Our promise to you:
Guaranteed product quality, expert customer support.
Thyroid cancer is a common endocrine malignancy and has rapidly increased in global incidence in recent decades. The vast majority of thyroid tumors arise from thyroid follicular epithelial cells, whereas 3-5% of cancers originate from parafollicular or C cells. The follicular cell-derived cancers are further subdivided into well-differentiated papillary carcinoma and follicular carcinoma, poorly differentiated carcinoma (insular carcinoma) and anaplastic carcinoma. Although the death rate of thyroid cancer is relatively low, the rate of disease recurrence or persistence is high, which is associated with increased incurability and patient morbidity and mortality.
As with other cancer types, thyroid cancer initiation and progression occurs through gradual accumulation of various genetic and epigenetic alterations, including activating and inactivating somatic mutations, alteration in gene expression patterns, aberrant gene methylation and microRNA (miRNA) dysregulation. Among these alterations, most of the data that have accumulated relate to somatic mutations, many of which occur early in the transformation process and are essential for cancer development. Thyroid cancer represents a type of neoplasia in which critical genes are frequently mutated through two distinct molecular mechanisms: point mutation or chromosomal rearrangement.
Most mutations in thyroid cancer involve the effectors of the MAPK pathway and the PI3K-AKT pathway MAPK activation is important for tumor initiation. The mutated genes that affect these pathways encode cell-membrane receptor tyrosine kinases RET and NTRK1 and intracellular signal transducers BRAF and RAS. These typically mutually exclusive mutations occur in approximately 70% of patients with papillary thyroid carcinomas and are associated with particular clinical, histopathological and biological tumor characteristics. In follicular thyroid cancer, in addition to the mutation of RAS, another common event is PAX8/PPARγ rearrangement. Thyroid cancer progression and dedifferentiation involves many additional mutations that affect the PI3K–AKT pathway and other cell signaling pathways.
The recent progress in understanding the molecular pathogenesis of thyroid cancer has shown great promise for the development of more effective treatment strategies for thyroid cancer. This has mainly resulted from the identification of molecular alterations, including the genetic and epigenetic alterations of signaling pathways — such as the RAS-RAF- MEK-MAPK-ERK pathway (MAPK pathway) and the PI3K-AKT pathway — which is reshaping thyroid cancer medicine. Creative Biogene, as a leading biotechnology company, is able to offer various thyroid cancer pathway related products including stable cell lines, viral particles and clones for your drug discovery projects.