Simulating the Dedifferentiation Process of Thyroid Cancer: Insights from Mouse Models and Ultrasound Imaging.
Authors
Affiliations (4)
Affiliations (4)
- Department of Ultrasound, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
- The Key Laboratory of Specialty Fiber Optics and Optical Access Networks, Joint International Research Laboratory of Specialty Fiber Optics and Advanced Communication, Shanghai Institute for Advanced Communication and Data Science, School of Communication and Information Engineering, Shanghai University, Shanghai, China.
- Department of Head and Neck Surgery, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
- Department of Ultrasound, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China. Electronic address: [email protected].
Abstract
Anaplastic thyroid carcinoma (ATC) may arise from the progression of differentiated thyroid cancers, but the mechanisms are not well understood. Establishing appropriate animal models and conducting ultrasound imaging monitoring can facilitate the study of this dedifferentiation process. We constructed mouse models of papillary thyroid carcinoma (PTC) and ATC by editing the Braf mutation and Trp53 deletion, and monitored the process using small-animal ultrasound. The you only look once computer model was employed to process ultrasound images, analyze the characteristics of ultrasound images from different tumors and build a lesion identification and diagnostic model. The molecular expression characteristics of PTC with potential for dedifferentiation were analyzed through RNA sequencing. Mice ATCs exhibited a characteristic five-phase growth curve, accompanied by earlier lung metastasis. The mice thyroid tumor lesion recognition model was capable of identifying different types of tumor lesions and simulating their progression process with an accuracy of 0.765. Some PTCs showed lower Thyroid Differentiation Scores and were associated with high expression of genes such as Ptprn2, Tnfsf18 and Cdkn2a. This study validated the hypothesis that Trp53 deletion and Braf mutation promote the progression of PTC to ATC through ultrasound monitoring and computer modeling. Certain PTCs with the potential for dedifferentiation exhibit a specific molecular expression profile, which may represent potential therapeutic targets.