From Standard of Care
Incidence increasing over the last three decades.
Most common endocrine neoplasm.
Lifelong risk is less than 1% with 0.83% for women and 0.33% for men (Horner MJ et al).
Estimated 48,020 new cases and 1,740 deaths in 2011.
Ranks 10th in incidence among solid organ malignancies.
Incidence among men has risen more dramatically than any other malignancy in recent years with a 2.4% annual increase.
Strong female predominance 2.7:1.
Rare in children below the age of 10 years.
Papillary carcinoma accounts for 90% of pediatric thyroid cancers.
Children with thyroid cancer usually present with more extensive thyroid disease than adults, and more than 80% have lymph node metastases, and 10-20% have lung metastases.
Children have excellent prognosis despite more advanced disease, with most having long-term survival.
Childhood thyroid cancer may be more responsive to thyroid suppression, or have a greater avidity to iodine and tend to have RET/PTC rearrangements.
Adults with papillary thyroid cancer often have BRAF mutation which may be associated with tumor recurrence and decreased iodine avidity.
Most cases arise from thyroid follicular cells.
Arise from follicular or para-follicular cells.
Differentiated and undifferentiated tumor is originated in follicular cells.
Vast majority are papillary (88%) or follicular (9%)-differentiated cancers.
Majority of lesions are differentiated cancers which includes papillary, follicular, and Hurthle cell variants.
Anaplastic thyroid cancer is the most uniformly fatal type of far right cancer, but most carcinoma depths are from papillary, follicular, and Hurthle cell carcinomas, which account for 95% of all thyroid cancers.
Poorly differentiated or undifferentiated thyroid cancers include anaplastic thyroid cancer.
Thyroid cancer occurs more often in women, but mortality rates are higher in men, because of an older age at diagnosis.
Medullary thyroid cancer is arise from parafollicular or C cells and may be familial or
Medullary thyroid cancer comprises 2-3% of all thyroid cancers.
Following surgery thyroid hormone is administered to compensate for the function of the resected thyroid disease and to prevent recurrence.
Strong association with pregnancy, especially with spontaneous or induced abortions.
Serum thyroglobulin measurements are the most sensitive indicators of recurrent disease.
Previous radiation exposure to the head and neck area is related to less favorable pathologic and clinical outcome in patients after surgical management (Seaberg R).
30-50% of adults patients with well differentiated thyroid cancer have palpable nodal disease.
Up to 90% of patients with well-differentiated disease have histologically proven lymph node metastases after elective modified radical neck dissection.
Before treatment with radioiodine it is standard practice to reduce the body’s stores of iodine by avoiding iodine rich diet and supplements which may contain iodine.
Most patients with differentiated forms of thyroid cancer are managed successfully with surgery, radioactive iodine and long-term thyroid hormone suppression treatment.
Following thyroidectomy for well differentiated thyroid cancer to ensure full eradication of remnant thyroid tissue and to treat microscopic residual disease, and patients with visible, inoperable, iodine avid metastases radioactive iodine is often administered.
For well differentiated advanced iodine avid thyroid cancer the administration of radioactive iodine results in reduced tumor recurrence and improved survival.
For patients with a well differentiated very low risk thyroid cancer treatment with radioactive iodine is of uncertain benefit.
Differentiated carcinomas of the thyroid had a 20 year overall survival of almost 90%.
Poorly differentiated thyroid cancer is having less radioactive avidity and anaplastic undifferentiated lesions or refractory to radioactive iodine.
Associated with several genetic alterations including the RET proto-oncogene, which coats were 80 cell membrane receptor tyrosine kinase.
RET proto-oncogene expressed in parafollicular C cells but not in follicular cells.
RET proto-oncogene can be activated in follicular cells by chromosomal translocation RET/PTC rearrangement.
RET/PTC is found at approximately 20% of adults sporadic papillary carcinoma patients.
An RET point mutation is commonly found in parafollicular C cells derived medullary thyroid cancers. 25-50% of metastatic differentiated thyroid cancers can lose functional iodine concentrating ability to become in sensitive to radioactive iodine therapy: When this occurs less than 50% of patients will be alive at 3 years (Wang W).
B-RAF kinase (BRAF) can activate the mitogen activated protein kinase (MAPK) signaling pathway, and point mutation was of the BRAF gene are found and 45% of thyroid papillary cancers.
PET scans can localize sites of metastases and demonstrate radioactive iodine resistance, as thyroid carcinomas were low iodine and daily at higher glucose metabolism and are more likely to be positive on PET scans.
Radioactive iodine has little or no therapeutic effect on PET scan positive tumors and tumors that concentrate radioactive iodine are not likely to be active on PET scan.
FDG avidity is the most practical and reproducible definition of radioactive iodine resistance disease in thyroid cancer with a median sensitivity and specificity of 77% in 78%, respectively.
RAS point mutations also activate the MAPK signaling pathway and occurs in all types of thyroid follicular cell adenomas and carcinomas, suggesting RAS hasn't role in the early tumor genesis of thyroid cancer.
Mutations of 1 of 3 genes: RET/PTC,BRAF,or RAS are found in greater than 70% of papillary carcinomas and they rarely overlap in the same malignancy.