Heterogeneous Transcriptional Landscapes in Human Sporadic Parathyroid Gland Tumors
- 1Laboratory of Experimental Biochemistry and Molecular Biology, IRCCS Ospedale Galeazzi-Sant'Ambrogio, 20157 Milan, Italy.
- 2Department of Medical Biotechnology and Translational Medicine, University of Milan, 20133 Milan, Italy.
- 3Endocrine Surgery, IRCCS Ospedale San Raffaele, 20132 Milan, Italy.
- 4Endocrine Unit, ASST Ospedale Niguarda, 20162 Milan, Italy.
- 5Bone Metabolism Diseases and Diabetes Unit, IRCCS Istituto Auxologico Italiano, 20145 Milan, Italy.
- 6Department of Biomedical, Surgical and Dental Sciences, University of Milan, 20122 Milan, Italy.
- 0Laboratory of Experimental Biochemistry and Molecular Biology, IRCCS Ospedale Galeazzi-Sant'Ambrogio, 20157 Milan, Italy.
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View abstract on PubMed
Summary
This summary is machine-generated.Parathyroid adenomas (PAds) exhibit diverse gene expression patterns, influencing primary hyperparathyroidism (PHPT) severity. Specific lncRNAs and gene alterations correlate with distinct PAd subtypes and clinical outcomes.
Area Of Science
- Endocrinology
- Oncology
- Molecular Biology
Background
- Parathyroid tumors (adenomas) show molecular alterations impacting tumorigenesis.
- Understanding these alterations is key to classifying parathyroid adenomas (PAds) and their clinical relevance.
Purpose Of The Study
- To investigate the transcriptomic profiles of sporadic parathyroid adenomas (PAds).
- To correlate gene and lncRNA expression patterns with clinical features of primary hyperparathyroidism (PHPT).
Main Methods
- Gene, microRNA, and lncRNA expression profiling of 32 PAd samples.
- Cluster analysis based on key tumorigenesis genes (e.g., MEN1, CDC73, CDKN1B).
- Correlation of transcriptomic clusters with clinical and biochemical data.
Main Results
- Two main transcriptomic clusters (C1, C2) identified, driven by CDC73 and CDKN1B expression.
- Subcluster C2A showed loss of TP73 and increased lncRNAs, linked to more severe PHPT.
- Subcluster C2B exhibited general gene downregulation, lower calcium/PTH, and smaller tumors.
Conclusions
- PArathyroid adenomas display heterogeneous transcriptomic profiles.
- These profiles correlate with clinical and biochemical variations in PHPT.
- Downregulated gene expression in some PAds suggests quiescent tumor cells; p73 loss and lncRNA deregulation may drive PHPT severity.
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