clinical pathway of thyroid cancer

Thyroid cancer is the most common endocrine malignancy; it generally has an excellent prognosis, although some tumors of follicular origin can turn metastatic or indolent and, after that, progress to radioiodine-resistant thyroid cancers. This study, crucial for understanding thyroid cancer clinical progression, aims to illuminate these intricate transformations and their implications for patient care. Our investigation focuses on the three well-recognized forms of thyroid cancer: papillary, follicular, and oncocytic types derived from thyroid follicular cells. Most cases of these well-recognized thyroid cancers are asymptomatic and are typically diagnosed during a physical exam or when appropriate imaging studies are performed on an individual. The findings of this study, which significantly contribute to the field of thyroid cancer, provide a comprehensive understanding of the disease's progression and its implications for patient care. Methods: ۸۲ articles were reviewed on PubMed, Science Direct, and Google Scholar until September ۲۰۲۴. After thoroughly reviewing titles and abstracts, ۱۵ articles met the inclusion criteria. More than ۱۰۰ hours were utilized to review and extract the content. Results: Aggressive forms include anaplastic thyroid cancer and medullary thyroid cancer of the parafollicular C cells. Microcarcinomas can be identified, while larger tumors may require Surgery with or without radioactive iodine. Symptoms emanating from the locoregional disease will require surgical resection, while symptoms emanating from metastatic disease will require Surgical techniques or stereotactic body irradiation. Multikinase inhibitors are used for thyroid cancer that does not respond to radioactive iodine, while targeted therapies like dabrafenib and selpercatinib target specific mutations (BRAF, RET, NTRK, MEK) in advanced cases. The molecular biology of these excrescences has stressed a hyperactive- activation of the Mitogen- Actuated Protein Kinases (MAPK) pathway (RAS-RAF-MEK-ERK), mainly secondary to the BRAFV۶۰۰E hotspot mutation, which is a significant driver of thyroid cancer. The Ras- Raf- MEK- ERK signaling pathway regulates cell proliferation, insulation, and survival. Overexpression and overactivation of members within the signaling cascade have been observed in multitudinous solid cancers, especially thyroid ones. These members are, therefore, the target of inhibitory antidotes, such as tyrosine kinase impediments or monoclonal antibodies. These drugs are formerly used in clinical practice. However, their effectiveness is not always satisfactory, and they may even suffer from "escape" in tumoral cells—the ability to develop resistance to these drugs over time. Conclusion: It seems that surgical intervention can cure most cases of thyroid cancer, and radioactive iodine can enhance survival in high-risk cases. The Anti-angiogenic therapies and targeted therapies for genetic mutations in metastatic thyroid cancer represent the single most important development that can hold hope for the treatment of thyroid cancer. However, it is the start of a very long journey. This promise intrinsic to targeted therapies brings hope regarding the future management of thyroid cancer; however, further research is needed to understand the differences in efficacy between thyroid cancers and other malignancies. Thus, this will enable us to shape our subsequent research efforts and commitment to studying thyroid cancer.

کلیدواژه ها:

thyroid cancer ، clinical pathway ، diagnostic pathways ، thyroid nodule