ArticleBMC cancer2015
Combined comparative genomic hybridization and transcriptomic analyses of ovarian granulosa cell tumors point to novel candidate driver genes.
Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Relevance of Molecular Pathology for the Diagnosis of Sex Cord-Stromal Tumors of the Ovary: A Narrative Review.Cancers · 2023Review
- Loss ofInternational journal of molecular sciences · 2022Article
- Transcriptomics and solid tumors: The next frontier in precision cancer medicine.Seminars in cancer biology · 2022Review
- Analysis of Non-Relapsed and Relapsed Adult Type Granulosa Cell Tumors Suggests Stable Transcriptomes during Tumor Progression.Current issues in molecular biology · 2022Article
- Adult-type granulosa cell tumor of the ovary: a FOXL2-centric disease.The journal of pathology. Clinical research · 2021Article
- FOXO1 mitigates the SMAD3/FOXL2Journal of translational medicine · 2021Article
- Review
- Whole Genome Analysis of Ovarian Granulosa Cell Tumors Reveals Tumor Heterogeneity and a High-Grade TP53-Specific Subgroup.Cancers · 2020Article
- Article
- Construction and Comprehensive Analyses of a METTL5-Associated Prognostic Signature With Immune Implication in Lung Adenocarcinomas.Frontiers in genetics · 2020Article
- FOXO1 Negates the Cooperative Action of FOXL2Journal of the Endocrine Society · 2019Article
- [Sex cord-stromal tumors of the ovary : Current aspects with a focus on granulosa cell tumors, Sertoli-Leydig cell tumors, and gynandroblastomas].Der Pathologe · 2019Review
- FOXL2C134W-Induced CYP19 Expression via Cooperation With SMAD3 in HGrC1 Cells.Endocrinology · 2018Article
- Ovarian Cancers: Genetic Abnormalities, Tumor Heterogeneity and Progression, Clonal Evolution and Cancer Stem Cells.Medicines (Basel, Switzerland) · 2018Review
- Integrated analysis of gene expression and copy number identified potential cancer driver genes with amplification-dependent overexpression in 1,454 solid tumors.Scientific reports · 2017Article
- Article
- The four and a half LIM domains 2 (FHL2) regulates ovarian granulosa cell tumor progression via controlling AKT1 transcription.Cell death & disease · 2016Article
- Article
- Molecular manipulation of keratin 8/18 intermediate filaments: modulators of FAS-mediated death signaling in human ovarian granulosa tumor cells.Journal of ovarian research · 2016Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOvarian granulosa cell tumors (GCTs) are the most frequent sex cord-stromal tumors. Several studies have shown that a somatic mutation leading to a C134W substitution in the transcription factor FOXL2 appears in more than 95% of adult-type GCTs. Its pervasive presence suggests that FOXL2 is the main cancer driver gene. However, other mutations and genomic changes might also contribute to tumor formation and/or progression.
methodsWe have performed a combined comparative genomic hybridization and transcriptomic analyses of 10 adult-type GCTs to obtain a picture of the genomic landscape of this cancer type and to identify new candidate co-driver genes.
resultsOur results, along with a review of previous molecular studies, show the existence of highly recurrent chromosomal imbalances (especially, trisomy 14 and monosomy 22) and preferential co-occurrences (i.e. trisomy 14/monosomy 22 and trisomy 7/monosomy 16q). In-depth analyses showed the presence of recurrently broken, amplified/duplicated or deleted genes. Many of these genes, such as AKT1, RUNX1 and LIMA1, are known to be involved in cancer and related processes. Further genomic explorations suggest that they are functionally related.
conclusionsOur combined analysis identifies potential candidate genes, whose alterations might contribute to adult-type GCT formation/progression together with the recurrent FOXL2 somatic mutation.
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