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A saliva-based surrogate associates with clinical outcome of oral potentially malignant disorders

ABSTRACT: The aim of this experiment was to identify the transcriptomic alterations and biological pathways associated with malignant transformation (MT) of oral potentially malignant disorders (OPMD) using RNA-sequencing (RNA-seq) analysis of tissues retrospectively collected in this study.

ORGANISM(S): Homo sapiens

PROVIDER: GSE305747 | GEO | 2026/08/16

REPOSITORIES: GEO

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Gene expression changes associated with malignant transformation of oral potentially malignant disorders

Project description:A large number of oral squamous cell carcinomas (OSCCs) are believed to be preceded by oral potentially malignant disorders (OPMD) that have an increased likelihood of malignant transformation compared to clinically normal mucosa. This study was performed to identify differentially expressed genes between OPMDs that underwent malignant transformation (MT) and those that did not, termed ‘non-transforming’ (NT) cases. Total RNA was extracted from formalin-fixed paraffin-embedded tissue biopsies of 20 OPMD cases with known clinical outcomes (10 MT vs. 10 NT). Samples were assessed for quantity, quality and integrity of RNA prior to sequencing. Analysis for differential gene expression between MT and NT was performed using statistical packages in R. Genes were considered to be significantly differentially expressed if the False Discovery Rate corrected p-value was < 0.05. RNA yield was variable but RNA purity was good (A260/A280 >1.90). Analysis of RNA-Sequencing outputs revealed 41 genes (34 protein-coding; 7 non-coding) that were significantly differentially expressed between MT and NT cases. The log2 fold change for the statistically significant differentially expressed genes ranged from -2.63 to 2.48, with 23 protein-coding genes being downregulated and 11 protein-coding genes being upregulated in MT cases compared to NT cases. Several candidate genes that may play a role in malignant transformation of OPMD have been identified. Experiments to validate these candidates are underway. It is anticipated that this work will contribute to better understanding of the aetiopathogenesis of OPMD and development of novel biomarkers.

2020-08-14 | GSE156208 | GEO

A saliva-based surrogate associates with clinical outcome of oral potentially malignant disorders

Project description:A saliva-based surrogate associates with clinical outcome of oral potentially malignant disorders

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Gene expression changes associated with malignant transformation of oral potentially malignant disorders

Project description:Gene expression changes associated with malignant transformation of oral potentially malignant disorders

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Transcriptomic analysis predicts the risk of progression of premalignant lesions in in human tongue.

Project description:The 5-year survival rate for patients with oral squamous cell carcinomas (SCC), including tongue SCC, has not significantly improved over the last several decades. Oral potentially malignant disorders (OPMD), including oral dysplasias, are oral epithelial disorders that can develop into oral SCCs. To identify molecular characteristics that might predict conversion of OPMDs to SCCs and guide treatment plans, we performed global transcriptomic analysis of human tongue OPMD (n=9) and tongue SCC (n=11) samples with paired normal margin tissue from patients treated at Weill Cornell Medicine. Compared to margin tissue, SCCs showed more transcript changes than OPMDs. OPMDs and SCCs shared some altered transcripts, but these changes were generally greater in SCCs than OPMDs. Both OPMDs and SCCs showed altered signaling pathways related to cell migration, basement membrane disruption, and metastasis. We suggest that OPMDs were on the path towards malignant transformation. Based in patterns of gene expression, both OPMD samples and SCC samples can be categorized into subclasses (mesenchymal, classical, basal, and atypical) similar to those seen in human head and neck SCC (HNSCC). These subclasses of OPMDs the potential to be used to stratify patient prognosis and therapeutic options for tongue OPMDs. Lastly, we developed Firth logistic regression models to classify OPMDs and SCCs using a signature gene set ELF5, RPTN, IGSF10, HTR3A, and CRMP1, and this predictive model is amenable to testing as data sets become available. We suggest that changes in these five transcripts relative to paired normal tissue could be used to predict of the likelihood of an OPMD developing into a SCC.

2023-10-08 | GSE202048 | GEO

Predicting the clinical outcome of oral potentially malignant disorders using transcriptomic-based molecular pathology.

Project description: Not available

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Porphyromonas gingivalis in saliva associates with chronic and aggressive periodontitis.

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Histopathology of the tongue in a mouse model of oculopharyngeal muscular dystrophy reveals progressive PABPN1 deposition associated with muscle wasting.

Project description:The tongue facilitates vital activities such as swallowing. Swallowing difficulties (dysphagia) are common in the elderly and in many adult-onset neuromuscular diseases. In oculopharyngeal muscular dystrophy (OPMD), dysphagia is often the first symptom. OPMD is an autosomal dominant myopathy caused by a trinucleotide expansion mutation in the gene encoding PABPN1. The expanded PABPN1 forms insoluble nuclear aggregates that reduce the levels of the soluble form. Clinical tongue involvement in OPMD has been documented but is poorly understood. Tongue histopathology was investigated in OPMD mouse models using light and electron microscopy. Muscle histopathology was predominantly affected by age. PABPN1 nuclear aggregates were found at moderate levels, whereas deposition of insoluble PABPN1 in blood vessels was already prominent in 4-month-old mice. RNA signatures of the OPMD tongue were enriched for mitochondrial and cytoskeletal genes, suggesting an energy and contractile deficit.

2024-12-04 | GSE263433 | GEO

Saliva metabolomic profile of COVID-19 patients associates with disease severity.

Project description: Not available

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Fanconi anemia: matrix remodeling and oral carcinogenesis

Project description:Fanconi anemia (FA) increases the risk of early-onset oral potentially malignant disorders (OPMD) and oral squamous cell carcinoma; however, the earliest stromal determinants of malignant progression remain undefined. We investigated whether extracellular matrix (ECM) remodeling constitutes an initial and quantifiable hallmark of FA-associated OPMD. A total of 119 participants were included: controls with normal mucosa or oral leukoplakia (OL) and individuals with FA. Histopathology, immunohistochemistry (p53, Ki-67, α-SMA, elastin), picrosirius red staining, and multiphoton microscopy combining second-harmonic generation and two-photon fluorescence were performed, complemented by salivary and transcriptomic profiling. Additionally, FANCA/p53EPI and p53 murine models were used to assess stromal remodeling. Compared with sporadic OL, FA-OL exhibited reduced collagen density and elastin autofluorescence, higher collagen-to-elastin ratio, and diminished p53 expression. Salivary procollagen type 1 N-terminal propeptide declined and correlated with matrix-derived optical parameters. RNA sequencing revealed upregulated ECM structural genes and downregulated ECM regulators in FA patients. In FA-mimicking mice, collagen and elastin signals progressively decreased. Collectively, multimodal imaging and transcriptomic data unveil ECM disruption as a defining feature of FA-OL. Matrix disorganization, coupled with epithelial p53 loss delineates a permissive stromal niche that links genomic instability to malignant transformation.

2026-08-17 | GSE313834 | GEO

Transcriptome of tibialis anterior muscle RNA samples from control and OPMD A17.1 mouse treated or not with a gene therapy approach

Project description:Oculopharyngeal muscular dystrophy (OPMD) is an adult-onset syndrome characterized by progressive degeneration of specific muscles. OPMD is caused by short GCN repeat expansions within the gene encoding the nuclear poly(A)-binding protein 1 (PABPN1) that extend an N-terminal polyalanine tract in the protein. Mutant PABPN1 aggregates as nuclear inclusions in OMPD patient muscles. We have used the transgenic mouse A17.1 OPMD model that recapitulates the features of the human disorder: progressive muscle weakness, atrophy and formation of PABPN1 nuclear inclusions. Wild-type human PABPN1 contains a stretch of 10 alanines following the initial methionine, which is expanded to 11–18 alanines in OPMD patients. Transgenic A17.1 mouse overexpress an 17 alanine expanded PABPN1 under the control of the HSA promoter. To evaluate a gene therapy approach based on AAV delivery of a ‘suppress and replace’ strategy in OPMD we performed a transcriptomic analysis in treated muscles 18 weeks after injection. Using microarrays, tibialis anterior gene expression was compared between control muscles (FvB), OPMD muscles (A17), AAV-shRNA3x treated muscles (A17 shRNA3X), AAVoptPABPN1 treated muscles (A17 optPABPN1), and AAV-shRNA3x+AAV-optPABPN1 treated muscles (A17 dual).

2017-06-12 | GSE89996 | GEO

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