Targeting Thyroid Cancer: From Biology to Therapeutic Strategies

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: closed (15 January 2024) | Viewed by 3645

Special Issue Editors


E-Mail Website1 Website2
Guest Editor
1. Faculty of Medicine, University of Porto, Porto, Portugal
2. i3S—Instituto de Investigação e Inovação em Saúde, Cancer Signaling and Metabolism Group, Porto, Portugal
3. IPATIMUP—Instituto de Patologia e Imunologia Molecular da Universidade do Porto, Porto, Portugal
Interests: thyroid cancer; neuroendocrine tumors; oncobiology

E-Mail Website
Guest Editor
1. i3S - Instituto de Investigação e Inovação em Saúde, Cancer Signaling and Metabolism Group, Porto, Portugal
2. IPATIMUP – Instituto de Patologia e Imunologia Molecular da Universidade do Porto, Porto, Portugal
3. Department of Pathology – Faculty of Medicine of the University of Porto, Porto, Portugal
Interests: oncobiology; cancer biomarkers; drug resistance; anticancer therapeutic strategies
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
1. i3S - Instituto de Investigação e Inovação em Saúde, Cancer Signaling and Metabolism Group, Porto, Portugal
2. IPATIMUP – Instituto de Patologia e Imunologia Molecular da Universidade do Porto, Porto, Portugal
Interests: metabolism; reactive oxygen species; apoptosis; oncobiology; mitochondrial biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Thyroid cancer-TC represents the most common endocrine malignancy (being the fifth cause of cancer in women), with its incidence rapidly increasing globally. Mostly, thyroid cancer patients are cured with surgery followed by radioactive iodine (RAI). Still, in 10-15% of the patients’ disease persists or recurs. Of these, 60% do not respond to treatment with RAI. Following RAI-refractory (RAI-R) disease, the outcome of those patients drops significantly, with 10-year survival rate of less than 10% and the mean life expectancy of 3–5 years.

The advances in targeted therapies, in particular tyrosine kinase inhibitors-TKI (targeting molecules/signaling pathways involved in TC pathogenesis) brought hope to RAI-R patients, for whom no therapies were available. This is particularly true for undifferentiated thyroid cancer where new genetic targets (as ALK or TRK) have demonstrated excellent responses, but it is also true in advanced follicular cell cancer and in medullary thyroid cancer.

However, and despite initial response, resistance can develop, with disease progression and patient death. TC complex heterogeneity is a major hurdle, going much beyond the simple action of known oncogenes and/or tumor suppressor genes. Indeed, it is becoming increasingly evident that genetic and epigenetic alterations occur during progression/metastasis (some of which driven by treatment selective pressure). Moreover, changes in tumor interactions with its microenvironment/immune cells further contribute to TC progression, aggressiveness and/or response to therapy.

This special issue will focus on the recent findings on TC research field, from its underlying biology to the players/mechanism involved in TC heterogeneity and response to therapy.

Your contributions, either through original research articles or review papers, will be relevant to further evolve in this field.

Prof. Dr. Paula Soares
Dr. Raquel T. Lima
Dr. Marcelo Correia
Guest Editors

Manuscript Submission Information

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Keywords

  • thyroid cancer
  • radio iodine therapy
  • therapy resistance
  • targeted therapies
  • tumor heterogeneity
  • signaling pathways
  • metastasis
  • tyrosine kinase receptors
  • Tyrosine Kinase inhibitors (TKI)
  • tumor microenvironment

Published Papers (2 papers)

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Research

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18 pages, 11400 KiB  
Article
Lysicamine Reduces Protein Kinase B (AKT) Activation and Promotes Necrosis in Anaplastic Thyroid Cancer
by Mariana Teixeira Rodrigues, Ana Paula Picaro Michelli, Gustavo Felisola Caso, Paloma Ramos de Oliveira, Dorival Mendes Rodrigues-Junior, Mirian Galliote Morale, Joel Machado Júnior, Karina Ramalho Bortoluci, Rodrigo Esaki Tamura, Tamiris Reissa Cipriano da Silva, Cristiano Raminelli, Eric Chau, Biana Godin, Jamile Calil-Silveira and Ileana G. Sanchez Rubio
Pharmaceuticals 2023, 16(12), 1687; https://doi.org/10.3390/ph16121687 - 04 Dec 2023
Viewed by 1243
Abstract
Anaplastic thyroid cancer (ATC) is an aggressive form of thyroid cancer (TC), accounting for 50% of total TC-related deaths. Although therapeutic approaches against TC have improved in recent years, the survival rate remains low, and severe adverse effects are commonly reported. However, unexplored [...] Read more.
Anaplastic thyroid cancer (ATC) is an aggressive form of thyroid cancer (TC), accounting for 50% of total TC-related deaths. Although therapeutic approaches against TC have improved in recent years, the survival rate remains low, and severe adverse effects are commonly reported. However, unexplored alternatives based on natural compounds, such as lysicamine, an alkaloid found in plants with established cytotoxicity against breast and liver cancers, offer promise. Therefore, this study aimed to explore the antineoplastic effects of lysicamine in papillary TC (BCPAP) and ATC (HTH83 and KTC-2) cells. Lysicamine treatment reduced cell viability, motility, colony formation, and AKT activation while increasing the percentage of necrotic cells. The absence of caspase activity confirmed apoptosis-independent cell death. Necrostatin-1 (NEC-1)-mediated necrosome inhibition reduced lysicamine-induced necrosis in KTC-2, suggesting necroptosis induction via a reactive oxygen species (ROS)-independent mechanism. Additionally, in silico analysis predicted lysicamine target proteins, particularly those related to MAPK and TGF-β signaling. Our study demonstrated lysicamine’s potential as an antineoplastic compound in ATC cells with a proposed mechanism related to inhibiting AKT activation and inducing cell death. Full article
(This article belongs to the Special Issue Targeting Thyroid Cancer: From Biology to Therapeutic Strategies)
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Review

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18 pages, 6390 KiB  
Review
Non-Apoptotic Programmed Cell Death in Thyroid Diseases
by Feihong Ji and Xinguang Qiu
Pharmaceuticals 2022, 15(12), 1565; https://doi.org/10.3390/ph15121565 - 15 Dec 2022
Cited by 1 | Viewed by 1809
Abstract
Thyroid disorders are among the most common endocrinological conditions. As the prevalence of thyroid diseases increases annually, the exploration of thyroid disease mechanisms and the development of treatments are also gradually improving. With the gradual advancement of therapies, non-apoptotic programmed cell death (NAPCD) [...] Read more.
Thyroid disorders are among the most common endocrinological conditions. As the prevalence of thyroid diseases increases annually, the exploration of thyroid disease mechanisms and the development of treatments are also gradually improving. With the gradual advancement of therapies, non-apoptotic programmed cell death (NAPCD) has immense potential in inflammatory and neoplastic diseases. Autophagy, pyroptosis, ferroptosis, and immunogenic cell death are all classical NAPCD. In this paper, we have compiled the recent mechanistic investigations of thyroid diseases and established the considerable progress by NAPCD in thyroid diseases. Furthermore, we have elucidated the role of various types of NAPCD in different thyroid disorders. This will help us to better understand the pathophysiology of thyroid-related disorders and identify new targets and mechanisms of drug resistance, which may facilitate the development of novel diagnostic and therapeutic strategies for patients with thyroid diseases. Here, we have reviewed the advances in the role of NAPCD in the occurrence, progression, and prognosis of thyroid diseases, and highlighted future research prospects in this area. Full article
(This article belongs to the Special Issue Targeting Thyroid Cancer: From Biology to Therapeutic Strategies)
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