Ask about this productRelated genes to: TSHR Blocking Peptide
- Gene:
- TSHR NIH gene
- Name:
- thyroid stimulating hormone receptor
- Previous symbol:
- -
- Synonyms:
- LGR3
- Chromosome:
- 14q24-q31
- Locus Type:
- gene with protein product
- Date approved:
- 1990-03-05
- Date modifiied:
- 2019-04-23
Related products to: TSHR Blocking Peptide
Related articles to: TSHR Blocking Peptide
- Sixty percent of papillary thyroid cancers (PTCs) are driven by BRAF, a mutation associated with high inter- and intra-tumoral heterogeneity. PTCs may become highly aggressive anaplastic thyroid cancers (ATCs). While single-cell transcriptomics may resolve this heterogeneity, it is potentially confounded by technical effects whose correction may dampen inter-tumor variations. Here we profiled ATCs and BRAF PTCs with single-nuclei RNA-seq and spatial transcriptomics, and an experimental design disentangling biological and technical variations. It reveals that much transcriptional variation in cancer cells and several immune cell types is idiosyncratic, that is, tumor-specific, a phenomenon obscured by batch integration in a number of single-cell studies. Idiosyncrasies are associated in some cases with genomic aberrations and global tissue states like hypoxia. Beyond idiosyncrasies, differentiation markers SLC5A5 (NIS), TPO, TG, and TSHR are lost in a sequence mirrored by their gain during human thyroid organoids maturation, suggesting a new classification of cancer cell states. PTC cells retain TSHR expression and show features of partial epithelial-mesenchymal transition (EMT) with a massive expression of FN1, which promotes proliferation via an autocrine loop. In contrast, ATCs undergo full-scale EMT, with expression of mesenchymal extracellular components and loss of TSHR. Finally, we show that the microenvironment of cancer cells is driven by inflammation. These findings may help future stratifications of BRAF PTCs. - Source: PubMed
Publication date: 2026/08/11
Tourneur AdrienVitória Joel RodriguesSaiselet ManuelCraciun LigiaLarsimont DenisLefort AnneLibert FrédérickMaenhaut CarineCostagliola SabineTarabichi MaximeRomitti MirianDetours Vincent - This study aims to investigate the expression and function of DNA methyltransferases (DNMTs) and histone methyltransferase EZH2 in regulating the expression of thyroid-stimulating hormone receptor (TSHR) and fibrotic markers by orbital fibroblasts from Graves' ophthalmopathy (GO) patients. - Source: PubMed
Chompoowong RajitPhankeaw PimchanokSuwannavong ApinyaVisamol SopitaPitikiadtikun SukonlaphatSaonanon PreamjitPruksakorn VannakornPotita PanidaPalaga TanapatVirakul Sita - [This corrects the article DOI: 10.3389/fonc.2021.718578.]. - Source: PubMed
Publication date: 2026/07/17
Feng FangHan HuiqinWu ShuqiWang Hui - Thyroid eye disease (TED), also referred to Graves' ophthalmopathy, is a disfiguring and vision-threatening autoimmune disease of the retroocular tissues occurring in patients with Graves' disease (GD). Among the extrathyroidal manifestations of GD, TED is the most frequent, being observed in roughly 30-50% of patients. In the immunopathogenesis of TED, the TSH-R/IGF-1R complex has a determinant role. TED is commonly bilateral, and during its active phase it presents with ocular redness, eyelid edema, photophobia, proptosis, and diplopia. In the most severe cases, the involvement of the optic nerve (dysthyroid optic neuropathy) may endanger vision and requires urgent treatment. Recommendations for the management of TED encompass three aspects: general measures, thyroid treatment, and eye treatment. The management of TED consists in control of hyperthyroidism, local therapies, intravenous pulses of methylprednisolone, and immunosuppressive agents. Recently, the deeper knowledge of TED pathophysiology has led to new potential therapeutic targets, and new biological drugs, such as teprotumumab, that is able to ameliorate clinical activity score and proptosis in these patients. Additional agents are currently under investigation, with promising results that suggest potential advances in the treatment of this disease. The aim of this review is to provide an updated outline of TED, in terms of immunopathogenesis, diagnosis, clinical management and current innovative drugs. - Source: PubMed
Publication date: 2026/07/31
Ferrari Silvia MartinaRagusa FrancescaElia GiusyBotrini ChiaraBalestri EugeniaRugani LiciaMazzi ValeriaMaglionico Maria NovellaFigus MicheleShoenfeld YehudaAntonelli AlessandroFallahi Poupak - Thyroid-Stimulating Hormone (TSH) suppression therapy is a key strategy in managing differentiated thyroid cancer (DTC) after surgery, but its clinical use has long faced the challenge of a "one-size-fits-all" approach. Previous studies mainly focus on balancing risks and benefits, yet the process of individualized decision-making still lacks systematic integration and synthesis. This article offers a comprehensive review of this issue from an individualized perspective. Mechanistically, it details the networked regulatory mechanisms by which TSH promotes the proliferation, invasion, and dedifferentiation of thyroid cancer cells through the activation of signaling pathways like Gαs and Gαq/11 via TSHR. It also uncovers the complex relationship where TSH collaborates with the key oncogenic drivers to advance tumor growth and the loss of oncogene-induced senescence after long-term stimulation. Clinically, we develop an individualized decision-making framework based on three dimensions: patient factors, tumor traits, and treatment process. Additionally, we synthesize existing evidence to define the benefit boundaries of TSH suppression, aiming to guide clinical practice. - Source: PubMed
Publication date: 2026/07/07
Li ZhaoqingWang TengfeiLiu Jia