Activating <i>BRAF</i>
 mutations in eruptive melanocytic naevi

Sekulic, Aleksander; Colgan, Michael; Davis, Mark D.P.; DiCaudo, David J.; Pittelkow, Mark R.

doi:10.1111/j.1365-2133.2010.09989.x

Cited by 26 publications

(18 citation statements)

References 14 publications

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“…It is also well documented that nevi can enlarge or erupt de novo in large numbers under immunosuppresion. Such eruptive nevi also frequently have BRAF mutations and favor sun-exposed sites, indicating that the initiating mechanisms are identical to other acquired nevi (47). In a liver model, hepatocytes that became senescent due to oncogenic RAS were effectively eliminated by immune cells (48).…”

Section: Melanocytic Neoplasms Originating From Epithelial Melanocytesmentioning

confidence: 96%

The Molecular Pathology of Melanoma: An Integrated Taxonomy of Melanocytic Neoplasia

Bastian

2014

Annu. Rev. Pathol. Mech. Dis.

436

388

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Melanomas are comprised of multiple biologically distinct categories, which differ in cell of origin, age of onset, clinical and histologic presentation, pattern of metastasis, ethnic distribution, causative role of UV radiation, predisposing germ line alterations, mutational processes, and patterns of somatic mutations. Neoplasms are initiated by gain of function mutations in one of several primary oncogenes, typically leading to benign melanocytic nevi with characteristic histologic features. The progression of nevi is restrained by multiple tumor suppressive mechanisms. Secondary genetic alterations override these barriers and promote intermediate or overtly malignant tumors along distinct progression trajectories. The current knowledge about pathogenesis, clinical, histological and genetic features of primary melanocytic neoplasms is reviewed and integrated into a taxonomic framework.

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Section: Melanocytic Neoplasms Originating From Epithelial Melanocytesmentioning

confidence: 96%

The Molecular Pathology of Melanoma: An Integrated Taxonomy of Melanocytic Neoplasia

Bastian

2014

Annu. Rev. Pathol. Mech. Dis.

436

388

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“…The purpose of the study was to investigate the molecular mechanisms underlying the development of eruptive melanocytic nevi (EMN) in a white male patient receiving 2 years of 6-mercaptopurine (6-MP) therapy for ulcerative colitis [1]. Over the course of the 6-MP treatment, the patient experienced an explosive growth of >200 melanocytic lesions on intermittently sun-exposed body sites.…”

Section: Summary Of Methods and Resultsmentioning

confidence: 99%

Identification ofBRAFmutations in eruptive melanocytic nevi: new insights into melanomagenesis?

John

Smalley

2011

Expert Review of Anticancer Therapy

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Eruptive melanocytic nevi (EMN) is an unusual phenomenon characterized by the abrupt, simultaneous appearance of hundreds of melanocytic nevi on previously uninvolved sun-exposed skin. The mechanisms underlying this phenomenon are not well understood, but have been associated with both systemic immunosuppression and bullous dermatoses. The paper under evaluation brings new insight into the molecular events underlying EMN development in a patient receiving 6-mercaptopurine immunosuppressive therapy for ulcerative colitis. Sequencing of DNA from 20 eruptive nevi revealed the presence of BRAF V600E mutations in 85% of the lesions tested. The role of mutated BRAF in the initiation and progression of melanoma in conjunction with the strong correlation between nevus number and melanoma risk suggests the need for photoprotection in patients receiving thiopurine therapy. The study under evaluation further points to the possible interaction between environmental mutagens and UV radiation in the acquisition of BRAF mutations that may in turn increase the risk of melanoma development.

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“…It remains plausible that this systemic population of susceptible nevus progenitor cells was derived from a single cell. Supporting evidence includes a recent case report by Sekulic et al that demonstrated a BRAF V600E mutation in 17 of 20 eruptive nevi removed from a single patient who was being treated with 6-Mercaptopurine [21]. Although the authors interpreted their results to imply that treatment with this immunosuppressive agent increases mutational frequency, it is also possible that most of these nevi share a monoclonal origin.…”

Section: Supporting Evidencementioning

confidence: 98%

Nevogenesis: A Benign Metastatic Process?

2011

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It is generally accepted that cutaneous nevogenesis is a localized event that occurs exclusively in the dermis and/or epidermis. However, the discovery of nevocytes circulating in the peripheral blood suggests that other, more systemic, benign metastatic processes could also be involved. The theoretical role of lymphatic and hematogenous dissemination of loosely adherent, immature nevus progenitor cells in the development of nodal nevi and eruptive melanocytic nevi will be reviewed.

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Activating BRAF mutations in eruptive melanocytic naevi

Cited by 26 publications

References 14 publications

The Molecular Pathology of Melanoma: An Integrated Taxonomy of Melanocytic Neoplasia

The Molecular Pathology of Melanoma: An Integrated Taxonomy of Melanocytic Neoplasia

Identification ofBRAFmutations in eruptive melanocytic nevi: new insights into melanomagenesis?

Nevogenesis: A Benign Metastatic Process?

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