ArticleHuman pathology2017
Mutation of NRAS is a rare genetic event in ovarian low-grade serous carcinoma.
Article in Human pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 26 citations in OpenAlex.
- Review
- An Analysis of Genetic Polymorphisms in 76 Genes Related to the Development of Ovarian Tumors of Different Aggressiveness.International journal of molecular sciences · 2024Article
- Eosinophilic Cells in Ovarian Borderline Serous Tumors as a Predictor of BRAF Mutation.Cancers · 2024Article
- Low-grade serous ovarian cancer: expert consensus report on the state of the science.International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · 2023Article
- KRAS mutation in primary ovarian serous borderline tumors correlates with tumor recurrence.Virchows Archiv : an international journal of pathology · 2023Article
- MicroRNAs miR-451a and Let-7i-5p Profiles in Circulating Exosomes Vary among Individuals with Different Sickle Hemoglobin Genotypes and Malaria.Journal of clinical medicine · 2022Article
- Role of RAS signaling in ovarian cancer.F1000Research · 2022Review
- Aberrant MAPK Signaling Offers Therapeutic Potential for Treatment of Ovarian Carcinoma.OncoTargets and therapy · 2022Review
- Loss of 1p36.33 Frequent in Low-Grade Serous Ovarian Cancer.Neoplasia (New York, N.Y.) · 2019Article
- Markers of MEK inhibitor resistance in low-grade serous ovarian cancer: EGFR is a potential therapeutic target.Cancer cell international · 2019Article
- Testing forDisease markers · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Activating mutations involving the members of the RAS signaling pathway, including KRAS, NRAS, and BRAF, have been reported in ovarian low-grade serous carcinoma and its precursor lesion, serous borderline tumor (SBT). Whether additional genetic alterations in the RAS oncogene family accumulate during the progression of SBT to invasive low-grade serous carcinoma (LGSC) remains largely unknown. Although mutations of KRAS and BRAF occur at a very early stage of progression, even preceding the development of SBT, additional driving events, such as NRAS mutations, have been postulated to facilitate progression. In this study, we analyzed NRAS exon 3 mutational status in 98 cases that were diagnosed with SBT/atypical proliferative serous tumor, noninvasive LGSC, or invasive LGSC. Of the latter, NRAS Q61R (CAA to CGA) mutations were detected in only 2 of 56 (3.6%) cases. The same mutation was not detected in any of the SBTs (atypical proliferative serous tumors) or noninvasive LGSCs. Mutational analysis for hotspots in KRAS and BRAF demonstrated a wild-type pattern of KRAS and BRAF in one of the NRAS-mutated cases. Interestingly, another LGSC case with NRAS mutation harbored a concurrent BRAF V600L mutation. These findings indicate that, although recurrent NRAS mutations are present, their low prevalence indicates that NRAS plays a limited role in the development of LGSC. Further studies to identify other oncogenic events that drive LGSC progression are warranted.
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