1,721,039 research outputs found

    Correction to: Lenvatinib as a salvage therapy for advanced metastatic medullary thyroid cancer (Journal of Endocrinological Investigation, (2021), 44, 10, (2139-2151), 10.1007/s40618-020-01491-3)

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    The article “Lenvatinib as a salvage therapy for advanced metastatic medullary thyroid cancer” written by A. Matrone, A. Prete, A. Nervo, A. Ragni, L. Agate, E. Molinaro, C. Giani, L. Valerio, E. Minaldi, A. Piovesan and R. Elise was originally published online on the publisher’s internet portal on 17th February 2021 with Open Access under a Creative Commons Attribution (CC BY) license 4.0 With the authors’ decision to cancel Open Access the copyright of the article changed on 28th April 2021 to © Italian Society of Endocrinology (SIE) 2021 with all rights reserved. The original article has been corrected

    State of the Art in 3D Culture Models Applied to Thyroid Cancer

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    Thyroid cancer (TC) is the prevalent endocrine tumor with a rising incidence, particularly in higher-income countries, leading to an increased interest in its management and treatment. While overall, survival rates for TC are usually favorable, advanced cases, especially with metastasis and specific histotypes, pose challenges with poorer outcomes, advocating the need of systemic treatments. Targeted therapies have shown efficacy in both preclinical models and clinical trials but face issues of resistance, since they usually induce partial and transient response. These resistance phenomena are currently only partially addressed by traditional preclinical models. This review explores the limitations of traditional preclinical models and emphasizes the potential of three-dimensional (3D) models, such as transwell assays, spheroids, organoids, and organ-on-chip technology in providing a more comprehensive understanding of TC pathogenesis and treatment responses. We reviewed their use in the TC field, highlighting how they can produce new interesting insights. Finally, the advent of organ-on-chip technology is currently revolutionizing preclinical research, offering dynamic, multi-cellular systems that replicate the complexity of human organs and cancer-host interactions

    Obesity as a risk factor for thyroid cancer

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    Purpose of review In this review, we evaluate recent findings related to the association between obesity and thyroid cancer. Recent findings During the last several decades, the prevalence of obesity and thyroid cancer have been increasing in parallel on a global scale. Current evidence suggests that the growing incidence of differentiated thyroid cancer (DTC) is pathogenically linked to the spread of obesity, but the biological mechanisms that may explain this connection have been only partially described. Furthermore, unlike other tumors, data on the impacts of obesity on the aggressiveness of DTC and response to treatment of DTC remain conflicting. Summary Emergent knowledge regarding the links between obesity and thyroid cancer suggests a relevant role for obesity as a risk factor for DTC, with no apparent impact on its aggressiveness

    Cabozantinib: An orphan drug for thyroid cancer

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    Introduction: Until recently, no therapeutic options were available for the treatment of advanced medullary thyroid cancer (MTC). Cabozantinib (XL184) is a novel tyrosine kinase inhibitor (TKI) that inhibits several tyrosine kinase receptors, in particular those coded by MET, VEGFR-2 and RET oncogenes that are considered to be involved in the pathogenesis of MTC.Areas covered: This article provides an overview of the phase I and III trials that demonstrated the efficacy of cabozantinib in two cohorts of advanced MTC patients who were naà ̄ve or previously treated with other TKIs. The benefits in terms of progression-free survival (PFS), overall survival (OS) and the demographic clinical and mutational status of the two cohorts of MTC patients are reported and discussed.Expert opinion: The possibility to have a therapeutic option for the treatment of patients with advanced and progressive MTC and, in particular, the evidence that the drug can be active also in those patients who already experienced disease progression while taking another TKI is a great opportunity as demonstrated in cases treated with cabozantinib after vandetanib such as the one reported in this paper

    Monoclonal antibody cetuximab impairs matrix metalloproteinases 2 and 9, epithelial–mesenchymal transition and cell migration in feline oral squamous cell carcinoma in vitro

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    Feline oral squamous cell carcinoma (FOSCC) is characterised by invasive and metastatic behaviour and is poorly responsive to current treatments, hence the need for new therapeutic strategies. FOSCC shares molecular targets with human head and neck squamous cell carcinoma (HNSCC), among these the epidermal growth factor receptor. Cetuximab is an anti-epidermal growth factor receptor monoclonal antibody employed in the therapy of HNSCC and, interestingly, previous work in vitro suggested that it displays cytostatic and cytotoxic properties also against FOSCC. With the present study, we aimed at further investigating the effects of cetuximab on invasion and metastasis pathways proven to be relevant in human patients. To this purpose, FOSCC cell lines SCCF1, SCCF2 and SCCF3 were treated with cetuximab for 48/72 h and subjected to Western blot for matrix metalloproteinases-2/9 (MMP-2/9) and epithelial–mesenchymal transition markers vimentin, E-, P- and N-cadherin. Treatment with cetuximab resulted in downregulation of MMP-2/-9 in all of the three cell lines in a dose-dependent manner. Moreover, cetuximab downregulated vimentin and P-cadherin in SCCF1, upregulated E-cadherin whilst downregulating P-/N-cadherins in SCCF2, and impaired P-/N-cadherins in SCCF3. An in vitro scratch test also demonstrated that cetuximab delayed cell migration in SCCF3. These data suggest that cetuximab mitigates invasion and metastasis processes by impairing MMPs and epithelial–mesenchymal transition pathways in FOSCC, indicating that this monoclonal antibody may help to counteract malignant progression and improve the management of locally invasive disease
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