ReviewInternational journal of molecular sciences2018
The Emerging Role of Insulin Receptor Isoforms in Thyroid Cancer: Clinical Implications and New Perspectives.
Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- The role of PI3K signaling pathway and its associated genes in papillary thyroid cancer.Journal of the Egyptian National Cancer Institute · 2021Pooled it
- The IGF signaling axis in thyroid cancer: biological complexity and therapeutic challenges.Endocrine connections · 2026Review
- Development of a prognostic model for thyroid cancer based on mitochondrial metabolism-related genes and immune profiling.World journal of surgical oncology · 2026Article
- Obesity and thyroid cancer: mechanisms and clinical implications.Frontiers in nutrition · 2026Review
- Brachyury and IGF1R: potential opposing roles in pediatric thyroid nodular pathology.Journal of endocrinological investigation · 2025Article
- Correlation between insulin receptor expression and tumor cell proliferation, recurrence and metastasis in well-differentiated pancreatic neuroendocrine neoplasms.Endocrine connections · 2025Article
- Gut microbiome versus thyroid cancer: Association and clinical implications (Review).Oncology letters · 2025Review
- Association between triglyceride-glucose index and papillary thyroid carcinoma among Chinese adults with thyroid nodules.Frontiers in endocrinology · 2025Article
- Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024Review
- A Brief Look at Hashimoto's Disease, Adrenal Incidentalomas, Obesity and Insulin Resistance-Could Endocrine Disruptors Be the Other Side of the Same Coin?Medicina (Kaunas, Lithuania) · 2023Review
- Metabolic syndrome and thyroid Cancer: risk, prognosis, and mechanism.Discover oncology · 2023Review
- Drug repositioning in thyroid cancer treatment: the intriguing case of anti-diabetic drugs.Frontiers in pharmacology · 2023Review
- Clinicopathological features and prognosis of papillary thyroid cancer patients with type 2 diabetes mellitus.Gland surgery · 2022Article
- Review
- Obesity and Thyroid Cancer Risk: An Update.International journal of environmental research and public health · 2022Review
- Single-Cell Transcriptome Analysis Reveals Inter-Tumor Heterogeneity in Bilateral Papillary Thyroid Carcinoma.Frontiers in immunology · 2022Article
- Discoidin Domain Receptor 1, a Potential Biomarker and Therapeutic Target in Hepatocellular Carcinoma.International journal of general medicine · 2022Review
- IGF2 is a potential factor in RAI-refractory differentiated thyroid cancer.Oncology letters · 2021Article
- The Journey of DDR1 and DDR2 Kinase Inhibitors as Rising Stars in the Fight Against Cancer.International journal of molecular sciences · 2021Review
- Knockdown of insulin-like growth factor 2 gene disrupts mitochondrial functions in the liver.Journal of molecular cell biology · 2021Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Thyroid cancer (TC) is the most common endocrine tumor. Although the majority of TCs show good prognoses, a minor proportion are aggressive and refractory to conventional therapies. So far, the molecular mechanisms underlying TC pathogenesis are incompletely understood. Evidence suggests that TC cells and their precursors are responsive to insulin and insulin-like growth factors (IGFs), and often overexpress receptors for insulin (IR) and IGF-1 (IGF-1R). IR exists in two isoforms, namely IR-A and IR-B. The first binds insulin and IGF-2, unlike IR-B, which only binds insulin. IR-A is preferentially expressed in prenatal life and contributes to development through IGF-2 action. Aggressive TC overexpresses IR-A, IGF-2, and IGF-1R. The over-activation of IR-A/IGF-2 loop in TC is associated with stem-like features and refractoriness to some targeted therapies. Importantly, both IR isoforms crosstalk with IGF-1R, giving rise to the formation of hybrids receptors (HR-A or HR-B). Other interactions have been demonstrated with other molecules such as the non-integrin collagen receptor, discoidin domain receptor 1 (DDR1), and the receptor for the hepatocyte growth factor (HGF), Met. These functional networks provide mechanisms for IR signaling diversification, which may also exert a role in TC stem cell biology, thereby contributing to TC initiation and progression. This review focuses on the molecular mechanisms by which deregulated IR isoforms and their crosstalk with other molecules and signaling pathways in TC cells and their precursors may contribute to thyroid carcinogenesis, progression, and resistance to conventional treatments. We also highlight how targeting these alterations starting from TC progenitors cells may represent new therapeutic strategies to improve the clinical management of advanced TCs.
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Registered trials
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