ArticleBioMed research international2015
Low mutational burden of eight genes involved in the MAPK/ERK, PI3K/AKT, and GNAQ/11 pathways in female genital tract primary melanomas.
Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Vulvar Melanoma: Molecular Characteristics, Diagnosis, Surgical Management, and Medical Treatment.American journal of clinical dermatology · 2021Review
- Clinical Implications of Acquired BRAF Inhibitors Resistance in Melanoma.International journal of molecular sciences · 2020Review
- The mutational landscape of mucosal melanoma.Seminars in cancer biology · 2020Review
- Predictive biomarkers and tumor microenvironment in female genital melanomas: a multi-institutional study of 55 cases.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020Article
- Targeting the ERK Signaling Pathway in Melanoma.International journal of molecular sciences · 2019Review
- Female genitourinary tract melanoma: mutation analysis with clinicopathologic correlation: a single-institution experience.Melanoma research · 2018Article
- Targeted next generation sequencing of mucosal melanomas identifies frequent NF1 and RAS mutations.Oncotarget · 2017Article
- Nonoverlapping Clinical and Mutational Patterns in Melanomas from the Female Genital Tract and Atypical Genital Nevi.The Journal of investigative dermatology · 2016Review
- Feasibility of Carbon Ion Radiotherapy in the Treatment of Gynecological Melanoma.In vivo (Athens, Greece)Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mucosal melanomas exhibit discrete genetic features compared to cutaneous melanoma. Limited studies on gynecological melanomas revealed significant heterogeneity and low mutational burden. To gain further insight into their genetics and DNA repair efficiency, we systematically investigated the status of eight genes whose products are critically involved in the MAPK/ERK, PI3K/AKT, and GNAQ/11 pathways, including BRAF, NRAS, HRAS, KRAS, c-KIT, PI3K, GNAQ, and GNA11, in a series of 16 primary gynecological melanomas, covering all anatomical locations, ranging from stages I to III. Analysis either by real-time PCR coupled with fluorescence melting curve analysis or by PCR followed by direct sequencing, along with studies for DNA mismatch repair status using immunohistochemistry, disclosed that 15 out of the 16 cases displayed wild-type genotypes, with a single case of vulvar primary melanoma, harboring the activating mutation BRAF(V600E). Investigations on whether this could reflect partly an efficient mismatch repair (MMR) mechanism were confirmed by normal expression of hMLH1 and hMSH2, suggesting that the lack of mutations could be explained by the operation of alternative pathogenetic mechanisms modulating downstream effectors of the signaling pathways. Our data suggest the presence of additional genetic components and provide the impetus for systematic approaches to reveal these yet unidentified genetic parameters.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.