Chapters authored
Molecular Mechanisms of Glucose Uptake Regulation in Thyroid Cancer
Common capabilities of thyroid malignant cells are accelerating metabolism and increasing glucose uptake to optimize energy supply for growth. In tumor cells, keeping the power load required for cell survival is essential and glucose transporters are capable of promoting this task. GLUT-1 and GLUT3 are promising goals for the development of anti-cancer strategies. The lack of oncosuppressors has dominant effect on the membrane expression of GLUT1 and glucose uptake. Overexpression of hypoxia-inducing factors, in thyroid cancer, modulates the expression of some glucose transporter genes. Although the physiology of the thyroid gland has been excellently explained, metabolic regulation in thyroid cancer is inevitable. In this section, we investigated the proliferation pathways of pivotal regulators and signal molecules around GLUT regulation in thyroid cancer, including PTEN, p53, MicroRNA, iodide, BRAF, HIF-1, PI3K-Akt, TSH, c-Myc, and AMPK. Impaired energy regulation and cell metabolism are the most critical symptoms of most cancers. As a result, understanding the mechanisms of glucose transport in the normal and pathological tissues of the thyroid may be very crucial and offer tremendous insights into the science of analysis and remedy of thyroid disease.
Part of the book: Hypothyroidism
RET Proto-Oncogene Mutations: Impact on Diagnosis, Treatment and Prognosis of MTC
Variants of MTC result from different mutations in exons of the RET gene. RET proto-oncogene is activated by a DNA rearrangement and it is one of the first tyrosine kinase receptor (RTK) proteins found to play a role in neoplasia. Early detection using genetic screening has become the gold standard of therapy, followed by prophylactic thyroidectomy. RET-kinase inhibitors have been developed recently for the treatment of MTC and are currently at various phases of pre- and clinical trials. Numerous autosomal dominantly inherited mutations have been demonstrated to activate RET constitutively. These mutations in separate populations are believed to be correlated with a rather heterogeneous prototype across countries. As such, one objective of this study was to demonstrate a geographical pattern of RET mutations in various populations. Advances in RET genetic screening have facilitated for the rapid recognition of hereditary MTCs and prophylactic thyroidectomy for relatives who may not show signs of the disease. In this chapter, we will discuss oncogenic RET signaling, RET inhibitors and the major RET mutations found in MTC and the necessity of RET genetic screening for the early diagnosis of MTC patients, using American Thyroid Association guidelines and genotype-phenotype correlation.
Part of the book: Thyroid Cancer