health (NIH) for classifying melanocytic lesions. In this classification, a nevus can be defined as benign, having atypia, or being a melanoma.

  • A benign nevus is read as (or understood as) having no cytologic or architectural atypia.
  • An atypical mole is read as having architectural atypia, and having (mild, moderate, or severe) cytologic (melanocytic) atypia.[1][2]

References

  1. ↑ Schanderdorf D, Kochs C, Livingstone E (2013). Handbook of Cutaneous Melanoma: A Guide to Diagnosis and Treatment. Springer.
  2. ↑ Mooi W, Krausz T (2007). Pathology of Melanocytic Disorders 2nd Ed. CRC Press.

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Pathophysiology

Pathophysiology


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Editors-In-Chief: Martin I. Newman, M.D., FACS, Cleveland Clinic Florida, [1];Associate Editor(s)-in-Chief: Qurrat-ul-ain Abid, M.D.[2] Michel C. Samson, M.D., FRCSC, FACS [3]

Overview

Melanocytic nevus is a benign growth on the skin (usually tan, brown, or flesh-colored) that contains a cluster of melanocytes and surrounding supportive tissue.

Pathophysiology

Congenital melanocytic nevi (CMN)

  • When melanocytic nevi are present at birth or within the first few months of life they are known as Congenital melanocytic nevi (CMN).
  • Congenital melanocytic nevi (CMN) are hamartomas lesions.
  • Small melanocytic nevi that appear during early childhood between three months and two years of age, resemble true CMN clinicaly and histologicaly and are known as “tardive CMN,” “early-onset nevi,” and “congenital nevus-like nevi.[1]
  • During embryogenesis clonal proliferations of benign melanocytes may give rise to melanocytic nevi.[2][3]
  • BRAF V600E mutations have a very high corelation with small congenital melanocytic nevi (CMN), acquired melanocytic nevi and cutaneous melanomas.[4][5]
  • While giant congenital melanocytic nevi (CMN) have somatic gain-of-function mutations in NRAS.[6][7]
  • Compared to acquired melanocytic nevi, CMN penetrate into deeper layers of dermis.[8]
  • Melanocytes in CMN follow pathyway of nerves and vessels and grow along adenxal structures (eg, hair follicles, sebaceous glands, eccrine ducts) and settle between collagen bundles in a single arrangement.[9][10]

Dermoscopic features of Congenital melanocytic nevi (CMN)

  • CMN and acquired melanocytic nevi appear as pigment network, aggregated globules, or diffuse homogeneous brown pigmentation on dermoscopy.[11]
  • Dermoscopic patterns that are commonly seen in CMN are:[12]
    • Reticular
    • Globular/cobblestoning
    • Homogenous
    • Or a mixture of these (ie, multicomponent)
  • CMN may exhibit exaggerated attributes on dermoscopy compared to acquired melanocytic nevi, they may show:[13][14][14]
    • Perifollicular hypopigmentation
    • Marked follicular structures
    • Skin hyperpigmentation
    • Hypertrichosis
    • Pigment changes surrounding follicles such as hypopigmentation

Proliferative nodules Melanocytic nevus

  • Benign melanocytic proliferations may occasionally appear within large or giant CMN.[15]
  • They may be congenital or develop in infancy or childhood.
  • They may grow rapidly with clinical characteristics of firmness or ulceration, in that case, a biopsy should be performed to eliminate melanoma.
  • Large, atypical melanocytes and mitoses may be present on microscopy that make it difficult to differentiate from Melanoma.
  • In case of difficulty in differentiating benign melanocytic proliferation from Melanoma on microscopy, an evaluation of an experienced doctor may be helpful. Other modalities of evaluation are comparative genomic hybridization or mass spectroscopy imaging proteomic analysis.[15][16]

Speckled lentiginous nevus (SLN)

  • CMN may appear as a hyperpigmented patch with, superimposed dark or brown macules and papules which is known as lentiginous nevus (SLN) or nevus spilus.
  • The “background” tan patch (café-au-lait macule-like) of an SLN is mostly present at birth or appear soon after birth, brown “spots” may appear in the lesions later.
  • SLN is of two types:[17][18]
    • With macular speckles
    • With papular and macular speckles

Acquired melanocytic nevi (moles)

  • Benign growth of a type of melanocyte known as a “nevus cell” is known as melanocytic nevi or mole.
  • Although both melanocytes and nevus cells produce the pigment melanin however Nevus cells are different from the Melanocytes due to the following characteristics:
    • Nevus cells have a tendency to cluster within the lower epidermis or dermis, while epidermal melanocyte tends to spread out in one group.
    • Nevus cells lack dendritic process
  • Appearance of moles may vary depending on their location in the skin:
    • Junctional nevi: melanocytes are at the dermal-epidermal junction.
    • Compound nevi, melanocytes are both at the dermal-epidermal junction and in the dermis.
    • Intradermal nevi, the nests of melanocytes are in the dermis.
    • Elevated and less pigmented nevi: migration of melanocytes from the dermal-epidermal junction into the dermis.

Predisposing factors for the development of acquired melanocytic nevi

  • Factors influencing to the development of all acquired nevi except blue and Spitz nevi are:[19][20][21]
    • Heredity, with a familial propensity to have many moles.[22]
    • Intense sun exposure during childhood. Other factors that may affect the development of acquired melanocytic nevi in children include lichen sclerosus, immunosuppression, chemotherapy, and endocrine disorders.[23][24][25]
    • Phenotypic attributes such as skin type, with more nevus in individuals with light skin. Dark skinned people have few nevi. Children with dark hair tend to have more moles compared to people with very fair skin and red hair. [24][21][26]

Complications of Melanocytic nevi

Melanoma

  • Melanoma may arise as a complication within congenital melanocytic nevi(CMN), the lifetime risk is lower than 1%.[2]
  • Melanoma arises at the dermal-epidermal junction, in giant CMN they may arise in the deeper layers.
  • In large or giant CMN, there is 2 to 5 percent lifetime risk of developing either cutaneous or extracutaneous melanoma.[27]
  • Half of the Melanoma may arise within the first five years of life.[28][29]
  • Early identification and assessment may be difficult in giant CMN, becuase of there subepidermal location in cutaneous melanomas.
  • Palpation of the lesion during physical exam may help in detecting deeper nodules.
  • Primary melanoma may arise in the central nervous system (CNS) or retroperitoneum.
  • Posterior axial giant CMN have the greateset risk of developing Melanomas, nevi of head and extrimities are less likely to develop melanomas.

Neurocutaneous melanosis

  • Rarely in CMN neurocutaneous melanosis(NCM) may arise, it is the growth of melanocytes in CNS and skin.
  • Neurocutaneous melanosis (NCM) includes leptomeningeal melanosis and CNS melanosis.[30]
  • NCM is diagnosed on MRI as it may stay asymptomatic or produce minimal symptoms.[28]
  • Symptomatic NCM has a poor prognosis with high mortality rate.[27]
  • Risk factors for NCM are:[31][32][33]
    • A large CMN >40 cm and in a posterior axial location
    • Multiple satellite nevi
    • Greater than two medium-sized CMN
  • According to a study CMN with >20 satellites had a fivefold increased risk for NCM compared with those with ≤20 satellites.[34]
  • NCM may cooccur with the structural abnormalities of CNS such as Dandy-Walker malformation/posterior fossa cysts, defects of the vertebrae or skull, and intraspinal lipomas.[34]
  • MRI with gadolinium contrast can pick NCM.[32]
  • Symptomatic NCM may present with hydrocephalus, seizures that may be consequence of intracranial hemorrhage, impaired cerebrospinal fluid circulation, spinal cord compression, or malignant transformation of the melanocytes.[35]
  • If symptomatic NCM have poor prognosis even with abscence of malignant changes.[36]

References

  1. ↑ Makkar HS, Frieden IJ (August 2002). “Congenital melanocytic nevi: an update for the pediatrician”. Curr. Opin. Pediatr. 14 (4): 397–403. PMID 12130901.
  2. ↑ 2.0 2.1 Tannous ZS, Mihm MC, Sober AJ, Duncan LM (February 2005). “Congenital melanocytic nevi: clinical and histopathologic features, risk of melanoma, and clinical management”. J. Am. Acad. Dermatol. 52 (2): 197–203. doi:10.1016/j.jaad.2004.07.020. PMID 15692463.
  3. ↑ Price HN, Schaffer JV (2010). “Congenital melanocytic nevi-when to worry and how to treat: Facts and controversies”. Clin. Dermatol. 28 (3): 293–302. doi:10.1016/j.clindermatol.2010.04.004. PMID 20541682.
  4. ↑ Ichii-Nakato N, Takata M, Takayanagi S, Takashima S, Lin J, Murata H, Fujimoto A, Hatta N, Saida T (September 2006). “High frequency of BRAFV600E mutation in acquired nevi and small congenital nevi, but low frequency of mutation in medium-sized congenital nevi”. J. Invest. Dermatol. 126 (9): 2111–8. doi:10.1038/sj.jid.5700366. PMID 16691193.
  5. ↑ Wu J, Rosenbaum E, Begum S, Westra WH (December 2007). “Distribution of BRAF T1799A(V600E) mutations across various types of benign nevi: implications for melanocytic tumorigenesis”. Am J Dermatopathol. 29 (6): 534–7. doi:10.1097/DAD.0b013e3181584950. PMID 18032947.
  6. ↑ Dessars B, De Raeve LE, Morandini R, Lefort A, El Housni H, Ghanem GE, Van den Eynde BJ, Ma W, Roseeuw D, Vassart G, Libert F, Heimann P (January 2009). “Genotypic and gene expression studies in congenital melanocytic nevi: insight into initial steps of melanotumorigenesis”. J. Invest. Dermatol. 129 (1): 139–47. doi:10.1038/jid.2008.203. PMID 18633438.
  7. ↑ Charbel C, Fontaine RH, Malouf GG, Picard A, Kadlub N, El-Murr N, How-Kit A, Su X, Coulomb-L’Hermine A, Tost J, Mourah S, Aractingi S, Guégan S (April 2014). “NRAS mutation is the sole recurrent somatic mutation in large congenital melanocytic nevi”. J. Invest. Dermatol. 134 (4): 1067–1074. doi:10.1038/jid.2013.429. PMID 24129063.
  8. ↑ Mark GJ, Mihm MC, Liteplo MG, Reed RJ, Clark WH (September 1973). “Congenital melanocytic nevi of the small and garment type. Clinical, histologic, and ultrastructural studies”. Hum. Pathol. 4 (3): 395–418. PMID 4756859.
  9. ↑ “Precursors to malignant melanoma. National Institutes of Health Consensus Development Conference Statement, Oct. 24-26, 1983”. J. Am. Acad. Dermatol. 10 (4): 683–8. April 1984. PMID 6715623.
  10. ↑ Kokta V, Hung T, Al Dhaybi R, Lugassy C, Barnhill RL (April 2013). “High prevalence of angiotropism in congenital melanocytic nevi: an analysis of 53 cases”. Am J Dermatopathol. 35 (2): 180–3. doi:10.1097/DAD.0b013e318260908c. PMID 22771898.
  11. ↑ Haliasos EC, Kerner M, Jaimes N, Zalaudek I, Malvehy J, Hofmann-Wellenhof R, Braun RP, Marghoob AA (2013). “Dermoscopy for the pediatric dermatologist part III: dermoscopy of melanocytic lesions”. Pediatr Dermatol. 30 (3): 281–93. doi:10.1111/pde.12041. PMID 23252411.
  12. ↑ Changchien L, Dusza SW, Agero AL, Korzenko AJ, Braun RP, Sachs D, Usman MH, Halpern AC, Marghoob AA (August 2007). “Age- and site-specific variation in the dermoscopic patterns of congenital melanocytic nevi: an aid to accurate classification and assessment of melanocytic nevi”. Arch Dermatol. 143 (8): 1007–14. doi:10.1001/archderm.143.8.1007. PMID 17709659.
  13. ↑ Seidenari S, Pellacani G, Martella A, Giusti F, Argenziano G, Buccini P, Carli P, Catricalà C, De Giorgi V, Ferrari A, Ingordo V, Manganoni AM, Peris K, Piccolo D, Pizzichetta MA (July 2006). “Instrument-, age- and site-dependent variations of dermoscopic patterns of congenital melanocytic naevi: a multicentre study”. Br. J. Dermatol. 155 (1): 56–61. doi:10.1111/j.1365-2133.2006.07182.x. PMID 16792752.
  14. ↑ 14.0 14.1 Ingordo V, Iannazzone SS, Cusano F, Naldi L (2006). “Dermoscopic features of congenital melanocytic nevus and Becker nevus in an adult male population: an analysis with a 10-fold magnification”. Dermatology (Basel). 212 (4): 354–60. doi:10.1159/000092286. PMID 16707885.
  15. ↑ 15.0 15.1 Phadke PA, Rakheja D, Le LP, Selim MA, Kapur P, Davis A, Mihm MC, Hoang MP (May 2011). “Proliferative nodules arising within congenital melanocytic nevi: a histologic, immunohistochemical, and molecular analyses of 43 cases”. Am. J. Surg. Pathol. 35 (5): 656–69. doi:10.1097/PAS.0b013e31821375ea. PMID 21436676.
  16. ↑ Lazova R, Yang Z, El Habr C, Lim Y, Choate KA, Seeley EH, Caprioli RM, Yangqun L (September 2017). “Mass Spectrometry Imaging Can Distinguish on a Proteomic Level Between Proliferative Nodules Within a Benign Congenital Nevus and Malignant Melanoma”. Am J Dermatopathol. 39 (9): 689–695. doi:10.1097/DAD.0000000000000849. PMC 5647999. PMID 28248717.
  17. ↑ Happle R (March 2009). “Speckled lentiginous naevus: which of the two disorders do you mean?”. Clin. Exp. Dermatol. 34 (2): 133–5. doi:10.1111/j.1365-2230.2008.02966.x. PMID 19040513.
  18. ↑ Schaffer JV, Orlow SJ, Lazova R, Bolognia JL (February 2001). “Speckled lentiginous nevus: within the spectrum of congenital melanocytic nevi”. Arch Dermatol. 137 (2): 172–8. PMID 11176689.
  19. ↑ Oliveria SA, Satagopan JM, Geller AC, Dusza SW, Weinstock MA, Berwick M, Bishop M, Heneghan MK, Halpern AC (January 2009). “Study of Nevi in Children (SONIC): baseline findings and predictors of nevus count”. Am. J. Epidemiol. 169 (1): 41–53. doi:10.1093/aje/kwn289. PMC 2720704. PMID 19001133.
  20. ↑ Aalborg J, Morelli JG, Mokrohisky ST, Asdigian NL, Byers TE, Dellavalle RP, Box NF, Crane LA (September 2009). “Tanning and increased nevus development in very-light-skinned children without red hair”. Arch Dermatol. 145 (9): 989–96. doi:10.1001/archdermatol.2009.193. PMC 2924169. PMID 19770437.
  21. ↑ 21.0 21.1 De Giorgi V, Gori A, Greco A, Savarese I, Alfaioli B, Grazzini M, Rossari S, Papi F, Scarfi F, Janowska A, D’Errico A, Salvati L, Covarelli P, Gandini S (October 2018). “Sun-Protection Behavior, Pubertal Development and Menarche: Factors Influencing the Melanocytic Nevi Development-The Results of an Observational Study of 1,512 Children”. J. Invest. Dermatol. 138 (10): 2144–2151. doi:10.1016/j.jid.2018.02.046. PMID 29614272.
  22. ↑ Orlow I, Satagopan JM, Berwick M, Enriquez HL, White KA, Cheung K, Dusza SW, Oliveria SA, Marchetti MA, Scope A, Marghoob AA, Halpern AC (April 2015). “Genetic factors associated with naevus count and dermoscopic patterns: preliminary results from the Study of Nevi in Children (SONIC)”. Br. J. Dermatol. 172 (4): 1081–9. doi:10.1111/bjd.13467. PMC 4382400. PMID 25307738.
  23. ↑ Dulon M, Weichenthal M, Blettner M, Breitbart M, Hetzer M, Greinert R, Baumgardt-Elms C, Breitbart EW (November 2002). “Sun exposure and number of nevi in 5- to 6-year-old European children”. J Clin Epidemiol. 55 (11): 1075–81. PMID 12507670.
  24. ↑ 24.0 24.1 Wiecker TS, Luther H, Buettner P, Bauer J, Garbe C (February 2003). “Moderate sun exposure and nevus counts in parents are associated with development of melanocytic nevi in childhood: a risk factor study in 1,812 kindergarten children”. Cancer. 97 (3): 628–38. doi:10.1002/cncr.11114. PMID 12548604.
  25. ↑ Harrison SL, MacLennan R, Buettner PG (September 2008). “Sun exposure and the incidence of melanocytic nevi in young Australian children”. Cancer Epidemiol. Biomarkers Prev. 17 (9): 2318–24. doi:10.1158/1055-9965.EPI-07-2801. PMID 18768500.
  26. ↑ Luther H, Altmeyer P, Garbe C, Ellwanger U, Jahn S, Hoffmann K, Segerling M (December 1996). “Increase of melanocytic nevus counts in children during 5 years of follow-up and analysis of associated factors”. Arch Dermatol. 132 (12): 1473–8. PMID 8961877.
  27. ↑ 27.0 27.1 Vourc’h-Jourdain M, Martin L, Barbarot S (March 2013). “Large congenital melanocytic nevi: therapeutic management and melanoma risk: a systematic review”. J. Am. Acad. Dermatol. 68 (3): 493–8.e1–14. doi:10.1016/j.jaad.2012.09.039. PMID 23182059.
  28. ↑ 28.0 28.1 Watt AJ, Kotsis SV, Chung KC (June 2004). “Risk of melanoma arising in large congenital melanocytic nevi: a systematic review”. Plast. Reconstr. Surg. 113 (7): 1968–74. PMID 15253185.
  29. ↑ Kinsler VA, Birley J, Atherton DJ (January 2009). “Great Ormond Street Hospital for Children Registry for congenital melanocytic naevi: prospective study 1988-2007. Part 1-epidemiology, phenotype and outcomes”. Br. J. Dermatol. 160 (1): 143–50. doi:10.1111/j.1365-2133.2008.08849.x. PMID 18811688.
  30. ↑ Foster RD, Williams ML, Barkovich AJ, Hoffman WY, Mathes SJ, Frieden IJ (April 2001). “Giant congenital melanocytic nevi: the significance of neurocutaneous melanosis in neurologically asymptomatic children”. Plast. Reconstr. Surg. 107 (4): 933–41. PMID 11252085.
  31. ↑ DeDavid M, Orlow SJ, Provost N, Marghoob AA, Rao BK, Wasti Q, Huang CL, Kopf AW, Bart RS (October 1996). “Neurocutaneous melanosis: clinical features of large congenital melanocytic nevi in patients with manifest central nervous system melanosis”. J. Am. Acad. Dermatol. 35 (4): 529–38. PMID 8859278.
  32. ↑ 32.0 32.1 Kinsler VA, Chong WK, Aylett SE, Atherton DJ (September 2008). “Complications of congenital melanocytic naevi in children: analysis of 16 years’ experience and clinical practice”. Br. J. Dermatol. 159 (4): 907–14. doi:10.1111/j.1365-2133.2008.08775.x. PMID 18671780.
  33. ↑ Lovett A, Maari C, Decarie JC, Marcoux D, McCuaig C, Hatami A, Savard P, Powell J (November 2009). “Large congenital melanocytic nevi and neurocutaneous melanocytosis: one pediatric center’s experience”. J. Am. Acad. Dermatol. 61 (5): 766–74. doi:10.1016/j.jaad.2008.11.022. PMID 19766348.
  34. ↑ 34.0 34.1 Marghoob AA, Dusza S, Oliveria S, Halpern AC (February 2004). “Number of satellite nevi as a correlate for neurocutaneous melanocytosis in patients with large congenital melanocytic nevi”. Arch Dermatol. 140 (2): 171–5. doi:10.1001/archderm.140.2.171. PMID 14967788.
  35. ↑ Di Rocco F, Sabatino G, Koutzoglou M, Battaglia D, Caldarelli M, Tamburrini G (January 2004). “Neurocutaneous melanosis”. Childs Nerv Syst. 20 (1): 23–8. doi:10.1007/s00381-003-0835-9. PMID 14576958.
  36. ↑ Schaffer JV, McNiff JM, Bolognia JL (2001). “Cerebral mass due to neurocutaneous melanosis: eight years later”. Pediatr Dermatol. 18 (5): 369–77. PMID 11737677.


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Causes

Causes

Editors-In-Chief: Martin I. Newman, M.D., FACS, Cleveland Clinic Florida, [1];Associate Editor(s)-in-Chief: Qurrat-ul-ain Abid, M.D.[2] Michel C. Samson, M.D., FRCSC, FACS [3]

Overview

Scientists suspect that overexposure to ultraviolet light, including excessive sunlight, may play a role in the formation of acquired moles. However, more research is needed in this area.

Causes

Dysplastic nevus arises from the epidermal melanocytes, which are neural crest cells involved in the synthesis of melanin (a brown pigment with photoprotective properties).

While melanoma may be caused by sporadic genetic mutations (e.g. BRAF and/or N-RAS) or may be part of familial syndromes.[1]

Sunlight

  • Some scientists suspect that overexposure to ultraviolet light, including excessive sunlight, may play a role in the formation of acquired moles.[2] However, more research is needed in this area.

Genes

  • Genes can also have an influence on a person’s moles.
  • Dysplastic nevi or atypical mole syndrome is a hereditary condition which causes the person to have a large number of moles (often 100 or more) with some larger than normal or atypical.
  • This often leads to a higher risk of melanoma, a serious skin cancer.[3]
  • A slight majority of melanomas do not form in an existing mole, but rather create a new growth on the skin. Nevertheless, those with more dysplastic nevi are at a higher risk of this type of melanoma occurrence.[4][5] Such persons need to be checked regularly for any changes in their moles and to note any new ones.

References

  1. ↑ O’Brien O, Lyons T, Murphy S, Feeley L, Power D, Heffron C (November 2017). “BRAF V600 mutation detection in melanoma: a comparison of two laboratory testing methods”. J. Clin. Pathol. 70 (11): 935–940. doi:10.1136/jclinpath-2017-204367. PMID 28424234. Vancouver style error: initials (help)
  2. ↑ Arne van Schanke, Gemma M.C.A.L. van Venrooij, Marjan J. Jongsma, H. Alexander Banus, Leon H.F. Mullenders, Henk J. van Kranen, and Frank R. de Gruijl. Induction of Nevi and Skin Tumors in Ink4a/ArfXpa Knockout Mice by Neonatal, Intermittent, or Chronic UVB Exposures. Cancer Res 2006; 66 (5), 2608-15.
  3. ↑ Burkhart, C.G MPH, MD. Dysplastic nevus declassified; even the NIH recommends elimination of confusing terminology. SKINmed: Dermatology for the Clinician 2(1):12-13, 2003.
  4. ↑ D.J. Pope, T. Sorahan, J.R. Marsden, P.M. Ball, R.P. Grimley, and I.M. Peck. Benign pigmented nevi in children. Arch of Dermatology 2006;142:1599-1604
  5. ↑ D.E. Goldgar, L.A. Cannon-Albright, L.J. Meyer, M.W. Pipekorn, J.J. Zone, M.H. Skolnick. Inheritance of Nevus Number and Size in Melanoma and Dysplastic Nevus Syndrome Kindreds. Journal of the National Cancer Institute 1991 83(23):1726-1733


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Differentiating Melanocytic Nevus from other Diseases

Differentiating Melanocytic Nevus from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qurrat-ul-ain Abid, M.D.[2]

Overview

Melanocytic nevus must be differentiated from a dysplastic nevus, epidermal nevus, and melanoma.

Differential diagnosis

Melanocytic nevus must be differentiated from several conditions including:

Diseases Skin examination Diagnosis Additional findings
Type Color Texture Size Distribution Dermoscopic Findings Histopathology
Cutaneous squamous cell carcinoma[1] SCC in situ (Bowen’s disease)
  • Scaly
  • Variable
  • Fair-skinned individuals: sun-exposed areas
Invasive squamous cell carcinoma
  • Skin colored
  • 0.5 to 1.5 cm
  • Fair-skinned individuals: sun-exposed areas
  • In black individuals: legs, anus, and areas of chronic inflammation
Keratoacanthoma[2]
  • 1 to 2.5 cm
Dermatofibroma[3][4]
  • Firm
  • 0.3- 1 cm
dermatofibrosarcoma protuberans[5][6]
  • Firm
  • 1-5 cm
Kaposi sarcoma[7][8]
  • Red/violaceous
  • Smooth
  • Rainbow pattern
  • scaly surface
  • Small brown globules
Merkel cell carcinoma[9]
  • Shiny
  • Flesh-colored or bluish-red
  • Firm
  • < 1 cm
  • Sun-exposed areas
  • Older individuals with light skin tones
  • Rapidly growing
Basal cell carcinoma[10] Nodular basal cell carcinoma
  • Flesh-colored
  • Variable
  • Focused, bright red, and branching arborizing vessels
  • Loosely arranged blue-gray dots
  • May have a “rolled” border
Superficial basal cell carcinoma
  • Scaly
  • 1 to > 10 cm
  • Sun-exposed areas
  • Head (cheek and nose)
  • Trunk
  • Large, hyperchromatic, oval nuclei
  • Minimal cytoplasm
  • Small basaloid nodules
Sclerosing basal cell carcinoma (morpheaform)[11]
  • Variable
  • Sun-exposed areas
Prurigo nodules[12][13]
  • Firm
  • Variable
Melanoma[14] Melanoma in situ (Lentigo Maligna)[15]
  • Variable (from light to dark brown, black, pink, red, or white)
  • Smooth
  • Around 1 cm
  • Asymmetric, pigmented follicular openings
  • Gray angulated lines
  • Gray areas, dots, and globules
  • Circle within a circle
Lentigo maligna melanoma[16]
  • Brown/tan
  • Variable
  • Asymmetric, pigmented follicular openings
  • Gray angulated lines
  • Gray areas, dots, and globules
  • Circle within a circle
  • Usually in older individuals
Superficial spreading melanoma[17]
  • Variably pigmented (red, blue, black, gray, and white)
  • Thin
  • 1 mm to > 1 cm
  • Asymmetry of shape
  • > 2 colors
  • Asymmetry of structures
Nodular melanoma[18][19]
  • Dark color
  • 6mm to > 1 cm
  • Two-thirds arise in normal skin, the rest in existing moles
  • Rapidly enlarging
Acral lentiginous melanoma[20]
  • Dark brown to black
  • Variable
  • Most common among dark skinned individuals
Amelanotic melanoma[21]
  • Around 6 mm
Common nevus[22][23]
  • 1 cm to > 20 cm
  • Also called Miescher nevus
Blue nevus[24]
  • Blue
  • Smooth
  • Variable
  • Structureless blue pigmentation
  • Structureless blue and white or blue and brown on some occasions
Spitz nevus[25][26] Nonpigmented Spitz nevus
  • Pink
  • Smooth
  • < 1 cm
Reed-like Spitz[27]
  • Smooth
  • < 1 cm
Solar lentigo[28]
  • Multiple spots
  • Brown
  • Smooth
  • Around 5mm
  • Associated with UV exposure and skin aging
Sebaceous hyperplasia[29]
  • Skin-colored to brownish
  • 2 – 6 mm
  • Structureless yellow to whitish center surrounded by short linear “crown vessels“
  • Usually in middle-aged or older patients
Lichen planus-like keratosis[30]
  • Gray to brown
  • Prominent
  • Variable
  • Appearance depends on stage of evolution

References

  1. ↑ Petter G, Haustein UF (2000). “Histologic subtyping and malignancy assessment of cutaneous squamous cell carcinoma”. Dermatol Surg. 26 (6): 521–30. PMID 10848931.
  2. ↑ Kwiek B, Schwartz RA (2016). “Keratoacanthoma (KA): An update and review”. J Am Acad Dermatol. 74 (6): 1220–33. doi:10.1016/j.jaad.2015.11.033. PMID 26853179.
  3. ↑ Lee, MiWoo; Lee, WooJin; Jung, JoonMin; Won, ChongHyun; Chang, SungEun; Choi, JeeHo; Moon, KeeChan (2015). “Clinical and histological patterns of dermatofibroma without gross skin surface change: A comparative study with conventional dermatofibroma”. Indian Journal of Dermatology, Venereology, and Leprology. 81 (3): 263. doi:10.4103/0378-6323.154795. ISSN 0378-6323.
  4. ↑ Mentzel, Thomas; Wiesner, Thomas; Cerroni, Lorenzo; Hantschke, Markus; Kutzner, Heinz; Rütten, Arno; Häberle, Michael; Bisceglia, Michele; Chibon, Frederic; Coindre, Jean-Michel (2012). “Malignant dermatofibroma: clinicopathological, immunohistochemical, and molecular analysis of seven cases”. Modern Pathology. 26 (2): 256–267. doi:10.1038/modpathol.2012.157. ISSN 0893-3952.
  5. ↑ Bernard, J.; Poulalhon, N.; Argenziano, G.; Debarbieux, S.; Dalle, S.; Thomas, L. (2013). “Dermoscopy of dermatofibrosarcoma protuberans: a study of 15 cases”. British Journal of Dermatology. 169 (1): 85–90. doi:10.1111/bjd.12318. ISSN 0007-0963.
  6. ↑ Acosta, Alvaro E.; Vélez, Catalina Santa (2017). “Dermatofibrosarcoma Protuberans”. Current Treatment Options in Oncology. 18 (9). doi:10.1007/s11864-017-0498-5. ISSN 1527-2729.
  7. ↑ Cesarman, Ethel; Damania, Blossom; Krown, Susan E.; Martin, Jeffrey; Bower, Mark; Whitby, Denise (2019). “Kaposi sarcoma”. Nature Reviews Disease Primers. 5 (1). doi:10.1038/s41572-019-0060-9. ISSN 2056-676X.
  8. ↑ Hu, S C-S; Ke, C-L K; Lee, C-H; Wu, C-S; Chen, G-S; Cheng, S-T (2009). “Dermoscopy of Kaposi’s sarcoma: Areas exhibiting the multicoloured ‘rainbow pattern‘“. Journal of the European Academy of Dermatology and Venereology. 23 (10): 1128–1132. doi:10.1111/j.1468-3083.2009.03239.x. ISSN 0926-9959.
  9. ↑ Albores-Saavedra J, Batich K, Chable-Montero F, Sagy N, Schwartz AM, Henson DE (2010). “Merkel cell carcinoma demographics, morphology, and survival based on 3870 cases: a population based study”. J Cutan Pathol. 37 (1): 20–7. doi:10.1111/j.1600-0560.2009.01370.x. PMID 19638070.
  10. ↑ Wolberink EA, Pasch MC, Zeiler M, van Erp PE, Gerritsen MJ (2013). “High discordance between punch biopsy and excision in establishing basal cell carcinoma subtype: analysis of 500 cases”. J Eur Acad Dermatol Venereol. 27 (8): 985–9. doi:10.1111/j.1468-3083.2012.04628.x. PMID 22759209.
  11. ↑ Wrone DA, Swetter SM, Egbert BM, Smoller BR, Khavari PA (1996). “Increased proportion of aggressive-growth basal cell carcinoma in the Veterans Affairs population of Palo Alto, California”. J Am Acad Dermatol. 35 (6): 907–10. PMID 8959949.
  12. ↑ Errichetti E, Piccirillo A, Stinco G (2015). “Dermoscopy of prurigo nodularis”. J Dermatol. 42 (6): 632–4. doi:10.1111/1346-8138.12844. PMID 25808786.
  13. ↑ Weigelt N, Metze D, Ständer S (2010). “Prurigo nodularis: systematic analysis of 58 histological criteria in 136 patients”. J Cutan Pathol. 37 (5): 578–86. doi:10.1111/j.1600-0560.2009.01484.x. PMID 20002240.
  14. ↑ Witt C, Krengel S (2010). “Clinical and epidemiological aspects of subtypes of melanocytic nevi (Flat nevi, Miescher nevi, Unna nevi)”. Dermatol Online J. 16 (1): 1. PMID 20137743.
  15. ↑ Connolly KL, Giordano C, Dusza S, Busam KJ, Nehal K (2019). “Follicular involvement is frequent in lentigo maligna: Implications for treatment”. J Am Acad Dermatol. 80 (2): 532–537. doi:10.1016/j.jaad.2018.07.071. PMC 6333487. PMID 30266559.
  16. ↑ Connolly KL, Giordano C, Dusza S, Busam KJ, Nehal K (2019). “Follicular involvement is frequent in lentigo maligna: Implications for treatment”. J Am Acad Dermatol. 80 (2): 532–537. doi:10.1016/j.jaad.2018.07.071. PMC 6333487. PMID 30266559.
  17. ↑ Argenziano G, Ferrara G, Francione S, Di Nola K, Martino A, Zalaudek I (2009). “Dermoscopy–the ultimate tool for melanoma diagnosis”. Semin Cutan Med Surg. 28 (3): 142–8. doi:10.1016/j.sder.2009.06.001. PMID 19782937.
  18. ↑ Argenziano G, Soyer HP, Chimenti S, Talamini R, Corona R, Sera F; et al. (2003). “Dermoscopy of pigmented skin lesions: results of a consensus meeting via the Internet”. J Am Acad Dermatol. 48 (5): 679–93. doi:10.1067/mjd.2003.281. PMID 12734496.
  19. ↑ Menzies, Scott W.; Moloney, Fergal J.; Byth, Karen; Avramidis, Michelle; Argenziano, Giuseppe; Zalaudek, Iris; Braun, Ralph P.; Malvehy, Josep; Puig, Susana; Rabinovitz, Harold S.; Oliviero, Margaret; Cabo, Horacio; Bono, Riccardo; Pizzichetta, Maria A.; Claeson, Magdalena; Gaffney, Daniel C.; Soyer, H. Peter; Stanganelli, Ignazio; Scolyer, Richard A.; Guitera, Pascale; Kelly, John; McCurdy, Olivia; Llambrich, Alex; Marghoob, Ashfaq A.; Zaballos, Pedro; Kirchesch, Herbert M.; Piccolo, Domenico; Bowling, Jonathan; Thomas, Luc; Terstappen, Karin; Tanaka, Masaru; Pellacani, Giovanni; Pagnanelli, Gianluca; Ghigliotti, Giovanni; Ortega, Blanca Carlos; Crafter, Greg; Ortiz, Ana María Perusquía; Tromme, Isabelle; Karaarslan, Isil Kilinc; Ozdemir, Fezal; Tam, Anthony; Landi, Christian; Norton, Peter; Kaçar, Nida; Rudnicka, Lidia; Slowinska, Monika; Simionescu, Olga; Di Stefani, Alessandro; Coates, Elliot; Kreusch, Juergen (2013). “Dermoscopic Evaluation of Nodular Melanoma”. JAMA Dermatology. 149 (6): 699. doi:10.1001/jamadermatol.2013.2466. ISSN 2168-6068.
  20. ↑ Phan A, Dalle S, Touzet S, Ronger-Savlé S, Balme B, Thomas L (2010). “Dermoscopic features of acral lentiginous melanoma in a large series of 110 cases in a white population”. Br J Dermatol. 162 (4): 765–71. doi:10.1111/j.1365-2133.2009.09594.x. PMID 19922528.
  21. ↑ Steglich RB, Meotti CD, Ferreira MS, Lovatto L, de Carvalho AV, de Castro CG (2012). “Dermoscopic clues in the diagnosis of amelanotic and hypomelanotic malignant melanoma”. An Bras Dermatol. 87 (6): 920–3. PMC 3699915. PMID 23197217.
  22. ↑ Witt C, Krengel S (2010). “Clinical and epidemiological aspects of subtypes of melanocytic nevi (Flat nevi, Miescher nevi, Unna nevi)”. Dermatol Online J. 16 (1): 1. PMID 20137743.
  23. ↑ Bauer J, Garbe C (2003). “Acquired melanocytic nevi as risk factor for melanoma development. A comprehensive review of epidemiological data”. Pigment Cell Res. 16 (3): 297–306. PMID 12753404.
  24. ↑ Granter SR, McKee PH, Calonje E, Mihm MC, Busam K (2001). “Melanoma associated with blue nevus and melanoma mimicking cellular blue nevus: a clinicopathologic study of 10 cases on the spectrum of so-called ‘malignant blue nevus‘“. Am J Surg Pathol. 25 (3): 316–23. PMID 11224601.
  25. ↑ Luo S, Sepehr A, Tsao H (2011). “Spitz nevi and other Spitzoid lesions part I. Background and diagnoses”. J Am Acad Dermatol. 65 (6): 1073–84. doi:10.1016/j.jaad.2011.04.040. PMC 3217183. PMID 22082838.
  26. ↑ Argenziano G, Agozzino M, Bonifazi E, Broganelli P, Brunetti B, Ferrara G; et al. (2011). “Natural evolution of Spitz nevi”. Dermatology. 222 (3): 256–60. doi:10.1159/000326109. PMID 21494025.
  27. ↑ Pedrosa AF, Lopes JM, Azevedo F, Mota A (2016). “Spitz/Reed nevi: a review of clinical-dermatoscopic and histological correlation”. Dermatol Pract Concept. 6 (2): 37–41. doi:10.5826/dpc.0602a07. PMC 4866625. PMID 27222770.
  28. ↑ Tanaka M, Sawada M, Kobayashi K (2011). “Key points in dermoscopic differentiation between lentigo maligna and solar lentigo”. J Dermatol. 38 (1): 53–8. doi:10.1111/j.1346-8138.2010.01132.x. PMID 21175756.
  29. ↑ Sato T, Tanaka M (2014). “Linear sebaceous hyperplasia on the chest”. Dermatol Pract Concept. 4 (1): 93–5. doi:10.5826/dpc.0401a16. PMC 3919849. PMID 24520522.
  30. ↑ Morgan MB, Stevens GL, Switlyk S (2005). “Benign lichenoid keratosis: a clinical and pathologic reappraisal of 1040 cases”. Am J Dermatopathol. 27 (5): 387–92. PMID 16148406.
Epidemiology and Demographics

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qurrat-ul-ain Abid, M.D.[2]

Overview

Darker skin shades tend to have fewer moles compared to fair complexion.

Epidemiology and demographics

Prevalence

  • The prevalence of congenital melanocytic nevi (CMN) in newborns is between 0.2 and 6% worldwide.[1]
  • The number of acquired moles among white children depends on the geographical area and sun exposure and its intensity.[2]

Age

  • According to the American Academy of Dermatology, the majority of moles appear during the first two decades of a person’s life. [3]

Race

  • Darker skin shades tend to have fewer moles.

Gender

  • Melanocytic nevi affect men and women equally.


References

  1. ↑ Ingordo V, Gentile C, Iannazzone SS, Cusano F, Naldi L (2007). “Congenital melanocytic nevus: an epidemiologic study in Italy”. Dermatology (Basel). 214 (3): 227–30. doi:10.1159/000099587. PMID 17377384.
  2. ↑ Valiukeviciene S, Miseviciene I, Gollnick H (May 2005). “The prevalence of common acquired melanocytic nevi and the relationship with skin type characteristics and sun exposure among children in Lithuania”. Arch Dermatol. 141 (5): 579–86. doi:10.1001/archderm.141.5.579. PMID 15897379.
  3. ↑ Gallagher RP, McLean DI (July 1995). “The epidemiology of acquired melanocytic nevi. A brief review”. Dermatol Clin. 13 (3): 595–603. PMID 7554507.
Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qurrat-ul-ain Abid, M.D.[2]

Overview

Most important risk factor for melanocytic nevus is sunlight however, genetic predisposition is an important factor as well.

Risk Factors

  • According to the American cancer society risk factors for melanocytic nevi are the following:[1]
    • Exposure to ultraviolet (UV) rays.
    • Genetic factors such as Dysplastic nevus syndrome (also known as familial atypical multiple mole melanoma syndrome, or FAMMM.
    • Fair skin, freckling, and light hair.
    • Family history of melanoma.
    • Personal history of melanoma or other skin cancers.
    • Having a weakened immune system.
    • Olde age
    • Male gender
    • Xeroderma pigmentosum

References

  1. ↑ “Risk Factors for Melanoma Skin Cancer”.
Screening

Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qurrat-ul-ain Abid, M.D.[2]

Overview

Presence of several melanocytic nevi is a strong risk factor for melanoma. Whole body nevus count can help in stratifying the high risk patients prone to developing malignant lesions.

Screening

  • Presence of several melanocytic nevi is a strong risk factor for melanoma.
  • In case of presence of numerous melanocytic nevi, one may perform whole body nevus count to identify at-risk patients.[1]
  • Two methods to count the nevus are used, whole body nevus count or the site-specific count.[2]

References

  1. ↑ Fariñas-Alvarez C, Ródenas JM, Herranz MT, Delgado-Rodríguez M (March 1999). “The naevus count on the arms as a predictor of the number of melanocytic naevi on the whole body”. Br. J. Dermatol. 140 (3): 457–62. PMID 10233266.
  2. ↑ Echeverría B, Bulliard JL, Guillén C, Nagore E (January 2014). “Indicators for the total number of melanocytic naevi: an adjunct for screening campaigns. Observational study on 292 patients”. Br. J. Dermatol. 170 (1): 144–9. doi:10.1111/bjd.12692. PMID 24443914.
Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editors-In-Chief: Martin I. Newman, M.D., FACS, Cleveland Clinic Florida, [1]; Associate Editor(s)-in-Chief: Qurrat-ul-ain Abid, M.D.[2]; Michel C. Samson, M.D., FRCSC, FACS [3]

Overview

Vast majority of moles are benign. Nonetheless, the National (U.S.) Cancer Institute reported 59,940 new cases of melanoma by June, 2007, with 8,110 deaths.[1]

Natural history of melanocytic nevi

Natural history of congenital melanocytic nevi

  • CMN grows as the child grows, with an approximate increase in size from infancy to adulthood in different regions of the body as follows:[2][3][4]
    • Head – 1.7-fold
    • Trunk and upper extremities – 2.8-fold
    • Lower extremities – 3.3-fold
  • CMN grows more quickly in early infancy.
  • In addition to changes in size, CMN may change in appearance.
  • Over the course f time CMN may change from flat, evenly pigmented patches to raised moles with a pebbly appearance, verrucous, or cerebriform surface, color may change from tan to darker, lighter, mottled, or uneven pigmentation.

Natural history of acquired melanocytic nevi

  • Common acquired melanocytic nevi start appearing within the first six months of life.[5][6]
  • Common acquired melanocytic nevi begin to appear after the first six months of life, increase in number during childhood and adolescence, reach a peak count in the third decade, and then slowly regress with age.
  • They may increase in number in childhood and adolescence, attaining maximum number in the third decade, and then slowly regress with age.[6][7]
  • Although a change in the appearance of nevus may raise suspicion for melanoma in adults, the ormal natural history of nevi in children and adolescents may include enlargement and elevation of nevi.[8]

Complications

Experts say that vast majority of moles are benign. Nonetheless, the National (U.S.) Cancer Institute reported 59,940 new cases of melanoma by June, 2007, with 8,110 deaths.[9]

References

  1. ↑ http://www.nci.nih.gov/cancertopics/types/melanoma
  2. ↑ Marghoob AA, Schoenbach SP, Kopf AW, Orlow SJ, Nossa R, Bart RS (February 1996). “Large congenital melanocytic nevi and the risk for the development of malignant melanoma. A prospective study”. Arch Dermatol. 132 (2): 170–5. PMID 8629825.
  3. ↑ Rhodes AR, Albert LS, Weinstock MA (January 1996). “Congenital nevomelanocytic nevi: proportionate area expansion during infancy and early childhood”. J. Am. Acad. Dermatol. 34 (1): 51–62. PMID 8543695.
  4. ↑ Ruiz-Maldonado R, Tamayo L, Laterza AM, Durán C (June 1992). “Giant pigmented nevi: clinical, histopathologic, and therapeutic considerations”. J. Pediatr. 120 (6): 906–11. PMID 1593350.
  5. ↑ Luther H, Altmeyer P, Garbe C, Ellwanger U, Jahn S, Hoffmann K, Segerling M (December 1996). “Increase of melanocytic nevus counts in children during 5 years of follow-up and analysis of associated factors”. Arch Dermatol. 132 (12): 1473–8. PMID 8961877.
  6. ↑ 6.0 6.1 Siskind V, Darlington S, Green L, Green A (March 2002). “Evolution of melanocytic nevi on the faces and necks of adolescents: a 4 y longitudinal study”. J. Invest. Dermatol. 118 (3): 500–4. doi:10.1046/j.0022-202x.2001.01685.x. PMID 11874490.
  7. ↑ Scope A, Dusza SW, Marghoob AA, Satagopan JM, Braga Casagrande Tavoloni J, Psaty EL, Weinstock MA, Oliveria SA, Bishop M, Geller AC, Halpern AC (August 2011). “Clinical and dermoscopic stability and volatility of melanocytic nevi in a population-based cohort of children in Framingham school system”. J. Invest. Dermatol. 131 (8): 1615–21. doi:10.1038/jid.2011.107. PMC 3136658. PMID 21562569.
  8. ↑ Scope A, Marchetti MA, Marghoob AA, Dusza SW, Geller AC, Satagopan JM, Weinstock MA, Berwick M, Halpern AC (October 2016). “The study of nevi in children: Principles learned and implications for melanoma diagnosis”. J. Am. Acad. Dermatol. 75 (4): 813–823. doi:10.1016/j.jaad.2016.03.027. PMC 5030195. PMID 27320410.
  9. ↑ http://www.nci.nih.gov/cancertopics/types/melanoma


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