Thyroid cancer

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Michael Maddaleni, B.S.

Thyroid Cancer Main Page

Patient Information

Overview

Classification

Papillary Thyroid Cancer
Follicular Thyroid Cancer
Medullary Thyroid Cancer
Anaplastic Thyroid Cancer
Thyroid Lymphoma

Causes

Differential diagnosis

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Overview

Historical Perspective

Pathophysiology

Epidemiology & Demographics

Risk Factors

Screening

Causes

Differentiating Thyroid cancer

Complications & Prognosis

Diagnosis

History and Symptoms | Physical Examination | Staging | Laboratory tests | Electrocardiogram | X Rays | CT | MRI Echocardiography or Ultrasound | Other images | Alternative diagnostics

Treatment

Medical therapy | Surgical options | Primary prevention | Secondary prevention | Financial costs | Future therapies


Classification

Thyroid cancers can be classified according to their pathological characteristics. The following variants can be distinguished (distribution over various subtypes may show regional variation):

Medullary thyroid cancer (MTC)

This form of thyroid carcinoma originates from the parafollicular cells (C cells), which produce the hormone calcitonin. While the increased serum concentration of calcitonin is not harmful, it is useful as a marker which can be tested in blood. A second marker, carcinoembryonic antigen (CEA), also produced by medullary thyroid carcinoma, is released into the blood and it is useful as a serum or blood tumor marker. In general measurement of serum CEA is less sensitive than serum calcitonin for detecting the presence of a tumor, but has less minute to minute variability and is therefore useful as an indicator of tumor mass.

The prognosis of MTC is poorer than that of follicular and papillary thyroid cancer when it has metastasized (spread) beyond the thyroid gland. Approximately 25% the cancer develops in families. When MTC occurs by itself it is termed familial MTC; when it coexists with tumors of the parathyroid gland and medullary component of the adrenal glands (pheochromocytoma) it is called multiple endocrine neoplasia type 2 (MEN2).

The genetics of medullary thyroid cancer

Mutations (DNA changes) in the RET proto-oncogene, located on chromosome 10, lead to the expression of a mutated receptor tyrosine kinase protein, termed RET. RET is involved in the regulation of cell growth and development and its mutation is responsible for nearly all cases of hereditary or familial medullary thyroid carcinoma. Its mutation may also be responsible for the development of hyperparathyroidism and pheochromocytoma. Hereditary medullary thyroid cancer is inherited as an autosomal dominant trait, meaning that each child of an affected parent has a 50/50 probability of inheriting the mutant RET proto-oncogene from the affected parent. DNA analysis makes it possible to identify children who carry the mutant gene; surgical removal of the thyroid in children who carry the mutant gene is curative if the entire thyroid gland is removed at an early age, before there is spread of the tumor. The parathyroid tumors and pheochromocytomas are removed when they cause clinical symptomatology. Hereditary medullary thyroid carcinoma or multiple endocrine neoplasia (MEN2) accounts for approximately 25% of all medullary thyroid carcinomas.

Seventy-five percent of medullary thyroid carcinoma occurs in individuals without an identifiable family history and is assigned the term "sporadic". Individuals who develop sporadic medullary thyroid carcinoma tend to be older and have more extensive disease at the time of initial presentation than those with a family history (screening is likely to be initiated at an early age in the hereditary form). Approximately 25% of sporadic medullary thyroid carcinomas have a somatic mutation (one that occurs within a single "parafollicular" cell) of the RET proto-oncogene. This mutation is presumed to be the initiating event, although there could be other as yet unidentified causes.

Clinical features of medullary thyroid carcinoma

The major clinical symptom of medullary thyroid carcinoma is diarrhea; occasionally a patient will have flushing episodes. Both occur particularly with liver metastasis. Occasionally, diarrhea or flushing will be the initial presenting complaint. The flushing that occurs in medullary thyroid carcinoma is indistinguishable from that associated with carcinoid syndrome. The presumed cause of flushing and diarrhea is the excessive production of calcitonin gene products (calcitonin or calcitonin gene-related peptide) and differs from the causation of flushing and diarrhea in carcinoid syndrome. Sites of spread of medullary thyroid carcinoma include local lymph nodes in the neck, lymph nodes in the central portion of the chest (mediastinum), liver, lung, and bone. Spread to other sites such as skin or brain occurs but is uncommon.

Adjuvant therapy for medullary thyroid cancer

Unlike differentiated thyroid carcinoma, there is no role for radioiodine treatment in medullary-type disease. External beam radiotherapy should be considered for patients at high risk of regional recurrence, even after optimum surgical treatment. Brierley et al., conducted a retrospective study of the treatment given to patients with microscopic residual disease, extraglandular invasion, or lymph-node metastases and found the locoregional relapse-free rate at 10 years was 86%, compared with 52% for those patients who did not receive adjuvant therapy. Typically, 40 Gy is given in 20 fractions to the cervical, supraclavicular, and upper mediastinal lymph nodes for 4 weeks, with subsequent booster doses of 10 Gy in five fractions to the thyroid bed, especially in the setting of gross residual disease.

After a long period during which surgery and radiation therapy formed the major treatments for medullary thyroid carcinoma, clinical trials of several new tyrosine kinase inhibitors [3] are now being studied. Preliminary results show clear evidence of response of a small percentage of patients, providing hope for future advances.

Anaplastic thyroid cancer

This form of thyroid cancer has a very poor prognosis (near 100% mortality) due to its aggressive behavior and resistance to cancer treatments. It rapidly invades surrounding tissues (such as the trachea). The presence of regional lymphadenopathy in older patients in whom FNA reveals characteristic vesicular appearance of the nuclei would support a diagnosis of anaplastic carcinoma.

Treatment

Unlike its differentiated counterparts, anaplastic thyroid cancer is highly unlikely to be curable either by surgery or by any other treatment modality, and is in fact usually unresectable due to its high propensity for invading surrounding tissues. Palliative treatment consists of radiation therapy usually combined with chemotherapy. However, with today's technology, new drugs, such as Bortezomib and TNF-Related Apoptosis Induced Ligand (TRAIL), are being introduced and trialed in clinical labs. Recent studies in Italy, have shown positive results against ATC, but more tests, outside the lab, are needed to confirm this, before it can be used in Chemotherapy. There has been some case studies where patients with aggressive Thyroid Cancer have survived outside the mean expected survival time. But the best treatment recommended at this stage is early detection and complete surgery, followed by Chemotherapy alongside Radiotherapy, for any chance of survival of ATC.

Adjuvant therapy for anaplastic thyroid cancer

Treatment of anaplastic-type carcinoma is generally palliative in its intent for a disease that is rarely cured and almost always fatal. The median survival from diagnosis ranges from 3 to 7 months, with worse prognosis associated with large tumours, distant metastases, acute obstructive symptoms, and leucocytosis. Death is attributable to upper airway obstruction and suffocation in half of patients, and to a combination of complications of local and distant disease, or therapy, or both in the remainder. In the absence of extracervical or unresectable disease, surgical excision should be followed by adjuvant radiotherapy. In the 18–24% of patients whose tumour seems both confined to the neck and grossly resectable, complete surgical resection followed by adjuvant radiotherapy and chemotherapy could yield a 75–80% survival at 2 years.

There are a number of clinical trials for anaplastic thyroid carcinoma[4] underway or being planned.

References

  • Bennedbæk F.N.; Perrild H.; Hegedüs L. (1999). "Diagnosis and treatment of the solitary thyroid nodule. Results of a European survey". Clinical Endocrinology. 50 (3): 357–363.
  • Carlo Ravetto, Luigia Colombo, Massimo E. Dottorini (2000). "Usefulness of fine-needle aspiration in the diagnosis of thyroid carcinoma". Cancer Cytopathology. 90 (6): 357–363.
  • Jacques Barbet, Loïc Campion, Françoise Kraeber-Bodéré, Jean-François Chatal, and the GTE Study Group (2005). "Prognostic Impact of Serum Calcitonin and Carcinoembryonic Antigen Doubling-Times in Patients with Medullary Thyroid Carcinoma". The Journal of Clinical Endocrinology & Metabolism. 90 (11): 6077–6084.

See also

External links

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