ArticleActa neuropathologica communications2014
Experimental treatment of NRAS-mutated neurocutaneous melanocytosis with MEK162, a MEK-inhibitor.
Article in Acta neuropathologica communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 61 citations in OpenAlex.
- Precision Medicine in Dermatology: MEK Inhibition and MAPK Pathway Modulation for Congenital Melanocytic Nevi.Biomedicines · 2026Review
- Efficacy of azacitidine and trametinib against leptomeningeal melanosis associated with congenital melanocytic nevus syndrome.Molecular and cellular pediatrics · 2026Review
- Prenatal Fetal Neurocutaneous Melanosis: A Case Report and Literature Review.Molecular genetics & genomic medicine · 2026Review
- Congenital melanocytic neoplasms: clinical, histopathological and recent molecular developments.Virchows Archiv : an international journal of pathology · 2025Review
- Review
- Missense mutation of NRAS is associated with malignant progression in neurocutaneous melanosis.Acta neuropathologica communications · 2024Article
- Neurocutaneous melanosis with an intracranial cystic-solid meningeal melanoma in an adult: A case report and review of literature.World journal of clinical cases · 2022Article
- Novel Insights into Diagnosis, Biology and Treatment of Primary Diffuse Leptomeningeal Melanomatosis.Journal of personalized medicine · 2021Article
- Symptomatic neurocutaneous melanosis: mild clinical onset in a teenager.BMJ case reports · 2020Review
- Conjunctival Melanoma in Childhood and Adolescence: A Systematic Review.Ocular oncology and pathology · 2019Review
- Immune synapses between mast cells and γδ T cells limit viral infection.The Journal of clinical investigation · 2019Article
- MEK1/2 as a Therapeutic Target in Sickle Cell Disease.International journal of blood research and disorders · 2019Article
- Tumor-specific hepatic stellate cells (tHSCs) induces DIgR2 expression in dendritic cells to inhibit T cells.Oncotarget · 2017Article
- The preclinical assessment of XL388, a mTOR kinase inhibitor, as a promising anti-renal cell carcinoma agent.Oncotarget · 2017Article
- MEK inhibition appears to improve symptom control in primary NRAS-driven CNS melanoma in children.British journal of cancer · 2017Article
- NRAS(Q61K) mutated primary leptomeningeal melanoma in a child: case presentation and discussion on clinical and diagnostic implications.BMC cancer · 2016Article
- The Antipancreatic Cancer Activity of OSI-027, a Potent and Selective Inhibitor of mTORC1 and mTORC2.DNA and cell biology · 2015Article
- Updates on Psoriasis and Cutaneous Oncology: Proceedings from the 2015 MauiDerm Meeting.The Journal of clinical and aesthetic dermatology · 2015Article
- Acute Inhibition of MEK Suppresses Congenital Melanocytic Nevus Syndrome in a Murine Model Driven by Activated NRAS and Wnt Signaling.The Journal of investigative dermatology · 2015Article
- Combination treatment with perifosine and MEK-162 demonstrates synergism against lung cancer cells in vitro and in vivo.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurocutaneous melanosis (NCM) is a rare congenital disorder characterized by the association of large and/or multiple congenital melanocytic nevi (CMN) of the skin with melanocytic lesions of the leptomeninges, including melanocytosis. Leptomeningeal melanocytosis carries a poor prognosis once neurological symptoms develop. Despite surgery, which is often not radical, few other treatment options exist. Recently, it was demonstrated that early embryonic, post-zygotic somatic mutations in the NRAS gene are implicated in the pathogenesis of NCM.In this report, we present a 13-year-old boy with NCM and progressive symptomatic leptomeningeal melanocytosis. A somatic NRASQ61K mutation was present in both CMN as well as the melanocytosis. Despite repeated surgery, the patient showed clinical progression. Therefore, treatment with MEK162, a MEK inhibitor, was started on compassionate use base. The patient died only five days later, i.e. too early to expect a clinical effect of MEK162 therapy. We therefore studied the effect of MEK162 at the protein level in the leptomeningeal tumor by immunohistochemical and Western Blot analyses using Ki67 and pERK antibodies. We observed lower MIB-1 expression and lower pERK expression in the post-treatment samples compared to pre-treatment, suggesting a potential effect of MEK inhibiting therapy. Further studies are needed to determine whether MEK inhibitors can effectively target NRAS-mutated symptomatic NCM, a rare but potentially fatal disease.
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