ReviewBiomedicines2022
Chromosome Translocations, Gene Fusions, and Their Molecular Consequences in Pleomorphic Salivary Gland Adenomas.
Review in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Recent developments in salivary gland pathology after the WHO 2024 classification: new developments in existing entities and evolving new entities.Virchows Archiv : an international journal of pathology · 2026Review
- Article
- Challenges in the detection and assembly of virus integration structures in human genomes.Frontiers in oncology · 2026Review
- Peptide‑based therapeutics targeting the SLC39A14‑PIWIL2 fusion in hepatocellular carcinoma.Genomics & informatics · 2025Article
- Integrative diagnostic approach to salivary gland tumors: from clinical evaluation to molecularly targeted therapy.Virchows Archiv : an international journal of pathology · 2025Review
- Single-cell transcriptomics reveals cellular evolution underlying pleomorphic adenoma recurrence and malignant transformation.Scientific reports · 2025Article
- Comparative transcriptomics of salivary basal cell adenoma and adenocarcinoma sustain linear neoplastic evolution and intertumor heterogeneity: classification and biological implications.The Journal of pathology · 2025Article
- Bilateral synchronous salivary gland tumors: report of three cases.Diagnostic pathology · 2025Article
- Recurrent MDM2 Amplification in the Spectrum of HMGA2-Altered Pleomorphic Adenoma, Atypical Pleomorphic Adenoma and Carcinoma Ex Pleomorphic Adenoma.Head and neck pathology · 2025Article
- Pleomorphic adenoma of the lip: a case report and literature review.Journal of surgical case reports · 2025Article
- Cytological features of oncocytic pleomorphic adenoma of the salivary gland: Using the Milan classification system to report 3 patients.Molecular and clinical oncology · 2025Article
- The Transcriptomic and Gene Fusion Landscape of Pleomorphic Salivary Gland Adenomas.Genes, chromosomes & cancer · 2025Article
- Distinct copy number signatures between residual benign and transformed areas of carcinoma ex pleomorphic adenoma.Scientific reports · 2024Article
- Pleomorphic Parotid Adenoma in a Child Affected with Cri du Chat Syndrome: Clinical, Cytogenetic, and Molecular Analysis.International journal of molecular sciences · 2024Article
- FGFR1/2/3-rearranged carcinoma of the head and neck: expanded histological spectrum crossing path with high-risk HPV in the sinonasal tract.Histopathology · 2024Article
- Molecular pathology in diagnosis and prognostication of head and neck tumors.Virchows Archiv : an international journal of pathology · 2024Review
- Single-cell transcriptomic analysis uncovers the origin and intratumoral heterogeneity of parotid pleomorphic adenoma.International journal of oral science · 2023Article
Corrections and comments
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Authors and funding
11 authors at 8 institutions in 9 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Salivary gland tumors are a heterogeneous group of tumors originating from the major and minor salivary glands. The pleomorphic adenoma (PA), which is the most common subtype, is a benign lesion showing a remarkable morphologic diversity and that, upon recurrence or malignant transformation, can cause significant clinical problems. Cytogenetic studies of >500 PAs have revealed a complex and recurrent pattern of chromosome rearrangements. In this review, we discuss the specificity and frequency of these rearrangements and their molecular/clinical consequences. The genomic hallmark of PA is translocations with breakpoints in 8q12 and 12q13-15 resulting in gene fusions involving the transcription factor genes PLAG1 and HMGA2. Until recently, the association between these two oncogenic drivers was obscure. Studies of the Silver−Russel syndrome, a growth retardation condition infrequently caused by mutations in IGF2/HMGA2/PLAG1, have provided new clues to the understanding of the molecular pathogenesis of PA. These studies have demonstrated that HMGA2 is an upstream regulator of PLAG1 and that HMGA2 regulates the expression of IGF2 via PLAG1. This provides a novel explanation for the 8q12/12q13-15 aberrations in PA and identifies IGF2 as a major oncogenic driver and therapeutic target in PA. These studies have important diagnostic and therapeutic implications for patients with PA.
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