Papillary thyroid cancer

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sahar Memar Montazerin, M.D.[2] Ammu Susheela, M.D. [3]

There is limited information about the historical perspective of papillary thyroid cancer. Papillary thyroid cancer may be classified according to histological subtypes. The most common subtypes include conventional, follicular and tall cell form. The exact pathogenesis of papillary thyroid cancer is not fully understood. Papillary thyroid cancer has been associated with somatic rearrangement of RET protooncogene. On gross pathology, an ill-defined tumor, irregular borders, and firm consistency are characteristic findings of papillary thyroid cancer. There is no unique consensus on the definition of histological subtypes of papillary thyroid cancer. Papillary thyroid cancer is caused by a mutation in the RET gene and BRAF gene. Papillary thyroid cancer must be differentiated from other diseases that cause neck mass, such as branchial cleft cyst, thyroglossal duct cyst, cystic metastasis, multiple neurofibromas, and other thyroid cancers. The incidence of thyroid cancer is approximately 15.8 per 100,000 men and women annually. Papillary cancer incidence has increased by 4.4% per year from 1974 till 2013. The majority of papillary thyroid cancers manifest in individuals between the ages of 20 to 55. It is more common among women, with female to male ratio of approximately 3:1. Common risk factors in the development of papillary thyroid cancer are radiation exposure, family history of thyroid cancer, and iodine deficiency. If left untreated, patients with papillary thyroid cancer may progress to develop metastasis. Common complications of papillary thyroid cancer include vocal cord compression, dysphagia, and dyspnea. The presence of metastasis is associated with a particularly poor prognosis among patients with papillary thyroid cancer. The 10-year survival rate papillary thyroid cancer is 99%. According to the American Joint Committee on Cancer (AJCC) there are 4 stages of papillary thyroid cancer based on the clinical features and findings on imaging. Each stage is assigned a letter and a number that designate the tumor size, number of involved lymph node regions, and metastasis. Papillary thyroid cancer is primarily diagnosed based on clinical presentation. There are no established criteria for the diagnosis of papillary thyroid cancer. The biopsy is the gold standard test for the diagnosis of papillary thyroid cancer. The most common symptoms of papillary thyroid cancer include swelling in the neck, pain in the front of the neck, and hoarseness of voice. Patients with papillary thyroid cancer usually appear thin and cachectic. Physical examination of patients with papillary thyroid cancer is usually remarkable for thyromegaly, lymphadenopathy and anxiety. Laboratory findings consistent with the diagnosis of papillary thyroid cancer include presence of tumor markers such as thyroglobulin. Thyroglobulin can be used as a tumor marker for well-differentiated papillary thyroid cancer. An x-ray may be helpful in the diagnosis of papillary thyroid cancer. Findings on an x-ray diagnostic of metastasis to the lungs or other tissues. CT scan may be helpful in the diagnosis of papillary thyroid cancer. Findings on CT scan suggestive of papillary thyroid cancer include nodal masses suggesting metastasis to the lymph node. MRI may be helpful in the diagnosis of papillary thyroid cancer. It may be suggestive of lymph node involvement as the first presentation of papillary thyroid cancer on MRI imaging. Neck ultrasound may be performed to detect papillary thyroid cancer. Ultrasound imaging findings suggestive of malignant thyroid nodule include microcalcification, peripheral and coarse calcification, solid, hypoechoic nodule, locally invaded nodule, and presence of posterior acoustic shadowing. Treatment options for papillary thyroid cancer differes according to the stage and invasion of the tumor and include surgery, external beam radiation therapy ( EBRT), Thyroid suppression therapy, and targeted therapy. Surgery is the mainstay of treatment for papillary thyroid cancer. Surgical interventions of papillary thyroid cancer include total thyroidectomy and lobectomy. Each of these has its indications.

There is limited information about the historical perspective of papillary thyroid cancer.

Papillary thyroid cancer may be classified according to histological subtypes. The most common subtypes include conventional, follicular and tall cell form.

The exact pathogenesis of papillary thyroid cancer is not fully understood. Papillary thyroid cancer has been associated with somatic rearrangement of RET protooncogene. On gross pathology, an ill-defined tumor, irregular borders, and firm consistency are characteristic findings of papillary thyroid cancer. There is no unique consensus on the definition of histological subtypes of papillary thyroid cancer.

Papillary thyroid cancer is caused by a mutation in the RET gene and BRAF gene.

Papillary thyroid cancer must be differentiated from other diseases that cause neck mass, such as branchial cleft cyst, thyroglossal duct cyst, cystic metastasis, multiple neurofibromas, and other thyroid cancers.

The incidence of thyroid cancer is approximately 15.8 per 100,000 men and women annually. Papillary cancer incidence has increased by 4.4% per year from 1974 till 2013. The majority of papillary thyroid cancers manifest in individuals between the ages of 20 to 55. It is more common among women, with female to male ratio of approximately 3:1.

Common risk factors in the development of papillary thyroid cancer are radiation exposure, family history of thyroid cancer, and iodine deficiency.

If left untreated, patients with papillary thyroid cancer may progress to develop metastasis. Common complications of papillary thyroid cancer include vocal cord compression, dysphagia, and dyspnea. The presence of metastasis is associated with a particularly poor prognosis among patients with papillary thyroid cancer. The 10-year survival rate papillary thyroid cancer is 99%.

According to the American Joint Committee on Cancer (AJCC) there are 4 stages of papillary thyroid cancer based on the clinical features and findings on imaging. Each stage is assigned a letter and a number that designate the tumor size, number of involved lymph node regions, and metastasis.

Papillary thyroid cancer is primarily diagnosed based on clinical presentation. There are no established criteria for the diagnosis of papillary thyroid cancer. The biopsy is the gold standard test for the diagnosis of papillary thyroid cancer.

The most common symptoms of papillary thyroid cancer include swelling in the neck, pain in the front of the neck, and hoarseness of voice.

Patients with papillary thyroid cancer usually appear thin and cachectic. Physical examination of patients with papillary thyroid cancer is usually remarkable for thyromegaly, lymphadenopathy and anxiety.

Laboratory findings consistent with the diagnosis of papillary thyroid cancer include presence of tumor markers such as thyroglobulin. Thyroglobulin can be used as a tumor marker for well-differentiated papillary thyroid cancer.

An x-ray may be helpful in the diagnosis of papillary thyroid cancer. Findings on an x-ray diagnostic of metastasis to the lungs or other tissues.

CT scan may be helpful in the diagnosis of papillary thyroid cancer. Findings on CT scan suggestive of papillary thyroid cancer include nodal masses suggesting metastasis to the lymph node.

MRI may be helpful in the diagnosis of papillary thyroid cancer. It may be suggestive of lymph node involvement as the first presentation of papillary thyroid cancer on MRI imaging.

Neck ultrasound may be performed to detect papillary thyroid cancer. Ultrasound imaging findings suggestive of malignant thyroid nodule include microcalcification, peripheral and coarse calcification, solid, hypoechoic nodule, locally invaded nodule, and presence of posterior acoustic shadowing.

Other imaging studies for papillary thyroid cancer include radioiodine scan, which demonstrates increased uptake of radioactive iodine at the areas of metastases and laryngoscopy which demonstrates vocal cord immobility.

There are no other diagnostic studies associated with papillary thyroid cancer.

Treatment options for papillary thyroid cancer differes according to the stage and invasion of the tumor and include surgery, external beam radiation therapy ( EBRT), Thyroid suppression therapy, and targeted therapy.

Surgery is the mainstay of treatment for papillary thyroid cancer. Surgical interventions of papillary thyroid cancer include total thyroidectomy and lobectomy. Each of these has its indications.

Effective measures for the prevention of papillary thyroid cancer include avoidance of diets low in iodine and avoidance of radiation exposure.

There are no established measures for the secondary prevention of papillary thyroid cancer.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [2]; Alison Leibowitz [3]

There is limited information about the historical perspective of papillary thyroid cancer.

• The most evident sign of thyroid pathology is goiter, which used to be referred to bronchocoele.
• In 1656, Thomas Wharton named the gland the “thyroid,” referring to its shield-like shape.
• In 1811, Bernard Courtois discovered iodine and in 1813, W. Prout used iodine to treat thyroid goiter.
• In 1835, James Graves provided the primary description of exophthalmic goiter.
• In 1833, Allan Burns and Gaspard Bayle distinguished thyroid cancer from goiter.^[1]
• There is limited information about the historical perspective of papillary thyroid cancer.

• In the 19th century, thyroid surgery became an increasingly standard practice with the help of anesthesia and antiseptics. ^[2]
• In 1880, Ludwig Rehn preformed the first total thyroidectomy.
• In 1885, J. Mikulicz-Radecki preformed the first subtotal thyroidectomy.
• In 1934, Frederic and Irene Joliot-Curie discovered radioactive iodine isotope, which catalyzed diagnosis and treatment methods for thyroid diseases.
• In 1909, Theodor Kocher was awarded the Nobel Prize for his research on the physiology and hormonal implications of the thyroid gland. ^[3]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sahar Memar Montazerin, M.D.[2] Ammu Susheela, M.D. [3]

Papillary thyroid cancer may be classified according to histological subtypes. The most common subtypes include conventional, follicular and tall cell form.

• WHO classification of papillary thyroid cancer is as follows:^[1]
  • Papillary microcarcinoma (<1 cm)
  • Encapsulated
  • Follicular
  • Diffuse sclerosing
  • Tall cell
  • Columnar cell
  • Cribriform-morular APC
  • Hobnail (micropapillary/discohesive)
  • Fibromatosis/ Fasciitis-like stroma
  • Solid/Trabecular
  • Oncocytic
  • Spindle cell
  • Clear cell
  • Warthin-like
• Another classification system for papillary thyroid cancer is:^[2]
  • Conventional
  • Follicular variant
  • Papillary microcarcinoma
  • Tall cell
  • Oncocytic
  • Columnar cell
  • Diffuse sclerosing
  • Solid
  • Clear cell
  • Cribriform morular
  • Macrofollicular
  • PTC with prominent hobnail features
  • PTC with fasciitis-like stroma
  • Combined papillary and medullary carcinoma
  • PTC with dedifferentiation to anaplastic carcinoma
• The most common subtypes are:
  • Conventional
  • Follicular
  • Tall cell

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sahar Memar Montazerin, M.D.[2] Ammu Susheela, M.D. [3]

The exact pathogenesis of papillary thyroid cancer is not fully understood. Papillary thyroid cancer has been associated with somatic rearrangement of RET protooncogene. On gross pathology, an ill-defined tumor, irregular borders, and firm consistency are characteristic findings of papillary thyroid cancer. There is no unique consensus on the definition of histological subtypes of papillary thyroid cancer.

• The mitogen-activated protein kinase (MAPK) pathway is involved in signal transduction of receptor tyrosine kinase such as RET and NTRK1.^[1]
• Tyrosine kinase receptor activation leads to RAS activation which subsequently result in GTP substitution of GDP. The GTP-bound form of RAS makes BRAF active which in turn activates MEK and ERK.
• ERK is engaged in the regulation of gene transcription including cell differentiation, proliferation, and survival.

Growth factor binds to Receptor tyrosine kinase (RET, NTRK1)

GDP substitution by GTP

RAS activation

BRAF activation

MEK ativation

ERK activation

cell differentiation

cell proliferation

cell survival

The above algorithm is adopted from Endocrine patology book[2]

• The exact pathogenesis of papillary thyroid cancer (PTC) is not fully understood.^[3][4][5]
• Papillary thyroid cancer has been associated with somatic rearrangement of RET protooncogene se well as point mutation in BRAF and RAS genes.
• All of the aforementioned genetic alterations leads to mitogen-activated protein kinase (MAPK) pathway activation.
• The RET rearrangement encodes for a tyrosine kinase receptor.
• This rearrangement has also been observed in mice with a history of ionizing radiation exposure.
• Ionizing radiation has been well recognized for its role in papillary thyroid cancer etiology.
• The rearranged form of this gene is well-known as ret/PCT rearrangement and is believed to be related to PTC carcinogenesis.
• Papillary thyroid cancer metastasize through lymphatics.

• Genetic alteration associated with papillary thyroid cancer include:^[6]
  • Mutations in RET proto-oncogene
  • Mutations in the BRAF oncogene
  • RAS mutations
  • TRK rearrangements
  • HMGA2 overexpression

• Papillary thyroid cancer may be associated with:^[6][7]
  • Gardner syndrome (especially seen with cribriform-Morular Variant of PTC)
  • Cowden syndrome

• On gross pathology, an ill-defined tumor, irregular borders, and firm consistency are characteristic findings of papillary thyroid cancer.^[2]
• Calcification may also be present.
• Other less common features include:
  • Cystic nodule with attached papillary growth
  • A well-circumscribed, encapsulated nodule with a fleshy appearance that may show some cystic change

• Papillary thyroid carcinoma has numerous histological subtypes. Each subtype has some specific characteristics.^[2][6][9]
• There is no unique consensus on the definition of each subtype, so different pathologists may not agree with these definitions.
• Cytologic features of papillary thyroid cancer are diagnostic for this tumor. These features include:
  • Enlarged, irregular, oval shape nuclei that are overlapped because of the nuclear enlargement
  • Nuclear clearing
  • Ground glass appearance with prominent nuclear grooves
  • Pink cytoplasmic invaginations

Papillary thyroid cancer subtype	Features on Histopathological Microscopic Analysis
Follicular	Follicles with variable size Dark, eosinophilic colloid with scalloping ‘‘bubble gum’’ appearance Cytologic features including prominent nucleoli and increased mitotic activity are diagnostic
Conventional	Papillae with fibrovascular cores Enlarged nuclei with nuclear clearing Squamous metaplasia may be present
Tall cell	With a height 2 to 3 times greater than the width Cytologic features are diagnostic
Columnar cell	Pseudostratified cells Overlapping enlarged nuclei
Oncocytic	Large cells with abundant eosinophilic cytoplasm Enlarged nuclei with nuclear clearing
Solid	Sheets of tumor cells with abundant cytoplasm Enlarged nuclei with nuclear clearing
Diffuse sclerosing	Abundant psammoma bodies, and squamoid changes in the tumor cells Lymphocytic infiltrates in the background
Papillary thyroid carcinoma with prominent hobnail features	Hobnail cells with loss of polarity High-grade cytologic features including prominent nucleoli increased mitotic activity
Clear cell	Clear cells with a papillary architecture Cytological features of papillary thyroid cancer
Cribriform-Morular	Cribriform pattern with solid and spindle cell areas Squamous morules Nuclei with clearing and groove Involving both thyroid lobes
Macrofollicular	Composed of macrofollicles Cytological features of papillary thyroid cancer

Papillary thyroid cancer	Image
Micrograph of papillary thyroid carcinoma, tall cell variant – high magnification “Tall cells”: the largest dimension is 3x the smaller dimension Abundant eosinophilic cytoplasm Lack of pseudostratification is a significant differentiator from columnar cell variant of papillary thyroid carcinoma
Micrograph showing oncocytic variant of papillary thyroid carcinoma Large cells with abundant eosinophilic cytoplasm
Micrograph showing cribriform-Morular variant of papillary thyroid carcinoma Cribriform pattern with solid and spindle cell areas Squamous morules
Micrograph (high power view) showing nuclear changes in papillary thyroid carcinoma (PTC), which include: Groove formation Optical clearing Eosinophilic inclusions and overlapping of nuclei
Micrograph (high power view) of PTC demonstrating nuclear clearing and overlapping nuclei
Micrograph of papillary thyroid carcinoma demonstrating prominent papillae with fibrovascular cores
Micrograph of metastatic papillary thyroid carcinoma to a lymph node Papillary architecture — papillae with fibrovascular cores are present Lymph node with several germinal centers (left, top/right of image) Adipose tissue (fat) is seen at the edge of the image (bottom and left)
Micrograph of psammoma body in papillary thyroid cancer A single necrotic tumor cell in the center of this structure acts as the nidus for its formation

• Papillary thyroid cancer may be positive for following markers:^[2]
  • TTF-1
  • Thyroglobulin
  • Thyroid peroxidase
  • CD56 (NCAM)
  • PAX8
  • HBME-1
  • CITED1
  • Cytokeratin 19
  • Galectin 3
• These markers are helpful in the confirmation of thyroid origin of the tumor particularly when the tumor is outside of the thyroid gland.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sahar Memar Montazerin, M.D.[2] Ammu Susheela, M.D. [3]

Papillary thyroid cancer is caused by a mutation in the RET gene and BRAF gene.

• Common causes of papillary thyroid cancer may include:^[1]
  • Mutation in RET gene
  • Mutation in BRAF gene
• For more information on the potential causes of papillary thyroid cancer please click here.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [2] Sahar Memar Montazerin, M.D.[3]

Papillary thyroid cancer must be differentiated from other diseases that cause neck mass, such as branchial cleft cyst, thyroglossal duct cyst, cystic metastasis, and multiple neurofibromas.

• The differential of a cystic neck mass(es) includes:

• Thyroglossal duct cyst (only if single)
• Branchial cleft cyst (only if single)
• Cystic metastasis
• Abscess including tuberculous lymphadenitis
• Multiple neurofibromas

• Papillary thyroid cancer must be differentiated from other thyroid cancers as well as other disorders such as:

Disease Name	Age of Onset	Gender Preponderance	Signs/Symptoms	Imaging Feature(s)	Macroscopic Feature(s)	Microscopic Feature(s)	Laboratory Findings(s)	Other Feature(s)	Microscopic Appearance
Papillary Thyroid Cancer[1][2][3]	More common in the middle aged (30 – 50 years of age)	More commonly affects women	Asymptomatic thyroid mass or nodule Compressive symptoms, such as: Difficulty swallowing/breathing Persistent cough Stridor Vocal chord paralysis Rapid enlarging mass	On ultrasound Solitary mass with an irregular outline Located in the sub-capsular region High vascularity Imaging features are not characteristic of this cancer	Solitary hypoechogenic nodule with lobulated margin which may extend into adjacent tissues Calcification may be present or not	Empty-appearing nuclei with central clearing (Orphan Annie eye) Psammoma bodies	Thyroid function tests can be normal Serum thyroglobulin can be used as a tumor marker	History of radiation to the head and neck BRAF and/or RET mutation may be present The most common type of thyroid cancer
Follicular Thyroid Cancer[2][3][4]	Peak incidence at 40 – 60 years of age	More commonly affects women	Asymptomatic thyroid mass or nodule Compressive symptoms, such as: Difficulty swallowing/breathing Persistent cough Stridor Vocal chord paralysis Rapid enlarging mass	On ultrasound: Solid hypoechoic nodule with a peripheral halo indicating fibrous capsule Irregular margin Imaging features are not characteristic of this cancer	Single encapsulated nodule Thick and irregular capsule Can be cystic or hemorrhagic in appearance	Invades thyroid capsule and vasculature Uniform follicles	Thyroid function tests can be normal Serum thyroglobulin can be used as a tumor marker	RAS mutation may be present PAX8–PPARγ translocations
Medullary Thyroid Cancer[5][6][7][3]	Incidence increases with age More common in the 3rd to 4th decades of life	Both genders are affected equally	Solitary thyroid nodule Mostly affects upper lobe of thyroid gland Possible systemic symptoms due to hormonal secretion by the tumor Cervical lymphadenopathy	On ultrasound: Solitary hypoechoic nodule with or without calcification Imaging features are not characteristic of this cancer	Single non-encapsulated mass Gray-tan color	Sheets of cells in an amyloid stroma	Secretes calcitonin Normal thyroid function tests Carcinoembryonic antigen (CEA) may be used as a tumor marker Rarely negative for calcitonin	Can be part of MEN 2A and 2B syndrome Can be associated with RET mutation
Anaplastic Thyroid Cancer[8][9][10]	More common among older individuals Mean age at diagnosis is 65 years	More commonly affects women	Rapidly enlarging thyroid mass May manifest with compressive symptoms Can present with signs/symptoms of metastasis Constitutional symptoms may be present Hard nodular goiter without tenderness	On ultrasound: Solid hypoechoic nodule with a peripheral halo indicating fibrous capsule Irregular margin Imaging features are not characteristic of this cancer	Solid tumor with areas of necrosis and hemorrhage Infiltrative pattern	Undifferentiated, devastatingly aggressive variant of papillary/follicular thyroid cancer	Normal thyroid function tests	Poor prognosis May be associated with TP53 mutation
Follicular Adenoma[11]	More commonly affects individuals older than 50 years of age	More commonly affects women	Asymptomatic or symptoms of hyperthyroidism	Solitary nodule which may show echogenicity or not	Solitary, spherical, and encapsulated lesion Well demarcated from the surrounding parenchyma	Uniform follicles Absence of capsular or vascular invasion	Functional adenoma: Elevated T3, T4 Decreased TSH	May be considered functional or hot May be considered non-functional or cold
Multinodular Goiter[12]	Commonly affects individuals older than 60 years of age	More commonly affects women	Thyroid enlargement Signs/symptoms of hypo/hyperthyroidism	Multiple nodules with different echogenicity Calcification may be present	Multiple thyroid nodules	Variable sized follicles Some may show papillary projections without nuclear characteristics of papillary thyroid cancer	Classified as toxic and non-toxic Toxic: Hyperthyroidism Non-toxic: Normal thyroid function tests	Benign condition
Thyroid Lymphoma[13] [14][15][16]	Affects adults or elderly	More common among women	Rapidly enlarging mass/nodule of thyroid Compressive symptoms may be present Constitiutional symptoms can be present in 10% P/E:Firm, hard thyroid Fixed to the nearby structures Immobile even during swallowing Cervical or supraclavicular lymphadenopathy may be present	On ultrasound: Hypoechogenic appearance Difficult to distinguish from chronic thyroiditis	Thyroid nodule/mass Fixed to adjacent tissue Firm texture	It is of B cell lineage in the majority of cases Dffuse, large B-cell lymphomas is the most common subtype Marginal zone lymphoma is the second most common type	No specific test Some patients may have hypothyroidism Patients can also have antibodies against thyroid peroxidase or thyroglobulin	Preexisting chronic autoimmune (Hashimoto’s) thyroiditis is a known risk factor for this condition

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [2] Sahar Memar Montazerin, M.D.[3] Alison Leibowitz [4] Seyedmahdi Pahlavani, M.D. [5]

The incidence of thyroid cancer is approximately 15.8 per 100,000 men and women annually. The papillary cancer incidence has increased by 4.4% per year from 1974 till 2013. The majority of papillary thyroid cancers manifest in individuals between the ages of 20 to 55. It is more common among women, with female to male ratio of approximately 3:1.

• The incidence of thyroid cancer is approximately 15.8 per 100,000 men and women annually.^[1]
• The papillary cancer incidence has increased 4.4% per year from 1974 till 2013.^[2]
• It is suggested that increase in adiposity in childhood and early adulthood is related with this increase in incidence rate.
• The papillary thyroid cancer incidence-based mortality increased per year during 1974-2013.^[2]

• Papillary thyroid cancer (as is the case with follicular thyroid cancer) typically occurs in middle-aged individuals, with a peak incidence in the 3rd and 4th decades.^[3]
• The majority of papillary thyroid cancers manifest in individuals between the ages of 20 to 55..^[4]

• It is more common among women, with female to male ratio of approximately 3:1.^[5]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sahar Memar Montazerin, M.D.[2] Ammu Susheela, M.D. [3]

Common risk factors in the development of papillary thyroid cancer are radiation exposure, and family history of thyroid cancer.

• In general, risk factors for the development of thyroid cancers are:^[1][2][3]
  • Radiation therapy
  • Exposure to (131)Iodine in childhood
  • Family history of thyroid disease (including thyroid cancer)
  • History of enlarged thyroid (goiter)
  • Female gender
  • Asian race
• Common risk factors in the development of papillary thyroid cancer are:^[4]
  • Childhood head and neck irradiation
  • Total body irradiation for bone marrow transplantation
  • Any ionizing radiation exposure
  • Positive family history

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [2] Sahar Memar Montazerin, M.D.[3]

If left untreated, patients with papillary thyroid cancer may progress to develop metastasis. Common complications of papillary thyroid cancer include vocal cord compression, dysphagia, and dyspnea. The presence of metastasis is associated with a particularly poor prognosis among patients with papillary thyroid cancer. The 10-year survival rate papillary thyroid cancer is 99%.

• The symptoms of papillary thyroid cancer usually develop in the third or fourth decade of life and start with symptoms such as a painless lump in the neck.^[1]
• Without treatment, the patient will develop symptoms of compression and metastasis, which may be fatal.

• Complications of papillary thyroid cancer include:^[1]
  • Metastasis
  • Involvement of recurrent laryngeal nerve
  • Dysphagia
  • Dyspnea

• Prognosis is generally excellent, and the 10-year relative survival rate of patients with papillary thyroid cancer is approximately 99%.^[2]
• Prognosis of patients with papillary thyroid cancer depends on the following features:^[3][4]
  • Patient’s age
  • Size of the tumor
  • Presence of metastatic disease
  • Presence of tumor invasion into adjacent tissues
  • Gender (male gender has been associated with higher mortality rate)

• 5-year relative survival rate of papillary thyroid cancer depends on the invasion of the tumor at the time of diagnosis.^[5]
  • Localized tumor: 100%
  • Tumor with regional metastasis: 100%
  • Tumor with distant metastasis: 78%

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