- Thyroid
- Metabolic Reprogramming in Thyroid Cancer
-
Sang-Hyeon Ju, Minchul Song, Joung Youl Lim, Yea Eun Kang, Hyon-Seung Yi, Minho Shong
-
Endocrinol Metab. 2024;39(3):425-444. Published online June 10, 2024
-
DOI: https://doi.org/10.3803/EnM.2023.1802
-
-
 Abstract
 PDF PubReader  ePub
- Thyroid cancer is a common endocrine malignancy with increasing incidence globally. Although most cases can be treated effectively, some cases are more aggressive and have a higher risk of mortality. Inhibiting RET and BRAF kinases has emerged as a potential therapeutic strategy for the treatment of thyroid cancer, particularly in cases of advanced or aggressive disease. However, the development of resistance mechanisms may limit the efficacy of these kinase inhibitors. Therefore, developing precise strategies to target thyroid cancer cell metabolism and overcome resistance is a critical area of research for advancing thyroid cancer treatment. In the field of cancer therapeutics, researchers have explored combinatorial strategies involving dual metabolic inhibition and metabolic inhibitors in combination with targeted therapy, chemotherapy, and immunotherapy to overcome the challenge of metabolic plasticity. This review highlights the need for new therapeutic approaches for thyroid cancer and discusses promising metabolic inhibitors targeting thyroid cancer. It also discusses the challenges posed by metabolic plasticity in the development of effective strategies for targeting cancer cell metabolism and explores the potential advantages of combined metabolic targeting.
- Thyroid
- Development of Metabolic Synthetic Lethality and Its Implications for Thyroid Cancer
-
Sang-Hyeon Ju, Seong Eun Lee, Yea Eun Kang, Minho Shong
-
Endocrinol Metab. 2022;37(1):53-61. Published online February 28, 2022
-
DOI: https://doi.org/10.3803/EnM.2022.1402
-
-
4,299
View
-
194
Download
-
1
Web of Science
-
2
Crossref
-
Abstract
PDFPubReader ePub
- Cancer therapies targeting genetic alterations are a topic of great interest in the field of thyroid cancer, which frequently harbors mutations in the RAS, RAF, and RET genes. Unfortunately, U.S. Food and Drug Administration-approved BRAF inhibitors have relatively low therapeutic efficacy against BRAF-mutant thyroid cancer; in addition, the cancer often acquires drug resistance, which prevents effective treatment. Recent advances in genomics and transcriptomics are leading to a more complete picture of the range of mutations, both driver and messenger, present in thyroid cancer. Furthermore, our understanding of cancer suggests that oncogenic mutations drive tumorigenesis and induce rewiring of cancer cell metabolism, which promotes survival of mutated cells. Synthetic lethality (SL) is a method of neutralizing mutated genes that were previously considered untargetable by traditional genotype-targeted treatments. Because these metabolic events are specific to cancer cells, we have the opportunity to develop new therapies that target tumor cells specifically without affecting healthy tissue. Here, we describe developments in metabolism-based cancer therapy, focusing on the concept of metabolic SL in thyroid cancer. Finally, we discuss the essential implications of metabolic reprogramming and its role in the future direction of SL for thyroid cancer.
-
Citations
Citations to this article as recorded by  - Toward Systems-Level Metabolic Analysis in Endocrine Disorders and Cancer
Aliya Lakhani, Da Hyun Kang, Yea Eun Kang, Junyoung O. Park
Endocrinology and Metabolism.2023; 38(6): 619. CrossRef - The Role of De novo Serine Biosynthesis from Glucose in Papillary Thyroid Cancer
Seong Eun Lee, Na Rae Choi, Jin-Man Kim, Mi Ae Lim, Bon Seok Koo, Yea Eun Kang
International Journal of Thyroidology.2023; 16(2): 175. CrossRef
|
KES
