Hypopharyngeal cancer

For patient information click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Gertrude Djouka, M.D.[2], Faizan Sheraz, M.D. [3]

Synonyms and keywords: Squamous cell carcinoma of the hypopharynx, SCC of the hypopharynx, hypopharyngeal squamous cell carcinoma

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Gertrude Djouka, M.D.[2], Faizan Sheraz, M.D. [3]

Overview

Hypopharyngeal cancer was discovered in 1970 by Dr.Harrison in London, U.K. Hypopharyngeal cancer is a disease in which malignant cells proliferate in the hypopharynx. Most hypopharyngeal cancers form in the squamous cells, which are thin, flat cells lining inside the hypopharynx. Hypopharyngeal cancer can be classified according to the anatomy regions and histopathological derivatives. The anatomic location of hypopharyngeal cancer is divided into 3 subtypes such as pyriform sinus cancer, postcricoid area cancer and posterior wall of the hypopharynx. There are no direct causes of hypopharyngeal cancer, however tobacco abuse, abuse of alcohol consumption, HPV infection, Plummer-Vinsom syndrome, and asbestos have been associated with hypopharyngeal cancer. Genes involved in the pathogenesis of hypopharyngeal cancer include p16, NOTCH1, cyclin D1, and TP53. Hypopharyngeal cancer is associated with sideropaenic dysphagia and Paterson Brown Kelly syndrome. On gross pathology, flattened plaques, mucosal ulceration, and raised margins of the lesion are characteristic findings of hypopharyngeal cancer. On microscopic histopathological analysis, spindle cells, basaloid cells, and nuclear atypia are characteristic findings of hypopharyngeal cancer. The prevalence of hypopharyngeal cancer is estimated to be 2,500 new cases annually in U.S and hypopharyngeal cancer is a very rare type of cancer. Hypopharyngeal cancer commonly affects patients in 55 to 65 years of age. Males are mostly affected with a hypopharyngeal cancer compare to women. Hypopharyngeal cancer comprises about 7% of all cancers of the head and neck. According to the National Cancer Institute and American Cancer Society, screening test for hypopharyngeal cancer is not recommended.The majority of patients with hypopharyngeal cancer are initially asymptomatic. Most patients with hypopharyngeal cancer clinically manisfest symptoms at a late stage (III and IV) because of the tumor aggression which metastasizes to lymph nodes and submucosa. Once the tumor has expanded from its original site, it may obstruct the aerodigestive tract. Most common clinical presentations are neck mass, dysphagia with weight loss, non healing sore throat, odynophagia, and hoarseness. Common complications of hypopharyngeal cancer include upper airway obstruction and disfigurement of the neck or face. The prognosis varies with the type of hypopharyngeal cancer. The Squamous cell carcinoma of the hypopharynx has a poor prognosis and small survival rate.The medical therapy with the combination of the radiotherapy has been used compared to surgical therapy for the treatment of hypopharyngeal cancer. Swallowing, speech and laryngeal preservation are important to consider during the treatment. The feasibility of surgery depends on the stage of hypopharyngeal cancer at the time of the diagnosis.The main goal of the surgery is to clear any margin that contains the tumor cells. The available surgery options are transoral laser surgery, total laryngectomy with partial pharyngectomy surgery, total laryngectomy and circumferential pharyngectomy.

Historical Prospective

Hypopharyngeal Cancer is a rare type of malignant tumor. Hypopharyngeal cancer was discovered by Harrisson in 1970 with more than half in the postcricoid part.

Classification

Hypopharyngeal cancer may be classified according to the location into 4 subtypes: pyriform sinus cancer, postcricoid area cancer, and posterior wall of hypopharynx cancer. A pyriform sinus cancer subtype is found in 60 to 85 percent of patients who are diagnosed with hypopharyngeal cancer. Hypopharyngeal cancer may also be classified based on the histopathology.

Pathophysiology

Hypopharyngeal cancer arises from squamous cells, which are cells that are normally involved in protection of aerodigestive tract. Hypopharyngeal cancer is a rare type of malignant cancer which has a delayed onset of clinical manifestations. Hypopharyngeal cancer is usually diagnosed at an advanced stage and it spreads to other organs such as lungs, mediastinum, bones, brain, liver, esophagus, and thyroid gland. The metastatic invasion depends on the anatomic location of the hypopharyngeal cancer. Hypopharyngeal cancer is mostly differentiated as squamous cell carcinoma, but the undifferentiated type can be found in the pyriform sinus region. The exact pathogenesis of the hypopharyngeal cancer is not exactly understood, but the p16, cyclin D1, NOTCH1, and TP53 gene mutations have been associated with the development of the hypopharyngeal cancer. Hypopharyngeal cancer is associated with sideropenic dysphagia and Paterson Brown Kelly syndrome. On gross pathology, flattened plaques, mucosal ulceration, and raised margins of the lesion are the characteristic findings of hypopharyngeal cancer. On microscopic histopathological analysis, spindle cells, basaloid cells, and nuclear atypia are the characteristic findings of hypopharyngeal cancer.

Causes

There are no direct causes for hypopharngeal cancer however, there are some common risk factors that may lead to gene mutations and cause the hypopharyngeal cancer. Common risk factors for hypopharyngeal cancer can be found here.

Differentiating Hypopharyngeal Cancer from other Diseases

Hypopharyngeal carcinoma must be differentiated from accessory salivary gland tumor, lymphoma, and retropharyngeal abscess.

Epidemiology and Demographics

The prevalence of hypopharyngeal cancer is estimated to be 2,500 new cases annually in U.S and hypopharyngeal cancer is a very rare type of cancer. Hypopharyngeal cancer commonly affects patients in 55 to 65 years of age. Males are mostly affected with a hypopharyngeal cancer compare to women. Hypopharyngeal cancer comprises about 7% of all cancers of the head and neck.

Risk Factors

Common risk factors in the development of hypopharyngeal cancer are tobacco use, and abuse of alcohol consumption.

Screening

According to the National Cancer Institute and American Cancer Society, screening test for hypopharyngeal cancer is not recommended.

Natural History, Complications and Prognosis

The majority of patients with hypopharyngeal cancer are initially asymptomatic. Most patients with hypopharyngeal cancer clinically manisfest symptoms at late stage (III and IV) because of the tumor aggression which metastasizes to lymph nodes and submucosa. Once the tumor has expanded from its site of origin, it may obstruct the aerodigestive tract. Most common clinical presentations are neck mass, dysphagia with weight loss, non healing sore throat, odynophagia, and hoarseness. Common complications of hypopharyngeal cancer include upper airway obstruction and disfigurement of the neck or face. The prognosis varies with the type of hypopharyngeal cancer. Squamous cell carcinoma of hypopharynx has poor prognosis and small survival rate.

Diagnostic Study of Choice and Staging

The diagnostic study of choice for hypopharyngeal cancer is CT scan with contrast of head and neck. The definitive diagnosis of hypopharyngeal cancer is biopsy of the tumor. According to the American Joint Committee of Cancer (AJCC) TNM staging system, there are 5 stages of hypopharyngeal cancer based on the tumor size, lymph node involvement, and distant metastasis.

History and Symptoms

The hallmark of hypopharyngeal cancer is dysphagia. A positive history of odynophagia and hoarseness is suggestive of hypopharyngeal cancer. Common symptoms include a lump in the neck, dysphagia, chronic sore throat and hoarseness.

Physical Examination

Patients with hypopharyngeal carcinoma are usually well appearing. Physical examination of the patients with hypopharyngeal carcinoma is usually remarkable for the neck swelling.

Laboratory Findings

There are no diagnostic laboratory findings associated with hypopharyngeal cancer.

Electrocardiogram

There are no ECG findings associated with hypopharyngeal cancer.

Chest X Ray

Chest X rays may be performed to detect metastasis of hypopharyngeal cancer to the lungs.

CT

Head and neck CT scan may be helpful in the diagnosis of hypopharyngeal cancer. Findings on CT scan suggestive of hypopharyngeal cancer include soft tissue mass, irregular thickening of the mucosa, and necrotic region which is a sign of metastasis.

MRI

MRI may be helpful in the diagnosis of hypopharyngeal cancer. Findings on the MRI suggestive of hypopharyneal cancer include tumors are hypointense on T1 and hyperintense on T2 for soft tissues.

Other Imaging Findings

Ultrasound may be helpful to assess hypopharyngeal cancer along with endoscopy. Ultrasound may be use to detect, and localize primary tumors that invade neighboring organs such as esophagus, thyroid gland, and postcricoid area.

Other Diagnostic Studies

Biopsy may be diagnostic of hypopharyngeal cancer. Findings on biopsy diagnostic of hypopharyngeal cancer include spindle cells, basaloid cells, and nuclear atypia.

Medical Therapy

The medical therapy with the combination of the radiotherapy has been used compared to surgical therapy for the treatment of hypopharyngeal cancer.The optimal therapy for hypopharyngeal cancer depends on the stage at the time of the diagnosis. The combined treatment helps with organ preservation. Swallowing, speech and laryngeal preservation are important to consider during the treatment.

Surgery

The feasibility of surgery depends on the stage of hypopharyngeal cancer at the time of diagnosis. The main goal of the surgery is to clear any margin that contains tumor cells. The available surgery options are transoral laser surgery, total laryngectomy with partial pharyngectomy surgery, total laryngectomy and circumferential pharyngectomy.

Primary Prevention

Effective measures for the primary prevention of hypopharyngeal cancer include smoking cessation, decrease alcohol consumption, increase vegetables and fruits consumption, and vaccination for HPV.

Secondary Prevention

Secondary prevention measures of hypopharyngeal cancer include routine physical examination of head and neck and thyroid Screening are recommended among the patients who had received radiation therapy to the head and neck regions.

References

Template:WH Template:WS

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Gertrude Djouka, M.D.[2]

Overview

Hypopharyngeal Cancer is a rare type of malignant tumor. Hypopharyngeal cancer was discovered by Harrisson in 1970 with more than half in the postcricoid part.

Historical Perspective

Discovery

Hypopharyngeal cancer is a rare type of malignant tumor.
Hypopharyngeal cancer was first discovered by Harrisson in 1970 in London, UK at his clinic. He also described that about 60 percent of hypopharyngeal cancer were derived from the postcricoid area.^[1]^[2]

References

↑ Helliwell TR (February 2003). “acp Best Practice No 169. Evidence based pathology: squamous carcinoma of the hypopharynx”. J. Clin. Pathol. 56 (2): 81–5. PMC 1769882. PMID 12560383.
↑ International Journal of Recent Scientific Research. doi:10.24327/IJRSR. ISSN 0976-3031. Missing or empty |title= (help)

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Gertrude Djouka, M.D.[2], Faizan Sheraz, M.D. [3]

Overview

Hypopharyngeal cancer may be classified according to the location into 4 subtypes: pyriform sinus cancer, postcricoid area cancer, and posterior wall of hypopharynx cancer. A pyriform sinus cancer subtype is found in 60 to 85 percent of patients who are diagnosed with hypopharyngeal cancer. Hypopharyngeal cancer may also be classified based on the histopathology.

Classification

Anatomic classification of hypoharyngeal cancer includes:^[1]^[2]^[3]

Histopathologic classification of hypopharyngeal cancer includes:^[4]

Squamous cell carcinomas
Basaloid squamoid carcinomas
Spindle–cell carcinomas
Small-cell carcinomas
Nasopharyngeal-type undifferentiate carcinomas
Carcinomas of the minor salivary glands

References

↑ Toland, Amanda Ewart; Joo, Young-Hoon; Lee, Youn-Soo; Cho, Kwang-Jae; Park, Jun-Ook; Nam, In-Chul; Kim, Chung-Soo; Kim, Sang-Yeon; Kim, Min-Sik (2013). “Characteristics and Prognostic Implications of High-Risk HPV-Associated Hypopharyngeal Cancers”. PLoS ONE. 8 (11): e78718. doi:10.1371/journal.pone.0078718. ISSN 1932-6203.
↑ Pracy P, Loughran S, Good J, Parmar S, Goranova R (May 2016). “Hypopharyngeal cancer: United Kingdom National Multidisciplinary Guidelines”. J Laryngol Otol. 130 (S2): S104–S110. doi:10.1017/S0022215116000529. PMC 4873926. PMID 27841124.
↑ “Hypopharyngeal Cancer Treatment (Adult) (PDQ(R)): Health Professional Version”. 2002. PMID 26389199.
↑ Rosai, Juan (1996). Ackerman’s surgical pathology. St. Louis: Mosby. ISBN 9780801670046.

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Gertrude Djouka, M.D.[2], Faizan Sheraz, M.D. [3]

Overview

Hypopharyngeal cancer arises from squamous cells, which are cells that are normally involved in protection of aerodigestive tract. Hypopharyngeal cancer is a rare type of malignant cancer which has a delayed onset of clinical manifestations. Hypopharyngeal cancer is usually diagnosed at an advanced stage and it spreads to other organs such as lungs, mediastinum, bones, brain, liver, esophagus, and thyroid gland. The metastatic invasion depends on the anatomic location of the hypopharyngeal cancer. Hypopharyngeal cancer is mostly differentiated as squamous cell carcinoma, however, the undifferentiated type may be found in the pyriform sinus region. The exact pathogenesis of the hypopharyngeal cancer is not exactly understood, but the p16, cyclin D1, NOTCH1, and TP53 gene mutations have been associated with the development of the hypopharyngeal cancer. Hypopharyngeal cancer is associated with sideropenic dysphagia and Paterson Brown Kelly syndrome. On gross pathology, flattened plaques, mucosal ulceration, and raised margins of the lesion are the characteristic findings of hypopharyngeal cancer. On microscopic histopathological analysis, spindle cells, basaloid cells, and nuclear atypia are the characteristic findings of hypopharyngeal cancer.

Pathophysiology

Hypopharyngeal cancer arises from squamous cells, which are cells that are normally involved in protection of aerodigestive tract.^[1]
Development of hypopharyngeal cancer is the result of multiple genetic mutations. These mutations lead to activation of oncogenes and inactivation of tumor suppression genes which ultimately results in deregulated cellular proliferation.
Overexpression of TP53 and cyclin D1 may lead to multiple primary cancers of the hypopharynx.

Genetics

Genes involved in the pathogenesis of hypopharyngeal cancer include:^[1]^[2]
- p16
- Cyclin D1
- TP53
- NOTCH1

Associated Diseases

Hypopharyngeal carcinoma is associated with:^[2]
- Sideropenic dysphagia
- Paterson-Brown-Kelly syndrome

Gross Pathology

On gross pathology, hypopharyngeal cancer is characterized by:^[2]
- Flattened plaques
- Raised margins of the lesion
- Mucosal ulceration
- Tumor spread to piriform sinus
- Exophytic

Microscopic Pathology

On microscopic histopathological analysis, hypopharyngeal carcinoma is characterized by:^[2]
- Spindle cells
- Basaloid cells
- Nuclear atypia
- Abundant chromatin

Immunohistochemistry

There are some immunohistochemistry markers involve in the hypopharyngeal cancer:^[2]

- Beta catenin positive
- C-erbB2 negative
- mRNA translation initial factor positive

References

↑ ^1.0 ^1.1 Kohmura, Takahide; Hasegawa, Yasuhisa; Ogawa, Tetsuya; Matsuura, Hidehiro; Takahashi, Masakatsu; Yanagita, Noriyuki; Nakashima, Tsutomu (1999). “Cyclin D1 and p53 Overexpression Predicts Multiple Primary Malignant Neoplasms of the Hypopharynx and Esophagus”. Archives of Otolaryngology–Head & Neck Surgery. 125 (12): 1351. doi:10.1001/archotol.125.12.1351. ISSN 0886-4470.
↑ ^2.0 ^2.1 ^2.2 ^2.3 ^2.4 Helliwell TR (February 2003). “acp Best Practice No 169. Evidence based pathology: squamous carcinoma of the hypopharynx”. J. Clin. Pathol. 56 (2): 81–5. PMC 1769882. PMID 12560383.

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Gertrude Djouka, M.D.[2], Faizan Sheraz, M.D. [3]

Overview

There are no direct causes for hypopharngeal cancer. However, there are some common risk factors that may lead to gene mutations and cause the hypopharyngeal cancer.

Causes

There are no established direct causes for hypopharngeal cancer. Common risk factors for hypopharyngeal cancer can be found here.^[1]

References

↑ What are the risk factors for laryngeal and hypopharyngeal cancers?. Cancer.org. Accessed on October 13, 2015. http://www.cancer.org/cancer/laryngealandhypopharyngealcancer/overviewguide/laryngeal-and-hypopharyngeal-cancer-overview-what-causes

Differentiating Hypopharyngeal Cancer from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Maneesha Nandimandalam, M.B.B.S.[2], Gertrude Djouka, M.D.[3], Qurrat-ul-ain Abid, M.D.[4]

Overview

Hypopharyngeal carcinoma must be differentiated from other diseases that present as a neck mass.

Differentiating Hypopharyngeal Cancer From other Diseases

Hypopharyngeal cancer should be differentiated from other diseases causing a neck mass such as congenital abnormalities, inflammatory, and malignant lesions.

Category	Diseases		Benign/ Malignant	Clinical manifestation						Paraclinical findings			Gold standard diagnosis	Associated findings
				Demography	History	Symptoms		Signs		Lab findings	Histopathology	Imaging
				Demography	History	Pain	Dysphagia	Mass exam	Others	Lab findings	Histopathology	Imaging
Congenital	Branchial cleft cyst^[1]		Benign	Age: 1-15 years old Familial occurrence	Lateral neck mass	−	±	Solitary Smooth Mobile Well-defined Non-pulsatile Fluctuant	A pit at the opening of the cyst	−	Squamous or ciliated epithelial lining Lymphoid tissue with germinal centers and subcapsular sinuses	CT: Well defined fluid attenuation with slight enhancement of the capsule Ultrasound: Typical features of a cyst are seen	−	Brachio-oto-renal syndrome Sinus or fistula
	Thyroglossal duct cyst^[2]^[3]		Benign	Age: 1-10 years old	Midline neck mass	−	−	Mobile Moves upwards with tongue protrusion and swallowing	−	−	Squamous or ciliated pseudostratified columnar lining Foci of thyroid gland tissue Granulation tissue or giant cells if it gets infected	Ultrasound: Anechoic, thin walls, and heterogeneous with internal septa CT with contrast: Well circumscribed, homogeneous fluid attenuation, & thin enhancing rim MRI: T1-dark, T2-bright images	−	−
	Hemangioma^[4]		Benign	Age: Birth−2 years old Female>male	Presents with a flat red or purple patch Regress gradually with age	−	−	Firm Rubbery Well-demarcated	Blanching Telangiectasias Erythematous patch	GLUT-1 VEGF	Lined by non-atypical endothelial cells Vascular structures with RBC	Ultrasound: High flow with vascular channels	MRI with or without gadolinium (Gd)	POEMS Castleman’s disease
	Vascular malformation^[5]^[6]		Benign	Incidence: 1 in 2000 to 5000 births Gender: No predilection	Venous: Present with a bluish swelling Arteriovenous: Present with purple/red swelling	±	−	Soft Compressible Non-tender Venous: No thrill, ↑ in size on valsalva AVM: Thrill, warm, pulsatile	Grow proportionally with age	Elevated D-dimer level in venous malfomations	Lined by single endothelial layer	Doppler ultrasound: Slow hypoechoic flow in Venous malformations – High flow in AVM MRI with gadolinium (Gd): Diffuse enhancement	MRI	−
Category	Diseases		Benign	Demography	History	Pain	Dysphagia	Mass exam	Others	Lab findings	Histopathology	Imaging	Gold standard diagnosis	Associated findings
Congenital	Lymphatic malformation^[7]^[8]		Benign	Age: Birth-5 years old Gender: No predilection	Presents with a large swelling mainly in the neck	−	+	Soft Non-compressible Non-pulsatile Fluctuant Positive transillumination	Never regress, expand/contract based on inflammation	−	Dilated lymphatic channels lined by endothelial cells Positive D2-40 stain	Ultrasound: Hypo/anechoic with thick septa and fluid CT: Homogeneous and cystic mass MRI: Hyperintense on T2 & peripheral wall enhancement on T1	−	Down syndrome Turner syndrome
	Laryngocele^[9]^[10]^[11]		Benign	More common in adults Male/female = 5:1	Presents with a neck swelling, hoarseness, stridor and globus sensation Episodic in nature	−	+	Soft Reducible Increase in size on valsalva	Common in glass blowers and trumpet players	−	Lined by pseudostratified ciliated columnar epithelium	X-ray & CT: Fluid and air containing cystic masses Direct laryngoscopy	CT scan	−
	Ranula^[12]^[13]		Benign	Age: 1st and 2nd decade Female/male = 1:1.4	Presents with a blue colored swelling in the floor of the mouth	−	−	Well circumscribed Fluctuant Soft	−	−	H&E: Mucin surrounded by inflammatory cells & fibrosis	CT: Cystic mass with tail sign	−	−
Category	Diseases		Benign	Demography	History	Pain	Dysphagia	Mass exam	Others	Lab findings	Histopathology	Imaging	Gold standard diagnosis	Associated findings
Congenital	Teratoma^[14]^[15]		Benign or malignant	Incidence: 1:4000 births Gender: No predilection	Presents as a firm lateral neck mass	−	−	Firm Non-tender	−	High ALP levels	Shows ectodermal, mesodermal, and endodermal tissues	CT & MRI: Shows calcification	−	−
	Dermoid cyst^[16]^[17]		Benign	Incidence: 3 in 10000 population Age: Birth-5 years old	Presents as a slow growing mass or a sinus	−	−	Freely mobile Solitary Rubbery Nonpulsatile Noncompressible	Usually normal Sometimes a pit or sinus A tuft of hair at the center of the pit for nasal dermoid cyst	−	Keratinizing squamous epithelium Occasional remnants of hair follicles, adipose tissue, and sweat glands	Ultrasound: Thin walled, unilocular CT with contrast: Well circumscribed, unilocular, sac-of-marbles appearance due to fatty tissue	−	−
	Thymic cyst^[18]		Benign	Age: 1-10 years old Males>Females	Presents as a soft mass, gradually enlarging, on left side of the neck (usual)	−	−	Soft Compressible	−	−	Squamous epithelium or cuboidal epithelium Lymphoid tissue in the cyst wall contains hassall’s corpuscles	Ultrasound: Unilocular cystic mass CT: Uni/multilocular, well circumscribed and nonenhancing	−	−
Category	Diseases		Benign	Demography	History	Pain	Dysphagia	Mass exam	Others	Lab findings	Histopathology	Imaging	Gold standard diagnosis	Associated findings
Inflammatory	Acute sialadenitis^[19]		Benign	Age: Occurs in all age groups Gender: No predilection	Presents with an unilateral erythematous swelling Bad breath Fever with chills	+	–	Tender Firm Purulent discharge expressed from the duct Smooth	Redness More common in people with bad oral hygiene	Elevated ESR Leukocytosis	Inflammatory infiltrate with microabscess formation	Ultrasound: Hypoechoic with ductal dilatation CT: Diffuse homogeneous enlargement	CT scan	−
	Chronic sialadenitis^[20]		Benign	Age: Occurs in all age groups Gender: No predilection	Presents with an unilateral swelling Recurrent episodes common	+	−	Non-tender Firm Smooth	Mostly due to obstruction by a stone or stricture	Elevated ESR Leukocytosis	Hyperplastic lymphoid infiltrates with loss of salivary gland acini Fibrosis	X-ray: Shows radiopaque stones CT: Reduced parenchymal volume	CT scan	−
	Reactive viral lymphadenopathy	CMV^[21]	Benign	Age: 10-35 years old Gender: No predilection	Flu-like illness	−	−	Non-tender Soft	Generalized or cervical lymphadenopathy	Elevated ESR Elevated SGOT/SGPT	H&E stain: Typical owl-eye inclusions (nuclear) Basophilic cytoplasmic inclusions	Usually not necessary	Fine needle aspiration cytology	−
		EBV^[22]^[23]	Benign	Age: Mainly adolescents Gender: No predilection	Sore throat Fever Malaise	−	−	Non-tender Firm	Bilateral posterior cervical, axillary, inguinal lymphadenopathy Ulcer or rash Redness	Atypical lymphocytosis Positive monospot test IgM & IgG antibodies against EBV ↑↑SGOT/SGPT	CD8+ lymphocytes Necrosis B lymphocyte blasts	Usually not necessary	Fine needle aspiration cytology	−
		HIV^[24]	Benign	Prevalence: 1.1 million in U.S Gender: Males>females	Flu-like illness Rash	−	−	Non-tender mass	Generalized lymphadenopathy	Leukopenia Thrombocytopenia Anemia Elevated AST/ALT Elevated CRP Elevated ESR	Lymphoid hyperplasia	Usually not necessary	Western blot & P24 antigen assay	−
		Viral URI^[25]	Benign	Incidence: More in fall & winter Age: Common in elderly and infants	Sore throat Cough Runny nose Sneezing	−	−	Non-tender	Mild cervical lymphadenopathy	Lymphocytosis Elevated ESR & C-reactive protein	Inflammatory infiltrate	No specific findings	−	−
Category	Diseases		Benign	Demography	History	Pain	Dysphagia	Mass exam	Others	Lab findings	Histopathology	Imaging	Gold standard diagnosis	Associated findings
Inflammatory	Bacterial lymphadenopathy	Tularemia^[26]^[27]	Benign	Age: Affects all age groups Gender: No predilection	Fever Chills Swelling Joint pains	+	−	Tender Edematous	Regional lymphadenopathy	Elevated ESR Elevated C-reactive protein	Caseating granuloma +/- multinucleated giant cells	No specific findings	PCR & serology	−
		Brucellosis^[28]	Benign	Incidence: 100-200 cases anually in USA Gender: Males>females	Flu-like illness	+	−	Tender	Cervical lymphadenopathy	Elevated ESR	Non-caseating granuloma + giant cells, epitheloid cells	No specific findings	Serology	−
		Cat-scratch disease^[29]^[30]	Benign	More common in the Southern of U.S among children and young adults	Cat exposure Fever Fatigue Headache	+	−	Tender cervical nodes	Vesicular Erythema Papule at site of inoculation Lymphadenopathy	Elevated ESR Serology: Positive antibody to Bartonella Henselae	Satellite micro–abscess with granuloma	−	−	Bacillary angiomatosis Bacillary peliosis
		Actinomycosis^[31]^[32]	Benign	No predilection in race, age [[Male] to female ratio : 1.5 to 3:1	History of dental procedure or trauma Poor oral hygiene Swelling mandible	−	−	Tender at the beginning Painless Fluctuant Non-tender at late stage	Red or blue skin rash	Elevated ESR Elevated CRP Gram positive filamentous rods	Sulfur granules Filamentous organism	−	Histological examination Bacterial culture of the abscess	Mandible osteomyelitis
		Mycobacterial infections^[22]^[33]^[34]	Benign	More common in adults and children in endemic continent such as Africa	Recent travel to endemic regions Exposure to TB patients	−	−	Matted cervical nodes Firm Non-tender	Lymphadenopathy	Positive PPD Presence of acid fast bacilli on Sputum smear	Chronic necrotizing caseating calcified granuloma	Neck Ultrasound: Multiple lymph nodes Fusion tendency Internal echoes	Culture for mycobacteria	−
		Streptococcal infection^[21]^[35]	Benign	More common in children and adolescents	Fever Absence of cough Difficulty swallowing Swollen pharynx	+	+	Tender anterior cervical nodes Tonsillar exudates	Lymphadenopathy	Rapid antigen detection tests: ±	Follicular hyperplasia Infiltration of polymorphonuclear cells	−	Throat culture	Acute rheumatic fever Post-streptoccocal glomerulonephritis
Category	Diseases		Benign	Demography	History	Pain	Dysphagia	Mass exam	Others	Lab findings	Histopathology	Imaging	Gold standard diagnosis	Associated findings
Inflammatory	Parasitic lymphadenopathy	Toxoplasma gondii^[36]^[37]	Benign	6 years old and older adults are more affected in U.S. Seen in hot climates	Cats or birds feces exposure Drinking unpasteurized milk Undercooked food Organ transplant recipients	+	−	Bilateral Non-tender Symmetrical Non-fluctuant	Lymphadenopathy	Serology: Positive IgG and IgM antibodies	Follicular hyperplasia	MRI: Multiple rings enhanced lesions	Serology Immunofluorescence MRI CT scan	−
	Sarcoidosis^[38]^[19]		Benign	More common in African American women aged 20-40 years	Family history of sarcoidosis Fatigue Swelling and pain in the joints	−	−	Swollen Non-tender parotid glands	Erythema nodosum Lupus pernios Bilateral lymphadenopathy	Elevated ESR Elevated ACE	Non-necrotizing epithelioid granuloma	CXR: B/L hilar adenopathy MRI: B/L multiples enlarged cervical lymph nodes	Biopsy	Heerfordt’s syndrome: uveitis, facial nerve paralysis, parotitis
	Sjögren syndrome^[39]		Benign	Female to male ratio: 9 to 1 May happen at any age Mean age: 40-50	History of RA, SLE, and non-hodgkin B-cell lymphoma Dry mouth, dry eyes	−	+	Firm mass B/L enlarged parotid glands	Pruritis Rashes Lymphadenopathy	Elevated ESR Anti-SSA/Ro: + Anti-SSB/La: + Cytopenia Wetting <5 mm on Schirmer’s test	Hyperactivity of B-cells and lymphocytes which lead to infiltration of the exocrine glands	US: Hypoechoic and inhomogeneous salivary glands	Biopsy	−
	Castleman disease (angiofollicular lymphoproliferative disease)^[40]^[41]		Benign	Mean age: 30-40 years	Asymptomatic at early onset B-symptoms	−	−	Non tender cervical node	Lymphadenopathy Papule Cherry hemangioma	Elevated ESR Elevated CRP Anemia Polyclonal hypergammaglobulinemia	Hyaline vascular variant Plasma cell variant Mixed variant	CT scan: Matted lymphadenopathy Solitary, noninvasive mass	Biopsy	HHV-8 Kaposi sarcoma Non-hodgkin lymphoma POEMS syndrome
Category	Diseases		Benign	Demography	History	Pain	Dysphagia	Mass exam	Others	Lab findings	Histopathology	Imaging	Gold standard diagnosis	Associated findings
Inflammatory	Kikuchi disease (histiocytic necrotizing lymphadenitis)^[42]		Benign	High prevalence in Japan More common in young adults < 30 years old	Fever Flu-like prodrome	+	−	Tender cervical nodes	Skin rash Lymphadenopathy	Elevated ESR Abnormal liver enzymes Leukopenia	Irregular paracortical areas of coagulative necrosis with abundant karyorrhectic debris	−	Biopsy	Hashimoto’s thyroiditis
	Kimura disease^[43]		Benign	More common in Asian males	History of painless cervical lump	−	−	Large Non-tender cervical node	Itching Lymphadenopathy	Elevated Eosinophils	Conserved lymph node structure Eosinophilic infiltration High postcapillary venules	−	Biopsy	Nephrotic syndrome Hypercoagulable state
	Rosai-Dorfman disease^[44]^[45]		Benign	More common in children	Fever	−	−	Non-tender enlarged cervical lymph nodes	Erythema Lymphadenopathy	Elevated ESR Polyclonal hypergammaglobulinemia	−	−	−	−
	Kawasaki disease^[46]^[47]		Benign	More common in children < 5 years old Highest incidence in Japan Most leading cause of acquired heart disease in U.S	High fever B/L conjunctivitis Rash Swelling of hands and feet Inflammation of lips Strawberry tongue	−	−	Large, single palpable cervical node	−	Elevated ESR Elevated CRP	Inflammation of medium sized arteries and organs	Echocardiography: Coronary artery dilation Coronary artery aneurysm	Clinical findings	−
Category	Diseases		Benign or Malignant	Demography	History	Pain	Dysphagia	Mass exam	Others	Lab findings	Histopathology	Imaging	Gold standard diagnosis	Associated findings
Neoplasm	Salivary gland neoplasm	Pleomorphic adenoma^[48]^[49]	Benign	More common in females Incidence increase with age Incidence: 2-3.5 cases per 100,000 population	History of swelling Dysphagia Hoarseness	−	+	Palpable mass of deep lobe of parotid gland Firm Mobile	−	−	Proliferation of epithelial cells and stromal matrix in the ducts	MRI: Homogenous on T1 Abundant myxochondroid stroma on T2	Biopsy	−
		Warthin’s tumor^[50]^[51]	Benign	Male to female ratio: 4:1 More common in people aged 60-70 years old	History of swollen salivary gland Jaw pain Tinnitus	−	+	Non tender Mobile Firm Solitary	−	−	Papillae Fibrous capsule Cystic spaces	Neck CT: Cystic lesion posteriorly within the parotid gland MRI: B/L heterogeneous lesions	Biopsy	−
		Oncocytoma ^[52]	Benign	Race: Caucasian patients predilection Gender: No gender preference Age: 50–70 years	Growing palpable painless mass Facial swelling Lymphadenopathy (if transformed to malignant)	±	±	Firm, multilobulated Mobile mass	Normal Redness Swelling Skin ulceration	Normal Anemia	Epithelial cells with eosinophilic Granular cytoplasm Rich in mitochondria	CT: Isodense expansive mass Enhancement after intravenous contrast Hypodense areas MRI: Isodensties on T1 Mass is hyperintense on T2 Enhancement on contrast	Incisional biopsy and histopathological examination	–
		Monomorphic adenoma ^[53]^[54]^[55]	Benign or malignant	Age: 26-76 years Rare in children Gender: No predilection	Growing palpable painless mass on jaw or in oral cavity Facial swelling Lymphadenopathy (if transformed to malignant) Pain and ulceration (in later stage)	±	±	Nodular Fluctuant swelling	Normal Redness Skin ulceration May have lymphadenopathy	Normal	Straw colored fluid on aspiration	Ultrasound: Used to biopsy the lesion May show cystic an solid components CT: useful for lesions with calcification and venous phleboliths MRI: Test of choice Differentiate benign from malignant Defines tumor extent Shows perineural spread	Incisional biopsy and histopathological examination	–
		Mucoepidermoid carcinoma ^[56]	Malignant	Age: Mean age of 59 Female predilection	Painlesss mass Swelling in oral cavity Lymphadenopathy	±	±	Cystic and solid mass	May have lymphadenopathy	−	Gross findings: Firm Tan-white to yellow Bosselated Cystic Microscopic findings: Encapsulated squamous and glandular components	Cystic and solid component with variable appearance on CT and MRI	Incisional biopsy and histopathological examination	Association with CMV
Category	Diseases		Benign	Demography	History	Pain	Dysphagia	Mass exam	Others	Lab findings	Histopathology	Imaging	Gold standard diagnosis	Associated findings
Neoplasm	Salivary gland neoplasm	Adenoid cystic carcinoma ^[57]	Malignant	Age: 40s-60s Gender: Female predominance	Slow growing rare tumor with low recurrence	±	±	Solid mass	Normal to ulcerated lesions May have lymphadenopathy	−	Gross findings: Tubular Cribriform Solid pattern of growth Microscopic findings: Components of large cells with pleomorphic nuclei Increased mitotic activity Focal necrosis	Imaging reveal dimensions of the tumor, local spread, and distant metastasis	Biopsy and histopathological examination	−
		Adenocarcinoma ^[58]	Malignant	Age: young age predilection	Its a tumor of minor salivary glands May present as small ulceration or nodules in oral cavity	−	−	Small nodules in oral cavity With or without lymphadenopathy	Normal to ulcerated lesions May have lymphadenopathy	May be normal Or may show anemia and blood cell disorders with distant bone invasion	On histology it is confused with Adeocyctic carcinoma Components of gland and cyst formations More perineural invasion	CT and MRI MRI being more accurate for adjacent tissue involvement and lymphadenopathy	Biopsy and histopathological examination	−
		Salivary duct cancer^[59]^[60]^[61]	Malignant (Highly aggressive)	Incidence: 1-3% Gender: Male predilection Mean age: 55-61 years old	Rapidly growing mass with jaw involvement	±	±	Painless Hard Non-compressible mass	Ulceration of mucosa and skin May have lymphadenopathy facial paralysis in case of facial nerve involvement	Pathomorphologically tumor of salivary ducts resembles tumor of breast ducts	Gross findings: Firm mass Cystic component of variable size and dimension Microscopic finding: Resembling ductal carcinoma of breast Intraductal components invading surrounding tissue in several forms: cribriform papillary Solid with comedo-like central necrosis	Non-specific features on CT and MRI Shows neural and jaw involvement	Biopsy and histopathological examination	−
		Squamous cell carcinoma^[62]^[63]	Malignant	Incidence: rare Age: Old age , 61-68 years Male predilection	Present as painful growing mass on jaw	+	−	Teneder Firm Solitary swelling on jaw	Submandibular gland predilection Thinning and discoloration of skin	Past radiation exposure is a strong risk factor	Gross findings: Thinning of skin Microscopically findings: Nest and solid sheets of tumor cells arranged in glandular pattern Immunohistochemical staining can be used to mark the squamous and keratin component	Tumor dimension can be delineated using both CT and MRI	Biopsy and histopathological examination	−
Category	Diseases		Benign	Demography	History	Pain	Dysphagia	Mass exam	Others	Lab findings	Histopathology	Imaging	Gold standard diagnosis	Associated findings
Neoplasm	Hypopharyngeal cancer^[64]^[65]^[66]		Malignant	More common in males Age: 55-65 years old Incidence: < 1/100,000 in U.S. More common in Japan, India, Iran	Tobacco use Abuse alcohol consumption HPV infection Lump in the neck Odynophagia Hoarseness	−	+	Non tender cervical node	Lymphadenopathy	−	Spindle cells Nuclear atypia Basaloid cells Abundant chromatin	Neck CT scan: Soft tissue mass Irregular thickening of mucosa Necrotic region MRI: Tumors are hypointense on T1 and hyperintense on T2	Biopsy	−
	Parathyroid cancer^[67]^[68]^[69]		Malignant	Incidence: Rare Mean age : 44-54 years old Gender: Female predilection	Presents with the hyperparathyroidism Bone pains Abdominal pain Nausea and vomiting Fatigue Confusion	+	+	Lower neck mass	Tachycardia Weight loss Sweating Neck swelling	Low TSH Increased T4 and T3 Hypercalcemia	Microscopic findings: Trabecular growth pattern High mitosis Surrounding thick fibrotic bands Capsular involvement Vascular invasion is common	CT and MRI shows more frequent lower lobe involvement, vascular involvement , lymph node metastasis, and perineural involvement Bone scan may show decreasing bone density	Biopsy and histopathological examination	Hereditary syndromes MEN-2B syndrome Neurofibromatosis type 1 VHL disease
	Carotid body tumors^[70]^[71]^[72]^[73]		Benign	Age: 26-55 years Male predominance	A slow growing neck mass	+	−	Mobile Non-tender neck mass (horizontally more than vertically) Pulsatile Bruit may be present	Change in voice Dizziness Tinnitus Headache	Rasised catecholamine levels	Microscopically they are extra-adrenal paragangliomas	Doppler ultrasound, CT, MRI and angiography is used to visualize the tumor Metaiodobenzylguanidine (MIBG) testing	Histopathology analysis and catecholamine levels	−
	Paraganglioma^[74]^[75]^[76]		Benign (Majority) Malignant (rare)	Age 50-70 years More in females	May be an accidental finding depending on their secretory nature or present with following symptoms: Palpitation Tremor Pulse-like vibratory sense Headache Change in voice Vertigo Catecholamine secreting paragangliomas presents with : Hypertension Headache Sweating Tachycardia	−	−	No visible mass Located deep in the the neck along the glossopharyngeal nerve	−	Biochemical testing may show catecholamine metabolites in serum or urine samples	Highly vascular tumors that involves nerves around vessels Gross findings: Fleshy tumor Pink to red-brown to gray in color Associated with hemorrhage or fibrosis Microscopic findings: Round or polygonal cells Nests or trabecular structures inside the capsule	Ultrasound Computed tomography Magnetic resonance imaging Angiography metaiodobenzylguanidine (MIBG) 18F-fluoro-2-deoxyglucose Positron emission tomography (FDG-PET)	Imaging and serum catecholamine analysis	−
Category	Diseases		Benign	Demography	History	Pain	Dysphagia	Mass exam	Others	Lab findings	Histopathology	Imaging	Gold standard diagnosis	Associated findings
Neoplasm	Schwannoma^[77]^[78]^[79]		Benign	Rare tumor Incidence: 1-10%	Slow growing mass Localized neural deficit depending on the site of peripheral nerve involved Vagus nerve or superior cervical sympathetic chain involvement (most common locations)	+	±	Multiple Slow growing nodules on the skin	Vagal involvement: Hoarseness Dysphagia Sympathetic nerve involvement may present as Horner’s syndrome: Dilated pupil Decrease sweating Dropping eyelid Vestibular nerve involvement & Hearing impairment (most common)	May be normal	Encapsulated neural tissue growth	Resembling Carotid body tumor on CT MRI and MRI angiography confirm the diagnosis	Imaging	neurofibromatosis type II
	Lymphoma ^[80]^[81]^[82]^[83]^[84]^[85]		Benign or malignant	Age: Predilection for older age Mean age: 55	Insidious onset slow growing lymph nodes Non-specific systemic B symptoms: Fever Night sweats Weight loss) Rash Waxing and waning lymphadenopathy Abdominal fullness	−	±	Multiple chain lymphadenopathy Hepatosplenomegaly Ascites Crackles heard on chest auscultation	Rash and pruritus	Pancytopenia Hypercalcemia Hyperuricemia (increased cell turnover) Monoclonal immunoglobulin (M-spike) Raised LDH levels	On complete node analysis four patterns are described: Nodular/follicular Diffuse pattern Transition from a nodular to a diffuse pattern in adjacent nodes Transition from a lower to a higher grade of involvement within a single node	Imaging to stage the disease Positron emission tomography with computed tomography is preferred over MRI	Lymph node biopsy coupled with cytometry	Infections due to cytopenias With acquired form of C1 inhibitor deficiency patients may develop angioedema
	Liposarcoma ^[86]^[87]^[88]^[89]		Malignant	Rare tumor Age: Relatively in older age Gender: No gender predilection	Mobile mass Few symptoms until they grow enough to compress the surrounding structures Symptoms of neural deficit, pain, tingling, or skin changes	±	−	Mobile soft mass Intact overlying skin Blue discoloration due to intra-lesion hemorrhage	Intact skin and normal color	Normal	Gross examination: Bulk of yellow colored fat tissue Microscopic features: Adipose tissue containing lipoblasts Atypical nucleus pushed to side by intracytoplasmic vacuoles Tissue biopsy may show histological sub-groups: Well-differentiated Myxoid/round cell Pleomorphic liposarcomas	Imaging not usually required for diagnosis May show deeper invasion Ultrasound shows homogeneous hyperechoic mass	Biopsy and histopathology analysis	−
Category	Diseases		Benign	Demography	History	Pain	Dysphagia	Mass exam	Others	Lab findings	Histopathology	Imaging	Gold standard diagnosis	Associated findings
Neoplasm	Lipoma ^[90]^[91]^[92]		Benign	Genetic predisposition Unspecific gender or age association	One or multiple soft, painless skin nodules May causes pain or compressive symptoms	±	−	Mobile soft nodule Intact overlying skin	Normal	Normal	Diagnoses is usually clinical Tissue biopsy may show: Bundle of well-demarcated lipocytes Single nuclei aligned to the side Intra-cytoplasimic fat granules	Diagnosis is usually clinical ultrasound is used to differentiate lipoma from other benign lesions such as: Epidermoid cyst A ganglion	Clinical evaluation	Multiple lipomas Associated with familial multiple lipomatosis
	Glomus vagale, glomus jugulare tumors^[93]^[94]^[95]^[96]^[97]^[98]		Benign	Rare tumor	Painless slowly enlarging mass in the neck	−	±	Non-compressible Firm Non-tender swelling No thrill or bruit Normal overlying skin	Secretory tumors May have compressive signs such as: Dysphagia Hoarseness Cranial nerves deficits Horner’s syndrome	Normal	Glomus tumors arise from Non Chromaffin cells histopathology reveals “salt and pepper” chromatin On immunohistochemistry tumor cells show chromogranin and S-100 positivity	MRI (Imaging of choice): Typical appearance of the tumor along vagus nerve Ultrasonography (early stage of diagnosis): Isoechoic to hypoechoic well defined tumor CT: Vascularity of the tumor Biochemical testing: Shows secretary nature of the tumor	Imaging and Metaiodobenzylguanidine (MIBG) testing	−
	Metastatic head and neck cancer^[99]^[100]		Malignant	Depends on the nature of metastatic tumor	Asymptomatic Painless lymphadenopathy Supra clavicular fullness in case of stomach cancer metastasis	−	±	Non-tender mass in the neck Non-tender lymphadenopathy	Majority of metastatic head and neck cancer Metastatise from GIT and lungs	Vary depending on the underlying cancer	Histology of primary cancer	CT and MRI to see extent of tumor	Biopsy and histopathology of the primary site of tumor	−
Category	Diseases		Benign	Demography	History	Pain	Dysphagia	Mass exam	Others	Lab findings	Histopathology	Imaging	Gold standard diagnosis	Associated findings
Other	Laryngeal cancer^[101]^[102]		Benign/Malignant	Older males Younger patients with HPV infection or smoking history	Neck mass Hoarseness Throat pain Snoring Obstructive sleep apnea	±	±	Examination of neck and oral cavity may show : mass lymphadenopathy Examination of laryngeal cancer is done using flexible laryngoscopy under anesthesia.	Smoking is the most common risk factor Smoking with alcohol increases the risk Oropharyngeal cancers presenting with neck masses are associated with human papillomavirus (HPV) infection	HPV testing may show HPV infection	FNA of neck mass Followed by biopsy of laryngeal cancer Show type cancer cells	CT, MRI and PET are used to see local infiltration by cancer Also to see distant metastases. Panendoscopy is done to see extent of the tumor.	Laryngoscopy and biopsy	−
	Arteriovenous fistula ^[103]^[104]		Benign/Malignant	Depends on the risk factors	Expanding neck mass Headaches Dizziness Neurological sequels	−	−	Pulsating neck mass Bruit	May be associated with vasculopathies metastatic invasion of vessels and neck surgery		Varies depending on the etiology	MR angiography	MR angiography	−
	Thyroid nodule/ Goiter ^[105]^[106]^[107]^[108]		Benign/ Malignant	Female predominance Young age (benign causes) Old age (malignant etiology)	Growing painless neck mass in front of neck Weight loss Palpitation Hoarseness Irritability	±	±	Painless Non-tender Asymmetrical neck mass in front of neck With smooth overlying skin Nodular surface Depending on the type: May be mobile Adherent to the underlying structure Lymphadenopathy in case of malignant features	Goiter is most commonly associated with iodine deficiency	Normal to low TSH levels in case of malignancy High TSH levels in case of goiter	FNA is done in case of goiter Core biopsy is performed if malignancy is suspected	USG: Shows nodular or non- nodular lesions in Thyroid US is better than CT. Thyroid radionuclide imaging: Shows radioiodine uptake Cold in case of malignancy Cold or hot in case of goiter.	Biopsy and histopathology of nodules	−
Category	Diseases		Benign	Demography	History	Pain	Dysphagia	Mass exam	Others	Lab findings	Histopathology	Imaging	Gold standard diagnosis	Associated findings

References

↑ Nahata, Vaishali (2016). “Branchial cleft cyst”. Indian Journal of Dermatology. 61 (6): 701. doi:10.4103/0019-5154.193718. ISSN 0019-5154.
↑ Amos J, Shermetaro C. PMID 30085599. Missing or empty |title= (help)
↑ Deaver MJ, Silman EF, Lotfipour S (August 2009). “Infected thyroglossal duct cyst”. West J Emerg Med. 10 (3): 205. PMC 2729228. PMID 19718389.
↑ Léauté-Labrèze, C.; Prey, S.; Ezzedine, K. (2011). “Infantile haemangioma: Part I. Pathophysiology, epidemiology, clinical features, life cycle and associated structural abnormalities”. Journal of the European Academy of Dermatology and Venereology. 25 (11): 1245–1253. doi:10.1111/j.1468-3083.2011.04102.x. ISSN 0926-9959.
↑ Cox JA, Bartlett E, Lee EI (May 2014). “Vascular malformations: a review”. Semin Plast Surg. 28 (2): 58–63. doi:10.1055/s-0034-1376263. PMC 4078214. PMID 25045330.
↑ Behravesh S, Yakes W, Gupta N, Naidu S, Chong BW, Khademhosseini A, Oklu R (December 2016). “Venous malformations: clinical diagnosis and treatment”. Cardiovasc Diagn Ther. 6 (6): 557–569. doi:10.21037/cdt.2016.11.10. PMC 5220204. PMID 28123976.
↑ Cox JA, Bartlett E, Lee EI (May 2014). “Vascular malformations: a review”. Semin Plast Surg. 28 (2): 58–63. doi:10.1055/s-0034-1376263. PMC 4078214. PMID 25045330.
↑ Guruprasad Y, Chauhan DS (September 2012). “Cervical cystic hygroma”. J Maxillofac Oral Surg. 11 (3): 333–6. doi:10.1007/s12663-010-0149-x. PMC 3428451. PMID 23997487.
↑ Werner RL, Schroeder JW, Castle JT (March 2014). “Bilateral laryngoceles”. Head Neck Pathol. 8 (1): 110–3. doi:10.1007/s12105-013-0478-4. PMC 3950389. PMID 23881550.
↑ Prasad KC, Vijayalakshmi S, Prasad SC (December 2008). “Laryngoceles – presentations and management”. Indian J Otolaryngol Head Neck Surg. 60 (4): 303–8. doi:10.1007/s12070-008-0108-8. PMC 3476818. PMID 23120570.
↑ Mahdoufi R, Barhmi I, Tazi N, Abada R, Roubal M, Mahtar M (July 2017). “Mixed Pyolaryngocele: A Rare Case of Deep Neck Infection”. Iran J Otorhinolaryngol. 29 (93): 225–228. PMC 5554815. PMID 28819622.
↑ Packiri S, Gurunathan D, Selvarasu K (September 2017). “Management of Paediatric Oral Ranula: A Systematic Review”. J Clin Diagn Res. 11 (9): ZE06–ZE09. doi:10.7860/JCDR/2017/28498.10622. PMC 5713871. PMID 29207849.
↑ Kokong D, Iduh A, Chukwu I, Mugu J, Nuhu S, Augustine S (June 2017). “Ranula: Current Concept of Pathophysiologic Basis and Surgical Management Options”. World J Surg. 41 (6): 1476–1481. doi:10.1007/s00268-017-3901-2. PMC 5422487. PMID 28194490.
↑ Chauhan DS, Guruprasad Y, Inderchand S (September 2011). “Congenital nasopharyngeal teratoma with a cleft palate: case report and a 7 year follow up”. J Maxillofac Oral Surg. 10 (3): 253–6. doi:10.1007/s12663-010-0140-6. PMC 3238564. PMID 22942597.
↑ Bahgat M, Bahgat Y, Bahgat A (July 2012). “Oropharyngeal teratoma, a rare cause of airway obstruction in neonates”. BMJ Case Rep. 2012. doi:10.1136/bcr-2012-006580. PMC 4543570. PMID 22814615.
↑ Paradis, Josée; Koltai, Peter J. (2015). “Pediatric Teratoma and Dermoid Cysts”. Otolaryngologic Clinics of North America. 48 (1): 121–136. doi:10.1016/j.otc.2014.09.009. ISSN 0030-6665.
↑ Gaddikeri S, Vattoth S, Gaddikeri RS, Stuart R, Harrison K, Young D, Bhargava P (2014). “Congenital cystic neck masses: embryology and imaging appearances, with clinicopathological correlation”. Curr Probl Diagn Radiol. 43 (2): 55–67. doi:10.1067/j.cpradiol.2013.12.001. PMID 24629659.
↑ Gaddikeri, Santhosh; Vattoth, Surjith; Gaddikeri, Ramya S.; Stuart, Royal; Harrison, Keith; Young, Daniel; Bhargava, Puneet (2014). “Congenital Cystic Neck Masses: Embryology and Imaging Appearances, With Clinicopathological Correlation”. Current Problems in Diagnostic Radiology. 43 (2): 55–67. doi:10.1067/j.cpradiol.2013.12.001. ISSN 0363-0188.
↑ ^19.0 ^19.1 Abdel Razek A, Mukherji S (June 2017). “Imaging of sialadenitis”. Neuroradiol J. 30 (3): 205–215. doi:10.1177/1971400916682752. PMC 5480791. PMID 28059621. Vancouver style error: initials (help)
↑ Orlandi MA, Pistorio V, Guerra PA (2013). “Ultrasound in sialadenitis”. J Ultrasound. 16 (1): 3–9. doi:10.1007/s40477-013-0002-4. PMC 3774898. PMID 24046793.
↑ ^21.0 ^21.1 Mohseni S, Shojaiefard A, Khorgami Z, Alinejad S, Ghorbani A, Ghafouri A (March 2014). “Peripheral lymphadenopathy: approach and diagnostic tools”. Iran J Med Sci. 39 (2 Suppl): 158–70. PMC 3993046. PMID 24753638.
↑ ^22.0 ^22.1 Mohseni S, Shojaiefard A, Khorgami Z, Alinejad S, Ghorbani A, Ghafouri A (March 2014). “Peripheral lymphadenopathy: approach and diagnostic tools”. Iran J Med Sci. 39 (2 Suppl): 158–70. PMC 3993046. PMID 24753638.
↑ Stuhlmann-Laeisz C, Oschlies I, Klapper W (December 2014). “Detection of EBV in reactive and neoplastic lymphoproliferations in adults-when and how?”. J Hematop. 7 (4): 165–170. doi:10.1007/s12308-014-0209-0. PMC 4243011. PMID 25478033.
↑ Moonim MT, Alarcon L, Freeman J, Mahadeva U, van der Walt JD, Lucas SB (March 2010). “Identifying HIV infection in diagnostic histopathology tissue samples–the role of HIV-1 p24 immunohistochemistry in identifying clinically unsuspected HIV infection: a 3-year analysis”. Histopathology. 56 (4): 530–41. doi:10.1111/j.1365-2559.2010.03513.x. PMID 20459560.
↑ Thomas M, Bomar PA. PMID 30422556. Missing or empty |title= (help)
↑ Grunow R, Splettstoesser W, McDonald S, Otterbein C, O’Brien T, Morgan C, Aldrich J, Hofer E, Finke EJ, Meyer H (January 2000). “Detection of Francisella tularensis in biological specimens using a capture enzyme-linked immunosorbent assay, an immunochromatographic handheld assay, and a PCR”. Clin. Diagn. Lab. Immunol. 7 (1): 86–90. PMC 95828. PMID 10618283.
↑ Koç, Sema (2012). “Clinical and laboratory findings of tularemia: a retrospective analysis”. The Turkish Journal of Ear Nose and Throat: 26–31. doi:10.5606/kbbihtisas.2012.005. ISSN 1300-7475.
↑ Golshani M, Buozari S (November 2017). “A review of Brucellosis in Iran: Epidemiology, Risk Factors, Diagnosis, Control, and Prevention”. Iran. Biomed. J. 21 (6): 349–59. PMC 5572431. PMID 28766326.
↑ “Cat-Scratch Disease in the United States, 2005–2013 – Volume 22, Number 10—October 2016 – Emerging Infectious Diseases journal – CDC”.
↑ Hansmann, Y.; DeMartino, S.; Piemont, Y.; Meyer, N.; Mariet, P.; Heller, R.; Christmann, D.; Jaulhac, B. (2005). “Diagnosis of Cat Scratch Disease with Detection of Bartonella henselae by PCR: a Study of Patients with Lymph Node Enlargement”. Journal of Clinical Microbiology. 43 (8): 3800–3806. doi:10.1128/JCM.43.8.3800-3806.2005. ISSN 0095-1137.
↑ Valour F, Sénéchal A, Dupieux C, Karsenty J, Lustig S, Breton P, Gleizal A, Boussel L, Laurent F, Braun E, Chidiac C, Ader F, Ferry T (2014). “Actinomycosis: etiology, clinical features, diagnosis, treatment, and management”. Infect Drug Resist. 7: 183–97. doi:10.2147/IDR.S39601. PMC 4094581. PMID 25045274.
↑ Bonnefond S, Catroux M, Melenotte C, Karkowski L, Rolland L, Trouillier S, Raffray L (June 2016). “Clinical features of actinomycosis: A retrospective, multicenter study of 28 cases of miscellaneous presentations”. Medicine (Baltimore). 95 (24): e3923. doi:10.1097/MD.0000000000003923. PMC 4998488. PMID 27311002.
↑ Suskind DL, Handler SD, Tom LW, Potsic WP, Wetmore RF (July 1997). “Nontuberculous mycobacterial cervical adenitis”. Clin Pediatr (Phila). 36 (7): 403–9. doi:10.1177/000992289703600705. PMID 9241478.
↑ Drobniewski FA, Caws M, Gibson A, Young D (March 2003). “Modern laboratory diagnosis of tuberculosis”. Lancet Infect Dis. 3 (3): 141–7. PMID 12614730.
↑ Kenealy T (November 2007). “Sore throat”. BMJ Clin Evid. 2007. PMC 2943825. PMID 19450346.
↑ Kumar GG, Mahadevan A, Guruprasad AS, Kovoor JM, Satishchandra P, Nath A, Ranga U, Shankar SK (June 2010). “Eccentric target sign in cerebral toxoplasmosis: neuropathological correlate to the imaging feature”. J Magn Reson Imaging. 31 (6): 1469–72. doi:10.1002/jmri.22192. PMC 2908244. PMID 20512900.
↑ [+https://www.cdc.gov/parasites/toxoplasmosis/diagnosis.html “CDC – Toxoplasmosis – Diagnosis”] Check |url= value (help).
↑ “Sarcoidosis | National Heart, Lung, and Blood Institute (NHLBI)”.
↑ Mavragani CP, Moutsopoulos HM (October 2014). “Sjögren syndrome”. CMAJ. 186 (15): E579–86. doi:10.1503/cmaj.122037. PMC 4203623. PMID 24566651.
↑ Dispenzieri A, Armitage JO, Loe MJ, Geyer SM, Allred J, Camoriano JK, Menke DM, Weisenburger DD, Ristow K, Dogan A, Habermann TM (November 2012). “The clinical spectrum of Castleman’s disease”. Am. J. Hematol. 87 (11): 997–1002. doi:10.1002/ajh.23291. PMC 3900496. PMID 22791417.
↑ Saeed-Abdul-Rahman I, Al-Amri AM (September 2012). “Castleman disease”. Korean J Hematol. 47 (3): 163–77. doi:10.5045/kjh.2012.47.3.163. PMC 3464333. PMID 23071471.
↑ Bosch X, Guilabert A (May 2006). “Kikuchi-Fujimoto disease”. Orphanet J Rare Dis. 1: 18. doi:10.1186/1750-1172-1-18. PMC 1481509. PMID 16722618.
↑ AlGhamdi FE, Al-Khatib TA, Marzouki HZ, AlGarni MA (March 2016). “Kimura disease: No age or ethnicity limit”. Saudi Med J. 37 (3): 315–9. doi:10.15537/smj.2016.3.14448. PMC 4800898. PMID 26905356.
↑ “Rosai-Dorfman disease | Genetic and Rare Diseases Information Center (GARD) – an NCATS Program”.
↑ Foucar E, Rosai J, Dorfman R (February 1990). “Sinus histiocytosis with massive lymphadenopathy (Rosai-Dorfman disease): review of the entity”. Semin Diagn Pathol. 7 (1): 19–73. PMID 2180012.
↑ “About Kawasaki Disease | Kawasaki Disease | CDC”.
↑ “Kawasaki Disease | National Heart, Lung, and Blood Institute (NHLBI)”.
↑ Debnath SC, Adhyapok AK (June 2010). “Pleomorphic adenoma (benign mixed tumour) of the minor salivary glands of the upper lip”. J Maxillofac Oral Surg. 9 (2): 205–8. doi:10.1007/s12663-010-0052-5. PMC 3244097. PMID 22190789.
↑ Kato H, Kawaguchi M, Ando T, Mizuta K, Aoki M, Matsuo M (August 2018). “Pleomorphic adenoma of salivary glands: common and uncommon CT and MR imaging features”. Jpn J Radiol. 36 (8): 463–471. doi:10.1007/s11604-018-0747-y. PMID 29845358.
↑ Chulam TC, Noronha Francisco AL, Goncalves Filho J, Pinto Alves CA, Kowalski LP (December 2013). “Warthin’s tumour of the parotid gland: our experience”. Acta Otorhinolaryngol Ital. 33 (6): 393–7. PMID 24376295.
↑ “Warthin tumor | Genetic and Rare Diseases Information Center (GARD) – an NCATS Program”.
↑ Chen B, Hentzelman JI, Walker RJ, Lai JP (2016). “Oncocytoma of the Submandibular Gland: Diagnosis and Treatment Based on Clinicopathology”. Case Rep Otolaryngol. 2016: 8719030. doi:10.1155/2016/8719030. PMC 5045990. PMID 27722003.
↑ Kim KH, Sung MW, Kim JW, Koo JW (July 2000). “Pleomorphic adenoma of the trachea”. Otolaryngol Head Neck Surg. 123 (1 Pt 1): 147–8. doi:10.1067/mhn.2000.102809. PMID 10889498.
↑ Pramod Krishna B (June 2013). “Pleomorphic Adenoma of Minor Salivary Gland in a 14 year Old Child”. J Maxillofac Oral Surg. 12 (2): 228–31. doi:10.1007/s12663-010-0125-5. PMC 3681990. PMID 24431845.
↑ Kessler AT, Bhatt AA (2018). “Review of the Major and Minor Salivary Glands, Part 2: Neoplasms and Tumor-like Lesions”. J Clin Imaging Sci. 8: 48. doi:10.4103/jcis.JCIS_46_18. PMC 6251244. PMID 30546932.
↑ Chenevert J, Barnes LE, Chiosea SI (February 2011). “Mucoepidermoid carcinoma: a five-decade journey”. Virchows Arch. 458 (2): 133–40. doi:10.1007/s00428-011-1040-y. PMID 21243374.
↑ Jones AV, Craig GT, Speight PM, Franklin CD (April 2008). “The range and demographics of salivary gland tumours diagnosed in a UK population”. Oral Oncol. 44 (4): 407–17. doi:10.1016/j.oraloncology.2007.05.010. PMID 17825603.
↑ Beltran D, Faquin WC, Gallagher G, August M (March 2006). “Selective immunohistochemical comparison of polymorphous low-grade adenocarcinoma and adenoid cystic carcinoma”. J. Oral Maxillofac. Surg. 64 (3): 415–23. doi:10.1016/j.joms.2005.11.027. PMID 16487803.
↑ Mlika M, Kourda N, Zidi Y, Aloui R, Zneidi N, Rammeh S, Zermani R, Jilani SB (January 2012). “Salivary duct carcinoma of the parotid gland”. J Oral Maxillofac Pathol. 16 (1): 134–6. doi:10.4103/0973-029X.92992. PMC 3303509. PMID 22434951.
↑ Schmitt NC, Kang H, Sharma A (November 2017). “Salivary duct carcinoma: An aggressive salivary gland malignancy with opportunities for targeted therapy”. Oral Oncol. 74: 40–48. doi:10.1016/j.oraloncology.2017.09.008. PMC 5685667. PMID 29103750.
↑ Simpson RH (July 2013). “Salivary duct carcinoma: new developments–morphological variants including pure in situ high grade lesions; proposed molecular classification”. Head Neck Pathol. 7 Suppl 1: S48–58. doi:10.1007/s12105-013-0456-x. PMC 3712088. PMID 23821208.
↑ Manvikar V, Ramulu S, Ravishanker ST, Chakravarthy C (May 2014). “Squamous cell carcinoma of submandibular salivary gland: A rare case report”. J Oral Maxillofac Pathol. 18 (2): 299–302. doi:10.4103/0973-029X.140909. PMC 4196305. PMID 25328317.
↑ Ying YL, Johnson JT, Myers EN (July 2006). “Squamous cell carcinoma of the parotid gland”. Head Neck. 28 (7): 626–32. doi:10.1002/hed.20360. PMID 16475198.
↑ Helliwell TR (February 2003). “acp Best Practice No 169. Evidence based pathology: squamous carcinoma of the hypopharynx”. J. Clin. Pathol. 56 (2): 81–5. PMC 1769882. PMID 12560383.
↑ International Journal of Recent Scientific Research. doi:10.24327/IJRSR. ISSN 0976-3031. Missing or empty |title= (help)
↑ Maasland, Denise HE; van den Brandt, Piet A; Kremer, Bernd; Goldbohm, R Alexandra; Schouten, Leo J (2014). “Alcohol consumption, cigarette smoking and the risk of subtypes of head-neck cancer: results from the Netherlands Cohort Study”. BMC Cancer. 14 (1). doi:10.1186/1471-2407-14-187. ISSN 1471-2407.
↑ Wei CH, Harari A (March 2012). “Parathyroid carcinoma: update and guidelines for management”. Curr Treat Options Oncol. 13 (1): 11–23. doi:10.1007/s11864-011-0171-3. PMID 22327883.
↑ Sahasranam P, Tran MT, Mohamed H, Friedman TC (August 2007). “Multiglandular parathyroid carcinoma: a case report and brief review”. South. Med. J. 100 (8): 841–4. doi:10.1097/SMJ.0b013e318073ca37. PMID 17713315.
↑ Holmes EC, Morton DL, Ketcham AS (April 1969). “Parathyroid carcinoma: a collective review”. Ann. Surg. 169 (4): 631–40. PMC 1387475. PMID 4886854.
↑ Sajid MS, Hamilton G, Baker DM (August 2007). “A multicenter review of carotid body tumour management”. Eur J Vasc Endovasc Surg. 34 (2): 127–30. doi:10.1016/j.ejvs.2007.01.015. PMID 17400487.
↑ Boedeker CC, Ridder GJ, Schipper J (2005). “Paragangliomas of the head and neck: diagnosis and treatment”. Fam. Cancer. 4 (1): 55–9. doi:10.1007/s10689-004-2154-z. PMID 15883711.
↑ Pellitteri PK, Rinaldo A, Myssiorek D, Gary Jackson C, Bradley PJ, Devaney KO, Shaha AR, Netterville JL, Manni JJ, Ferlito A (July 2004). “Paragangliomas of the head and neck”. Oral Oncol. 40 (6): 563–75. doi:10.1016/j.oraloncology.2003.09.004. PMID 15063383.
↑ Darouassi Y, Alaoui M, Mliha Touati M, Al Maghraoui O, En-Nouali A, Bouaity B, Ammar H (August 2017). “Carotid Body Tumors: A Case Series and Review of the Literature”. Ann Vasc Surg. 43: 265–271. doi:10.1016/j.avsg.2017.03.167. PMID 28478173.
↑ Neumann HP, Pawlu C, Peczkowska M, Bausch B, McWhinney SR, Muresan M, Buchta M, Franke G, Klisch J, Bley TA, Hoegerle S, Boedeker CC, Opocher G, Schipper J, Januszewicz A, Eng C (August 2004). “Distinct clinical features of paraganglioma syndromes associated with SDHB and SDHD gene mutations”. JAMA. 292 (8): 943–51. doi:10.1001/jama.292.8.943. PMID 15328326.
↑ Erickson D, Kudva YC, Ebersold MJ, Thompson GB, Grant CS, van Heerden JA, Young WF (November 2001). “Benign paragangliomas: clinical presentation and treatment outcomes in 236 patients”. J. Clin. Endocrinol. Metab. 86 (11): 5210–6. doi:10.1210/jcem.86.11.8034. PMID 11701678.
↑ O’Riordain DS, Young WF, Grant CS, Carney JA, van Heerden JA (September 1996). “Clinical spectrum and outcome of functional extraadrenal paraganglioma”. World J Surg. 20 (7): 916–21, discussion 922. PMID 8678971.
↑ Hilton DA, Hanemann CO (April 2014). “Schwannomas and their pathogenesis”. Brain Pathol. 24 (3): 205–20. doi:10.1111/bpa.12125. PMID 24450866.
↑ Albert P, Patel J, Badawy K, Weissinger W, Brenner M, Bourhill I, Parnell J (2017). “Peripheral Nerve Schwannoma: A Review of Varying Clinical Presentations and Imaging Findings”. J Foot Ankle Surg. 56 (3): 632–637. doi:10.1053/j.jfas.2016.12.003. PMID 28237565.
↑ Wong B, Bathala S, Grant D (January 2017). “Laryngeal schwannoma: a systematic review”. Eur Arch Otorhinolaryngol. 274 (1): 25–34. doi:10.1007/s00405-016-4013-6. PMID 27020268. Vancouver style error: initials (help)
↑ Anderson T, Chabner BA, Young RC, Berard CW, Garvin AJ, Simon RM, DeVita VT (December 1982). “Malignant lymphoma. 1. The histology and staging of 473 patients at the National Cancer Institute”. Cancer. 50 (12): 2699–707. PMID 7139563.
↑ Anderson T, Chabner BA, Young RC, Berard CW, Garvin AJ, Simon RM, DeVita VT (December 1982). “Malignant lymphoma. 1. The histology and staging of 473 patients at the National Cancer Institute”. Cancer. 50 (12): 2699–707. PMID 7139563.
↑ Negri E, Little D, Boiocchi M, La Vecchia C, Franceschi S (August 2004). “B-cell non-Hodgkin’s lymphoma and hepatitis C virus infection: a systematic review”. Int. J. Cancer. 111 (1): 1–8. doi:10.1002/ijc.20205. PMID 15185336.
↑ Moormeier JA, Williams SF, Golomb HM (February 1990). “The staging of non-Hodgkin’s lymphomas”. Semin. Oncol. 17 (1): 43–50. PMID 2406917.
↑ Negri E, Little D, Boiocchi M, La Vecchia C, Franceschi S (August 2004). “B-cell non-Hodgkin’s lymphoma and hepatitis C virus infection: a systematic review”. Int. J. Cancer. 111 (1): 1–8. doi:10.1002/ijc.20205. PMID 15185336.
↑ Anderson T, Chabner BA, Young RC, Berard CW, Garvin AJ, Simon RM, DeVita VT (December 1982). “Malignant lymphoma. 1. The histology and staging of 473 patients at the National Cancer Institute”. Cancer. 50 (12): 2699–707. PMID 7139563.
↑ Evans HL (January 2007). “Atypical lipomatous tumor, its variants, and its combined forms: a study of 61 cases, with a minimum follow-up of 10 years”. Am. J. Surg. Pathol. 31 (1): 1–14. doi:10.1097/01.pas.0000213406.95440.7a. PMID 17197914.
↑ Conyers R, Young S, Thomas DM (2011). “Liposarcoma: molecular genetics and therapeutics”. Sarcoma. 2011: 483154. doi:10.1155/2011/483154. PMC 3021868. PMID 21253554.
↑ Alaggio R, Coffin CM, Weiss SW, Bridge JA, Issakov J, Oliveira AM, Folpe AL (May 2009). “Liposarcomas in young patients: a study of 82 cases occurring in patients younger than 22 years of age”. Am. J. Surg. Pathol. 33 (5): 645–58. doi:10.1097/PAS.0b013e3181963c9c. PMID 19194281.
↑ Serpell JW, Chen RY (July 2007). “Review of large deep lipomatous tumours”. ANZ J Surg. 77 (7): 524–9. doi:10.1111/j.1445-2197.2007.04042.x. PMID 17610686.
↑ de Bree E, Karatzanis A, Hunt JL, Strojan P, Rinaldo A, Takes RP, Ferlito A, de Bree R (May 2015). “Lipomatous tumours of the head and neck: a spectrum of biological behaviour”. Eur Arch Otorhinolaryngol. 272 (5): 1061–77. doi:10.1007/s00405-014-3065-8. PMID 24800932.
↑ Rydholm A, Berg NO (December 1983). “Size, site and clinical incidence of lipoma. Factors in the differential diagnosis of lipoma and sarcoma”. Acta Orthop Scand. 54 (6): 929–34. PMID 6670522.
↑ Myhre-Jensen O (June 1981). “A consecutive 7-year series of 1331 benign soft tissue tumours. Clinicopathologic data. Comparison with sarcomas”. Acta Orthop Scand. 52 (3): 287–93. PMID 7282321.
↑ Urquhart AC, Johnson JT, Myers EN, Schechter GL (April 1994). “Glomus vagale: paraganglioma of the vagus nerve”. Laryngoscope. 104 (4): 440–5. doi:10.1288/00005537-199404000-00008. PMID 8164483.
↑ Valavanis A, Schubiger O, Oguz M (1983). “High-resolution CT investigation of nonchromaffin paragangliomas of the temporal bone”. AJNR Am J Neuroradiol. 4 (3): 516–9. PMID 6308990.
↑ Urquhart AC, Johnson JT, Myers EN, Schechter GL (April 1994). “Glomus vagale: paraganglioma of the vagus nerve”. Laryngoscope. 104 (4): 440–5. doi:10.1288/00005537-199404000-00008. PMID 8164483.
↑ Stein PP, Black HR (January 1991). “A simplified diagnostic approach to pheochromocytoma. A review of the literature and report of one institution’s experience”. Medicine (Baltimore). 70 (1): 46–66. PMID 1988766.
↑ Sajid MS, Hamilton G, Baker DM (August 2007). “A multicenter review of carotid body tumour management”. Eur J Vasc Endovasc Surg. 34 (2): 127–30. doi:10.1016/j.ejvs.2007.01.015. PMID 17400487.
↑ Boedeker CC, Ridder GJ, Schipper J (2005). “Paragangliomas of the head and neck: diagnosis and treatment”. Fam. Cancer. 4 (1): 55–9. doi:10.1007/s10689-004-2154-z. PMID 15883711.
↑ Gluckman JL, Robbins KT, Fried MP (1990). “Cervical metastatic squamous carcinoma of unknown or occult primary source”. Head Neck. 12 (5): 440–3. PMID 2211107.
↑ Waltonen JD, Ozer E, Hall NC, Schuller DE, Agrawal A (October 2009). “Metastatic carcinoma of the neck of unknown primary origin: evolution and efficacy of the modern workup”. Arch. Otolaryngol. Head Neck Surg. 135 (10): 1024–9. doi:10.1001/archoto.2009.145. PMID 19841343.
↑ Feldman PS, Kaplan MJ, Johns ME, Cantrell RW (November 1983). “Fine-needle aspiration in squamous cell carcinoma of the head and neck”. Arch Otolaryngol. 109 (11): 735–42. PMID 6639441.
↑ Grénman R, Koivunen P, Minn H (2015). “[Laryngeal cancer in Finland]”. Duodecim (in Finnish). 131 (4): 331–7. PMID 26237923.
↑ Guneyli S, Cinar C, Bozkaya H, Korkmaz M, Oran I (September 2016). “Endovascular management of congenital arteriovenous fistulae in the neck”. Diagn Interv Imaging. 97 (9): 871–5. doi:10.1016/j.diii.2015.08.006. PMID 26972281.
↑ Gobin YP, Garcia de la Fuente JA, Herbreteau D, Houdart E, Merland JJ (November 1993). “Endovascular treatment of external carotid-jugular fistulae in the parotid region”. Neurosurgery. 33 (5): 812–6. PMID 8264877.
↑ Madjar S, Weissberg D (July 1995). “Retrosternal goiter”. Chest. 108 (1): 78–82. PMID 7606997.
↑ Hedayati N, McHenry CR (March 2002). “The clinical presentation and operative management of nodular and diffuse substernal thyroid disease”. Am Surg. 68 (3): 245–51, discussion 251–2. PMID 11893102.
↑ Hughes K, Eastman C (August 2012). “Goitre – causes, investigation and management”. Aust Fam Physician. 41 (8): 572–6. PMID 23145396.
↑ Hermus AR, Huysmans DA (August 2000). “[Diagnosis and therapy of patients with euthyroid goiter]”. Ned Tijdschr Geneeskd (in Dutch; Flemish). 144 (34): 1623–7. PMID 10972051.

Template:WH Template:WS

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Gertrude Djouka, M.D.[2], Faizan Sheraz, M.D. [3]

Overview

The prevalence of hypopharyngeal cancer is estimated to be 2,500 new cases in the U.S annually and hypopharyngeal cancer is a very rare type of cancer. Hypopharyngeal cancer commonly affects patients in 55 to 65 years of age. Males are commonly affected with a hypopharyngeal cancer compared to women. Hypopharyngeal cancer comprises about 7% of all cancers of the head and neck.

Epidemiology and Demographics

Prevalence

The prevalence of hypopharyngeal cancer is estimated to be 2,500 new cases in the United states, annually.^[1]
Hypopharyngeal cancer comprises about 7% of all cancers of head and neck.^[2]

Incidence

The incidence of hypopharyngeal cancer is estimated to less than 1 per 100,000 individuals in the United States, annually.^[3]^[2]

Age

Hypopharyngeal cancer commonly affects patients in 55 to 65 years of age.^[4]

Gender

Males are commonly affected with a hypopharyngeal cancer compared to females.
Women are commonly affected with postcricoid carcinoma.^[2]^[5]
Males are commonly affected with piriform sinuses and posterior pharyngeal wall carcinoma.^[2]

Region

Hypopharyngeal cancer is more common in Japan, India and Iran.^[2]

References

↑ DeVita, Vincent (2011). DeVita, Hellman, and Rosenberg’s cancer : principles & practice of oncology. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 978-1-4511-0545-2.
↑ ^2.0 ^2.1 ^2.2 ^2.3 ^2.4 International Journal of Recent Scientific Research. doi:10.24327/IJRSR. ISSN 0976-3031. Missing or empty |title= (help)
↑ Hypopharyngeal cancer epidemiology and treatment. http://www.cancer.gov/types/head-and-neck/hp/hypopharyngeal-treatment-pdq
↑ Barnes, Leon (2001). Surgical pathology of the head and neck. New York: M. Dekker. ISBN 0-8247-0109-7.
↑ Barnes, Leon (2001). Surgical pathology of the head and neck. New York: M. Dekker. ISBN 0-8247-0109-7.

Template:WH Template:WS

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Gertrude Djouka, M.D.[2], Faizan Sheraz, M.D. [3]

Overview

Common risk factors in the development of hypopharyngeal cancer are tobacco use, and abuse of alcohol consumption.

Risk Factors

Common Risk Factors

Common risk factors for the development of hypopharyngeal cancer include^[1]:

Tobacco use.
Abuse of alcohol consumption.

Less Common Risk Factors

Less common risk factors for development of hypopharangeal cancer include:

Plummer-Vinson syndrome.^[2]
HPV infection.^[3]
Areca nut and betel quid chewing habit.^[4]^[5]
Diet with insufficient nutrients.
Occupational exposures such as:

Asbestos^[6]

References

↑ Maasland, Denise HE; van den Brandt, Piet A; Kremer, Bernd; Goldbohm, R Alexandra; Schouten, Leo J (2014). “Alcohol consumption, cigarette smoking and the risk of subtypes of head-neck cancer: results from the Netherlands Cohort Study”. BMC Cancer. 14 (1). doi:10.1186/1471-2407-14-187. ISSN 1471-2407.
↑ Novacek, Gottfried (2006). Orphanet Journal of Rare Diseases. 1 (1): 36. doi:10.1186/1750-1172-1-36. ISSN 1750-1172. Missing or empty |title= (help)
↑ Toland, Amanda Ewart; Joo, Young-Hoon; Lee, Youn-Soo; Cho, Kwang-Jae; Park, Jun-Ook; Nam, In-Chul; Kim, Chung-Soo; Kim, Sang-Yeon; Kim, Min-Sik (2013). “Characteristics and Prognostic Implications of High-Risk HPV-Associated Hypopharyngeal Cancers”. PLoS ONE. 8 (11): e78718. doi:10.1371/journal.pone.0078718. ISSN 1932-6203.
↑ Guha, Neela; Warnakulasuriya, Saman; Vlaanderen, Jelle; Straif, Kurt (2014). “Betel quid chewing and the risk of oral and oropharyngeal cancers: A meta-analysis with implications for cancer control”. International Journal of Cancer. 135 (6): 1433–1443. doi:10.1002/ijc.28643. ISSN 0020-7136.
↑ Auluck A, Hislop G, Poh C, Zhang L, Rosin MP (2009). “Areca nut and betel quid chewing among South Asian immigrants to Western countries and its implications for oral cancer screening”. Rural Remote Health. 9 (2): 1118. PMC 2726113. PMID 19445556.
↑ Langevin SM, O’Sullivan MH, Valerio JL, Pawlita M, Applebaum KM, Eliot M, McClean MD, Kelsey KT (December 2013). “Occupational asbestos exposure is associated with pharyngeal squamous cell carcinoma in men from the greater Boston area”. Occup Environ Med. 70 (12): 858–63. doi:10.1136/oemed-2013-101528. PMC 4227396. PMID 24142981.

Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Gertrude Djouka, M.D.[2], Faizan Sheraz, M.D. [3]

Overview

According to the National Cancer Institute and American Cancer Society, screening test for hypopharyngeal cancer is not recommended.

Screening

According to the National Cancer Institute and American Cancer Society, screening test for hypopharyngeal cancer is not recommended.

References

Natural History, Complications and Prognosis

Please help WikiDoc by adding content here. It’s easy! Click here to learn about editing.

References

Template:WH Template:WS

 complications and prognosis

Diagnosis

Treatment

Case Studies

Case #1

Template:WH Template:WS

[pmid12560383-1] Helliwell TR (February 2003). “acp Best Practice No 169. Evidence based pathology: squamous carcinoma of the hypopharynx”. J. Clin. Pathol. 56 (2): 81–5. PMC 1769882. PMID 12560383.

[2] International Journal of Recent Scientific Research. doi:10.24327/IJRSR. ISSN 0976-3031. Missing or empty |title= (help)

[TolandJoo2013-1] Toland, Amanda Ewart; Joo, Young-Hoon; Lee, Youn-Soo; Cho, Kwang-Jae; Park, Jun-Ook; Nam, In-Chul; Kim, Chung-Soo; Kim, Sang-Yeon; Kim, Min-Sik (2013). “Characteristics and Prognostic Implications of High-Risk HPV-Associated Hypopharyngeal Cancers”. PLoS ONE. 8 (11): e78718. doi:10.1371/journal.pone.0078718. ISSN 1932-6203.

[pmid27841124-2] Pracy P, Loughran S, Good J, Parmar S, Goranova R (May 2016). “Hypopharyngeal cancer: United Kingdom National Multidisciplinary Guidelines”. J Laryngol Otol. 130 (S2): S104–S110. doi:10.1017/S0022215116000529. PMC 4873926. PMID 27841124.

[3] “Hypopharyngeal Cancer Treatment (Adult) (PDQ(R)): Health Professional Version”. 2002. PMID 26389199.

[4] Rosai, Juan (1996). Ackerman’s surgical pathology. St. Louis: Mosby. ISBN 9780801670046.

[KohmuraHasegawa1999-1] 1.0 ^1.1 Kohmura, Takahide; Hasegawa, Yasuhisa; Ogawa, Tetsuya; Matsuura, Hidehiro; Takahashi, Masakatsu; Yanagita, Noriyuki; Nakashima, Tsutomu (1999). “Cyclin D1 and p53 Overexpression Predicts Multiple Primary Malignant Neoplasms of the Hypopharynx and Esophagus”. Archives of Otolaryngology–Head & Neck Surgery. 125 (12): 1351. doi:10.1001/archotol.125.12.1351. ISSN 0886-4470.

[pmid12560383-2] 2.0 ^2.1 ^2.2 ^2.3 ^2.4 Helliwell TR (February 2003). “acp Best Practice No 169. Evidence based pathology: squamous carcinoma of the hypopharynx”. J. Clin. Pathol. 56 (2): 81–5. PMC 1769882. PMID 12560383.

[aaa-1] What are the risk factors for laryngeal and hypopharyngeal cancers?. Cancer.org. Accessed on October 13, 2015. http://www.cancer.org/cancer/laryngealandhypopharyngealcancer/overviewguide/laryngeal-and-hypopharyngeal-cancer-overview-what-causes

[Nahata20162-1] Nahata, Vaishali (2016). “Branchial cleft cyst”. Indian Journal of Dermatology. 61 (6): 701. doi:10.4103/0019-5154.193718. ISSN 0019-5154.

[pmid30085599-2] Amos J, Shermetaro C. PMID 30085599. Missing or empty |title= (help)

[pmid19718389-3] Deaver MJ, Silman EF, Lotfipour S (August 2009). “Infected thyroglossal duct cyst”. West J Emerg Med. 10 (3): 205. PMC 2729228. PMID 19718389.

[Léauté-LabrèzePrey2011-4] Léauté-Labrèze, C.; Prey, S.; Ezzedine, K. (2011). “Infantile haemangioma: Part I. Pathophysiology, epidemiology, clinical features, life cycle and associated structural abnormalities”. Journal of the European Academy of Dermatology and Venereology. 25 (11): 1245–1253. doi:10.1111/j.1468-3083.2011.04102.x. ISSN 0926-9959.

[pmid25045330-5] Cox JA, Bartlett E, Lee EI (May 2014). “Vascular malformations: a review”. Semin Plast Surg. 28 (2): 58–63. doi:10.1055/s-0034-1376263. PMC 4078214. PMID 25045330.

[pmid28123976-6] Behravesh S, Yakes W, Gupta N, Naidu S, Chong BW, Khademhosseini A, Oklu R (December 2016). “Venous malformations: clinical diagnosis and treatment”. Cardiovasc Diagn Ther. 6 (6): 557–569. doi:10.21037/cdt.2016.11.10. PMC 5220204. PMID 28123976.

[pmid250453302-7] Cox JA, Bartlett E, Lee EI (May 2014). “Vascular malformations: a review”. Semin Plast Surg. 28 (2): 58–63. doi:10.1055/s-0034-1376263. PMC 4078214. PMID 25045330.

[pmid23997487-8] Guruprasad Y, Chauhan DS (September 2012). “Cervical cystic hygroma”. J Maxillofac Oral Surg. 11 (3): 333–6. doi:10.1007/s12663-010-0149-x. PMC 3428451. PMID 23997487.

[pmid23881550-9] Werner RL, Schroeder JW, Castle JT (March 2014). “Bilateral laryngoceles”. Head Neck Pathol. 8 (1): 110–3. doi:10.1007/s12105-013-0478-4. PMC 3950389. PMID 23881550.

[pmid23120570-10] Prasad KC, Vijayalakshmi S, Prasad SC (December 2008). “Laryngoceles – presentations and management”. Indian J Otolaryngol Head Neck Surg. 60 (4): 303–8. doi:10.1007/s12070-008-0108-8. PMC 3476818. PMID 23120570.

[pmid28819622-11] Mahdoufi R, Barhmi I, Tazi N, Abada R, Roubal M, Mahtar M (July 2017). “Mixed Pyolaryngocele: A Rare Case of Deep Neck Infection”. Iran J Otorhinolaryngol. 29 (93): 225–228. PMC 5554815. PMID 28819622.

[pmid29207849-12] Packiri S, Gurunathan D, Selvarasu K (September 2017). “Management of Paediatric Oral Ranula: A Systematic Review”. J Clin Diagn Res. 11 (9): ZE06–ZE09. doi:10.7860/JCDR/2017/28498.10622. PMC 5713871. PMID 29207849.

[pmid28194490-13] Kokong D, Iduh A, Chukwu I, Mugu J, Nuhu S, Augustine S (June 2017). “Ranula: Current Concept of Pathophysiologic Basis and Surgical Management Options”. World J Surg. 41 (6): 1476–1481. doi:10.1007/s00268-017-3901-2. PMC 5422487. PMID 28194490.

[pmid22942597-14] Chauhan DS, Guruprasad Y, Inderchand S (September 2011). “Congenital nasopharyngeal teratoma with a cleft palate: case report and a 7 year follow up”. J Maxillofac Oral Surg. 10 (3): 253–6. doi:10.1007/s12663-010-0140-6. PMC 3238564. PMID 22942597.

[pmid22814615-15] Bahgat M, Bahgat Y, Bahgat A (July 2012). “Oropharyngeal teratoma, a rare cause of airway obstruction in neonates”. BMJ Case Rep. 2012. doi:10.1136/bcr-2012-006580. PMC 4543570. PMID 22814615.

[ParadisKoltai2015-16] Paradis, Josée; Koltai, Peter J. (2015). “Pediatric Teratoma and Dermoid Cysts”. Otolaryngologic Clinics of North America. 48 (1): 121–136. doi:10.1016/j.otc.2014.09.009. ISSN 0030-6665.

[pmid24629659-17] Gaddikeri S, Vattoth S, Gaddikeri RS, Stuart R, Harrison K, Young D, Bhargava P (2014). “Congenital cystic neck masses: embryology and imaging appearances, with clinicopathological correlation”. Curr Probl Diagn Radiol. 43 (2): 55–67. doi:10.1067/j.cpradiol.2013.12.001. PMID 24629659.

[GaddikeriVattoth2014-18] Gaddikeri, Santhosh; Vattoth, Surjith; Gaddikeri, Ramya S.; Stuart, Royal; Harrison, Keith; Young, Daniel; Bhargava, Puneet (2014). “Congenital Cystic Neck Masses: Embryology and Imaging Appearances, With Clinicopathological Correlation”. Current Problems in Diagnostic Radiology. 43 (2): 55–67. doi:10.1067/j.cpradiol.2013.12.001. ISSN 0363-0188.

[pmid28059621-19] 19.0 ^19.1 Abdel Razek A, Mukherji S (June 2017). “Imaging of sialadenitis”. Neuroradiol J. 30 (3): 205–215. doi:10.1177/1971400916682752. PMC 5480791. PMID 28059621. Vancouver style error: initials (help)

[pmid24046793-20] Orlandi MA, Pistorio V, Guerra PA (2013). “Ultrasound in sialadenitis”. J Ultrasound. 16 (1): 3–9. doi:10.1007/s40477-013-0002-4. PMC 3774898. PMID 24046793.

[pmid247536382-21] 21.0 ^21.1 Mohseni S, Shojaiefard A, Khorgami Z, Alinejad S, Ghorbani A, Ghafouri A (March 2014). “Peripheral lymphadenopathy: approach and diagnostic tools”. Iran J Med Sci. 39 (2 Suppl): 158–70. PMC 3993046. PMID 24753638.

[pmid24753638-22] 22.0 ^22.1 Mohseni S, Shojaiefard A, Khorgami Z, Alinejad S, Ghorbani A, Ghafouri A (March 2014). “Peripheral lymphadenopathy: approach and diagnostic tools”. Iran J Med Sci. 39 (2 Suppl): 158–70. PMC 3993046. PMID 24753638.

[pmid25478033-23] Stuhlmann-Laeisz C, Oschlies I, Klapper W (December 2014). “Detection of EBV in reactive and neoplastic lymphoproliferations in adults-when and how?”. J Hematop. 7 (4): 165–170. doi:10.1007/s12308-014-0209-0. PMC 4243011. PMID 25478033.

[pmid20459560-24] Moonim MT, Alarcon L, Freeman J, Mahadeva U, van der Walt JD, Lucas SB (March 2010). “Identifying HIV infection in diagnostic histopathology tissue samples–the role of HIV-1 p24 immunohistochemistry in identifying clinically unsuspected HIV infection: a 3-year analysis”. Histopathology. 56 (4): 530–41. doi:10.1111/j.1365-2559.2010.03513.x. PMID 20459560.

[pmid30422556-25] Thomas M, Bomar PA. PMID 30422556. Missing or empty |title= (help)

[pmid10618283-26] Grunow R, Splettstoesser W, McDonald S, Otterbein C, O’Brien T, Morgan C, Aldrich J, Hofer E, Finke EJ, Meyer H (January 2000). “Detection of Francisella tularensis in biological specimens using a capture enzyme-linked immunosorbent assay, an immunochromatographic handheld assay, and a PCR”. Clin. Diagn. Lab. Immunol. 7 (1): 86–90. PMC 95828. PMID 10618283.

[Koç2012-27] Koç, Sema (2012). “Clinical and laboratory findings of tularemia: a retrospective analysis”. The Turkish Journal of Ear Nose and Throat: 26–31. doi:10.5606/kbbihtisas.2012.005. ISSN 1300-7475.

[pmid28766326-28] Golshani M, Buozari S (November 2017). “A review of Brucellosis in Iran: Epidemiology, Risk Factors, Diagnosis, Control, and Prevention”. Iran. Biomed. J. 21 (6): 349–59. PMC 5572431. PMID 28766326.

[urlCat-Scratch_Disease_in_the_United_States,_2005–2013_-_Volume_22,_Number_10—October_2016_-_Emerging_Infectious_Diseases_journal_-_CDC-29] “Cat-Scratch Disease in the United States, 2005–2013 – Volume 22, Number 10—October 2016 – Emerging Infectious Diseases journal – CDC”.

[HansmannDeMartino2005-30] Hansmann, Y.; DeMartino, S.; Piemont, Y.; Meyer, N.; Mariet, P.; Heller, R.; Christmann, D.; Jaulhac, B. (2005). “Diagnosis of Cat Scratch Disease with Detection of Bartonella henselae by PCR: a Study of Patients with Lymph Node Enlargement”. Journal of Clinical Microbiology. 43 (8): 3800–3806. doi:10.1128/JCM.43.8.3800-3806.2005. ISSN 0095-1137.

[pmid25045274-31] Valour F, Sénéchal A, Dupieux C, Karsenty J, Lustig S, Breton P, Gleizal A, Boussel L, Laurent F, Braun E, Chidiac C, Ader F, Ferry T (2014). “Actinomycosis: etiology, clinical features, diagnosis, treatment, and management”. Infect Drug Resist. 7: 183–97. doi:10.2147/IDR.S39601. PMC 4094581. PMID 25045274.

[pmid27311002-32] Bonnefond S, Catroux M, Melenotte C, Karkowski L, Rolland L, Trouillier S, Raffray L (June 2016). “Clinical features of actinomycosis: A retrospective, multicenter study of 28 cases of miscellaneous presentations”. Medicine (Baltimore). 95 (24): e3923. doi:10.1097/MD.0000000000003923. PMC 4998488. PMID 27311002.

[pmid9241478-33] Suskind DL, Handler SD, Tom LW, Potsic WP, Wetmore RF (July 1997). “Nontuberculous mycobacterial cervical adenitis”. Clin Pediatr (Phila). 36 (7): 403–9. doi:10.1177/000992289703600705. PMID 9241478.

[pmid12614730-34] Drobniewski FA, Caws M, Gibson A, Young D (March 2003). “Modern laboratory diagnosis of tuberculosis”. Lancet Infect Dis. 3 (3): 141–7. PMID 12614730.

[pmid19450346-35] Kenealy T (November 2007). “Sore throat”. BMJ Clin Evid. 2007. PMC 2943825. PMID 19450346.

[pmid20512900-36] Kumar GG, Mahadevan A, Guruprasad AS, Kovoor JM, Satishchandra P, Nath A, Ranga U, Shankar SK (June 2010). “Eccentric target sign in cerebral toxoplasmosis: neuropathological correlate to the imaging feature”. J Magn Reson Imaging. 31 (6): 1469–72. doi:10.1002/jmri.22192. PMC 2908244. PMID 20512900.

[urlCDC_-_Toxoplasmosis_-_Diagnosis-37] [+https://www.cdc.gov/parasites/toxoplasmosis/diagnosis.html “CDC – Toxoplasmosis – Diagnosis”] Check |url= value (help).

[urlSarcoidosis_|_National_Heart,_Lung,_and_Blood_Institute_(NHLBI)-38] “Sarcoidosis | National Heart, Lung, and Blood Institute (NHLBI)”.

[pmid24566651-39] Mavragani CP, Moutsopoulos HM (October 2014). “Sjögren syndrome”. CMAJ. 186 (15): E579–86. doi:10.1503/cmaj.122037. PMC 4203623. PMID 24566651.

[pmid22791417-40] Dispenzieri A, Armitage JO, Loe MJ, Geyer SM, Allred J, Camoriano JK, Menke DM, Weisenburger DD, Ristow K, Dogan A, Habermann TM (November 2012). “The clinical spectrum of Castleman’s disease”. Am. J. Hematol. 87 (11): 997–1002. doi:10.1002/ajh.23291. PMC 3900496. PMID 22791417.

[pmid23071471-41] Saeed-Abdul-Rahman I, Al-Amri AM (September 2012). “Castleman disease”. Korean J Hematol. 47 (3): 163–77. doi:10.5045/kjh.2012.47.3.163. PMC 3464333. PMID 23071471.

[pmid16722618-42] Bosch X, Guilabert A (May 2006). “Kikuchi-Fujimoto disease”. Orphanet J Rare Dis. 1: 18. doi:10.1186/1750-1172-1-18. PMC 1481509. PMID 16722618.

[pmid26905356-43] AlGhamdi FE, Al-Khatib TA, Marzouki HZ, AlGarni MA (March 2016). “Kimura disease: No age or ethnicity limit”. Saudi Med J. 37 (3): 315–9. doi:10.15537/smj.2016.3.14448. PMC 4800898. PMID 26905356.

[urlRosai-Dorfman_disease_|_Genetic_and_Rare_Diseases_Information_Center_(GARD)_–_an_NCATS_Program-44] “Rosai-Dorfman disease | Genetic and Rare Diseases Information Center (GARD) – an NCATS Program”.

[pmid2180012-45] Foucar E, Rosai J, Dorfman R (February 1990). “Sinus histiocytosis with massive lymphadenopathy (Rosai-Dorfman disease): review of the entity”. Semin Diagn Pathol. 7 (1): 19–73. PMID 2180012.

[urlAbout_Kawasaki_Disease_|_Kawasaki_Disease_|_CDC-46] “About Kawasaki Disease | Kawasaki Disease | CDC”.

[urlKawasaki_Disease_|_National_Heart,_Lung,_and_Blood_Institute_(NHLBI)-47] “Kawasaki Disease | National Heart, Lung, and Blood Institute (NHLBI)”.

[pmid22190789-48] Debnath SC, Adhyapok AK (June 2010). “Pleomorphic adenoma (benign mixed tumour) of the minor salivary glands of the upper lip”. J Maxillofac Oral Surg. 9 (2): 205–8. doi:10.1007/s12663-010-0052-5. PMC 3244097. PMID 22190789.

[pmid29845358-49] Kato H, Kawaguchi M, Ando T, Mizuta K, Aoki M, Matsuo M (August 2018). “Pleomorphic adenoma of salivary glands: common and uncommon CT and MR imaging features”. Jpn J Radiol. 36 (8): 463–471. doi:10.1007/s11604-018-0747-y. PMID 29845358.

[pmid24376295-50] Chulam TC, Noronha Francisco AL, Goncalves Filho J, Pinto Alves CA, Kowalski LP (December 2013). “Warthin’s tumour of the parotid gland: our experience”. Acta Otorhinolaryngol Ital. 33 (6): 393–7. PMID 24376295.

[urlWarthin_tumor_|_Genetic_and_Rare_Diseases_Information_Center_(GARD)_–_an_NCATS_Program-51] “Warthin tumor | Genetic and Rare Diseases Information Center (GARD) – an NCATS Program”.

[pmid277220032-52] Chen B, Hentzelman JI, Walker RJ, Lai JP (2016). “Oncocytoma of the Submandibular Gland: Diagnosis and Treatment Based on Clinicopathology”. Case Rep Otolaryngol. 2016: 8719030. doi:10.1155/2016/8719030. PMC 5045990. PMID 27722003.

[pmid10889498-53] Kim KH, Sung MW, Kim JW, Koo JW (July 2000). “Pleomorphic adenoma of the trachea”. Otolaryngol Head Neck Surg. 123 (1 Pt 1): 147–8. doi:10.1067/mhn.2000.102809. PMID 10889498.

[pmid24431845-54] Pramod Krishna B (June 2013). “Pleomorphic Adenoma of Minor Salivary Gland in a 14 year Old Child”. J Maxillofac Oral Surg. 12 (2): 228–31. doi:10.1007/s12663-010-0125-5. PMC 3681990. PMID 24431845.

[pmid30546932-55] Kessler AT, Bhatt AA (2018). “Review of the Major and Minor Salivary Glands, Part 2: Neoplasms and Tumor-like Lesions”. J Clin Imaging Sci. 8: 48. doi:10.4103/jcis.JCIS_46_18. PMC 6251244. PMID 30546932.

[pmid21243374-56] Chenevert J, Barnes LE, Chiosea SI (February 2011). “Mucoepidermoid carcinoma: a five-decade journey”. Virchows Arch. 458 (2): 133–40. doi:10.1007/s00428-011-1040-y. PMID 21243374.

[pmid17825603-57] Jones AV, Craig GT, Speight PM, Franklin CD (April 2008). “The range and demographics of salivary gland tumours diagnosed in a UK population”. Oral Oncol. 44 (4): 407–17. doi:10.1016/j.oraloncology.2007.05.010. PMID 17825603.

[pmid16487803-58] Beltran D, Faquin WC, Gallagher G, August M (March 2006). “Selective immunohistochemical comparison of polymorphous low-grade adenocarcinoma and adenoid cystic carcinoma”. J. Oral Maxillofac. Surg. 64 (3): 415–23. doi:10.1016/j.joms.2005.11.027. PMID 16487803.

[pmid22434951-59] Mlika M, Kourda N, Zidi Y, Aloui R, Zneidi N, Rammeh S, Zermani R, Jilani SB (January 2012). “Salivary duct carcinoma of the parotid gland”. J Oral Maxillofac Pathol. 16 (1): 134–6. doi:10.4103/0973-029X.92992. PMC 3303509. PMID 22434951.

[pmid29103750-60] Schmitt NC, Kang H, Sharma A (November 2017). “Salivary duct carcinoma: An aggressive salivary gland malignancy with opportunities for targeted therapy”. Oral Oncol. 74: 40–48. doi:10.1016/j.oraloncology.2017.09.008. PMC 5685667. PMID 29103750.

[pmid23821208-61] Simpson RH (July 2013). “Salivary duct carcinoma: new developments–morphological variants including pure in situ high grade lesions; proposed molecular classification”. Head Neck Pathol. 7 Suppl 1: S48–58. doi:10.1007/s12105-013-0456-x. PMC 3712088. PMID 23821208.

[pmid25328317-62] Manvikar V, Ramulu S, Ravishanker ST, Chakravarthy C (May 2014). “Squamous cell carcinoma of submandibular salivary gland: A rare case report”. J Oral Maxillofac Pathol. 18 (2): 299–302. doi:10.4103/0973-029X.140909. PMC 4196305. PMID 25328317.

[pmid16475198-63] Ying YL, Johnson JT, Myers EN (July 2006). “Squamous cell carcinoma of the parotid gland”. Head Neck. 28 (7): 626–32. doi:10.1002/hed.20360. PMID 16475198.

[pmid12560383-64] Helliwell TR (February 2003). “acp Best Practice No 169. Evidence based pathology: squamous carcinoma of the hypopharynx”. J. Clin. Pathol. 56 (2): 81–5. PMC 1769882. PMID 12560383.

[65] International Journal of Recent Scientific Research. doi:10.24327/IJRSR. ISSN 0976-3031. Missing or empty |title= (help)

[Maaslandvan_den_Brandt2014-66] Maasland, Denise HE; van den Brandt, Piet A; Kremer, Bernd; Goldbohm, R Alexandra; Schouten, Leo J (2014). “Alcohol consumption, cigarette smoking and the risk of subtypes of head-neck cancer: results from the Netherlands Cohort Study”. BMC Cancer. 14 (1). doi:10.1186/1471-2407-14-187. ISSN 1471-2407.

[pmid22327883-67] Wei CH, Harari A (March 2012). “Parathyroid carcinoma: update and guidelines for management”. Curr Treat Options Oncol. 13 (1): 11–23. doi:10.1007/s11864-011-0171-3. PMID 22327883.

[pmid17713315-68] Sahasranam P, Tran MT, Mohamed H, Friedman TC (August 2007). “Multiglandular parathyroid carcinoma: a case report and brief review”. South. Med. J. 100 (8): 841–4. doi:10.1097/SMJ.0b013e318073ca37. PMID 17713315.

[pmid4886854-69] Holmes EC, Morton DL, Ketcham AS (April 1969). “Parathyroid carcinoma: a collective review”. Ann. Surg. 169 (4): 631–40. PMC 1387475. PMID 4886854.

[pmid174004872-70] Sajid MS, Hamilton G, Baker DM (August 2007). “A multicenter review of carotid body tumour management”. Eur J Vasc Endovasc Surg. 34 (2): 127–30. doi:10.1016/j.ejvs.2007.01.015. PMID 17400487.

[pmid158837112-71] Boedeker CC, Ridder GJ, Schipper J (2005). “Paragangliomas of the head and neck: diagnosis and treatment”. Fam. Cancer. 4 (1): 55–9. doi:10.1007/s10689-004-2154-z. PMID 15883711.

[pmid15063383-72] Pellitteri PK, Rinaldo A, Myssiorek D, Gary Jackson C, Bradley PJ, Devaney KO, Shaha AR, Netterville JL, Manni JJ, Ferlito A (July 2004). “Paragangliomas of the head and neck”. Oral Oncol. 40 (6): 563–75. doi:10.1016/j.oraloncology.2003.09.004. PMID 15063383.

[pmid28478173-73] Darouassi Y, Alaoui M, Mliha Touati M, Al Maghraoui O, En-Nouali A, Bouaity B, Ammar H (August 2017). “Carotid Body Tumors: A Case Series and Review of the Literature”. Ann Vasc Surg. 43: 265–271. doi:10.1016/j.avsg.2017.03.167. PMID 28478173.

[pmid15328326-74] Neumann HP, Pawlu C, Peczkowska M, Bausch B, McWhinney SR, Muresan M, Buchta M, Franke G, Klisch J, Bley TA, Hoegerle S, Boedeker CC, Opocher G, Schipper J, Januszewicz A, Eng C (August 2004). “Distinct clinical features of paraganglioma syndromes associated with SDHB and SDHD gene mutations”. JAMA. 292 (8): 943–51. doi:10.1001/jama.292.8.943. PMID 15328326.

[pmid11701678-75] Erickson D, Kudva YC, Ebersold MJ, Thompson GB, Grant CS, van Heerden JA, Young WF (November 2001). “Benign paragangliomas: clinical presentation and treatment outcomes in 236 patients”. J. Clin. Endocrinol. Metab. 86 (11): 5210–6. doi:10.1210/jcem.86.11.8034. PMID 11701678.

[pmid8678971-76] O’Riordain DS, Young WF, Grant CS, Carney JA, van Heerden JA (September 1996). “Clinical spectrum and outcome of functional extraadrenal paraganglioma”. World J Surg. 20 (7): 916–21, discussion 922. PMID 8678971.

[pmid24450866-77] Hilton DA, Hanemann CO (April 2014). “Schwannomas and their pathogenesis”. Brain Pathol. 24 (3): 205–20. doi:10.1111/bpa.12125. PMID 24450866.

[pmid28237565-78] Albert P, Patel J, Badawy K, Weissinger W, Brenner M, Bourhill I, Parnell J (2017). “Peripheral Nerve Schwannoma: A Review of Varying Clinical Presentations and Imaging Findings”. J Foot Ankle Surg. 56 (3): 632–637. doi:10.1053/j.jfas.2016.12.003. PMID 28237565.

[pmid27020268-79] Wong B, Bathala S, Grant D (January 2017). “Laryngeal schwannoma: a systematic review”. Eur Arch Otorhinolaryngol. 274 (1): 25–34. doi:10.1007/s00405-016-4013-6. PMID 27020268. Vancouver style error: initials (help)

[pmid7139563-80] Anderson T, Chabner BA, Young RC, Berard CW, Garvin AJ, Simon RM, DeVita VT (December 1982). “Malignant lymphoma. 1. The histology and staging of 473 patients at the National Cancer Institute”. Cancer. 50 (12): 2699–707. PMID 7139563.

[pmid71395632-81] Anderson T, Chabner BA, Young RC, Berard CW, Garvin AJ, Simon RM, DeVita VT (December 1982). “Malignant lymphoma. 1. The histology and staging of 473 patients at the National Cancer Institute”. Cancer. 50 (12): 2699–707. PMID 7139563.

[pmid15185336-82] Negri E, Little D, Boiocchi M, La Vecchia C, Franceschi S (August 2004). “B-cell non-Hodgkin’s lymphoma and hepatitis C virus infection: a systematic review”. Int. J. Cancer. 111 (1): 1–8. doi:10.1002/ijc.20205. PMID 15185336.

[pmid2406917-83] Moormeier JA, Williams SF, Golomb HM (February 1990). “The staging of non-Hodgkin’s lymphomas”. Semin. Oncol. 17 (1): 43–50. PMID 2406917.

[pmid151853362-84] Negri E, Little D, Boiocchi M, La Vecchia C, Franceschi S (August 2004). “B-cell non-Hodgkin’s lymphoma and hepatitis C virus infection: a systematic review”. Int. J. Cancer. 111 (1): 1–8. doi:10.1002/ijc.20205. PMID 15185336.

[pmid71395633-85] Anderson T, Chabner BA, Young RC, Berard CW, Garvin AJ, Simon RM, DeVita VT (December 1982). “Malignant lymphoma. 1. The histology and staging of 473 patients at the National Cancer Institute”. Cancer. 50 (12): 2699–707. PMID 7139563.

[pmid171979142-86] Evans HL (January 2007). “Atypical lipomatous tumor, its variants, and its combined forms: a study of 61 cases, with a minimum follow-up of 10 years”. Am. J. Surg. Pathol. 31 (1): 1–14. doi:10.1097/01.pas.0000213406.95440.7a. PMID 17197914.

[pmid21253554-87] Conyers R, Young S, Thomas DM (2011). “Liposarcoma: molecular genetics and therapeutics”. Sarcoma. 2011: 483154. doi:10.1155/2011/483154. PMC 3021868. PMID 21253554.

[pmid19194281-88] Alaggio R, Coffin CM, Weiss SW, Bridge JA, Issakov J, Oliveira AM, Folpe AL (May 2009). “Liposarcomas in young patients: a study of 82 cases occurring in patients younger than 22 years of age”. Am. J. Surg. Pathol. 33 (5): 645–58. doi:10.1097/PAS.0b013e3181963c9c. PMID 19194281.

[pmid176106862-89] Serpell JW, Chen RY (July 2007). “Review of large deep lipomatous tumours”. ANZ J Surg. 77 (7): 524–9. doi:10.1111/j.1445-2197.2007.04042.x. PMID 17610686.

[pmid24800932-90] Bree E, Karatzanis A, Hunt JL, Strojan P, Rinaldo A, Takes RP, Ferlito A, de Bree R (May 2015). “Lipomatous tumours of the head and neck: a spectrum of biological behaviour”. Eur Arch Otorhinolaryngol. 272 (5): 1061–77. doi:10.1007/s00405-014-3065-8. PMID 24800932.

[pmid6670522-91] Rydholm A, Berg NO (December 1983). “Size, site and clinical incidence of lipoma. Factors in the differential diagnosis of lipoma and sarcoma”. Acta Orthop Scand. 54 (6): 929–34. PMID 6670522.

[pmid7282321-92] Myhre-Jensen O (June 1981). “A consecutive 7-year series of 1331 benign soft tissue tumours. Clinicopathologic data. Comparison with sarcomas”. Acta Orthop Scand. 52 (3): 287–93. PMID 7282321.

[pmid8164483-93] Urquhart AC, Johnson JT, Myers EN, Schechter GL (April 1994). “Glomus vagale: paraganglioma of the vagus nerve”. Laryngoscope. 104 (4): 440–5. doi:10.1288/00005537-199404000-00008. PMID 8164483.

[pmid6308990-94] Valavanis A, Schubiger O, Oguz M (1983). “High-resolution CT investigation of nonchromaffin paragangliomas of the temporal bone”. AJNR Am J Neuroradiol. 4 (3): 516–9. PMID 6308990.

[pmid81644832-95] Urquhart AC, Johnson JT, Myers EN, Schechter GL (April 1994). “Glomus vagale: paraganglioma of the vagus nerve”. Laryngoscope. 104 (4): 440–5. doi:10.1288/00005537-199404000-00008. PMID 8164483.

[pmid1988766-96] Stein PP, Black HR (January 1991). “A simplified diagnostic approach to pheochromocytoma. A review of the literature and report of one institution’s experience”. Medicine (Baltimore). 70 (1): 46–66. PMID 1988766.

[pmid17400487-97] Sajid MS, Hamilton G, Baker DM (August 2007). “A multicenter review of carotid body tumour management”. Eur J Vasc Endovasc Surg. 34 (2): 127–30. doi:10.1016/j.ejvs.2007.01.015. PMID 17400487.

[pmid15883711-98] Boedeker CC, Ridder GJ, Schipper J (2005). “Paragangliomas of the head and neck: diagnosis and treatment”. Fam. Cancer. 4 (1): 55–9. doi:10.1007/s10689-004-2154-z. PMID 15883711.

[pmid2211107-99] Gluckman JL, Robbins KT, Fried MP (1990). “Cervical metastatic squamous carcinoma of unknown or occult primary source”. Head Neck. 12 (5): 440–3. PMID 2211107.

[pmid19841343-100] Waltonen JD, Ozer E, Hall NC, Schuller DE, Agrawal A (October 2009). “Metastatic carcinoma of the neck of unknown primary origin: evolution and efficacy of the modern workup”. Arch. Otolaryngol. Head Neck Surg. 135 (10): 1024–9. doi:10.1001/archoto.2009.145. PMID 19841343.

[pmid6639441-101] Feldman PS, Kaplan MJ, Johns ME, Cantrell RW (November 1983). “Fine-needle aspiration in squamous cell carcinoma of the head and neck”. Arch Otolaryngol. 109 (11): 735–42. PMID 6639441.

[pmid26237923-102] Grénman R, Koivunen P, Minn H (2015). “[Laryngeal cancer in Finland]”. Duodecim (in Finnish). 131 (4): 331–7. PMID 26237923.

[pmid26972281-103] Guneyli S, Cinar C, Bozkaya H, Korkmaz M, Oran I (September 2016). “Endovascular management of congenital arteriovenous fistulae in the neck”. Diagn Interv Imaging. 97 (9): 871–5. doi:10.1016/j.diii.2015.08.006. PMID 26972281.

[pmid8264877-104] Gobin YP, Garcia de la Fuente JA, Herbreteau D, Houdart E, Merland JJ (November 1993). “Endovascular treatment of external carotid-jugular fistulae in the parotid region”. Neurosurgery. 33 (5): 812–6. PMID 8264877.

[pmid7606997-105] Madjar S, Weissberg D (July 1995). “Retrosternal goiter”. Chest. 108 (1): 78–82. PMID 7606997.

[pmid11893102-106] Hedayati N, McHenry CR (March 2002). “The clinical presentation and operative management of nodular and diffuse substernal thyroid disease”. Am Surg. 68 (3): 245–51, discussion 251–2. PMID 11893102.

[pmid23145396-107] Hughes K, Eastman C (August 2012). “Goitre – causes, investigation and management”. Aust Fam Physician. 41 (8): 572–6. PMID 23145396.

[pmid10972051-108] Hermus AR, Huysmans DA (August 2000). “[Diagnosis and therapy of patients with euthyroid goiter]”. Ned Tijdschr Geneeskd (in Dutch; Flemish). 144 (34): 1623–7. PMID 10972051.

[1] DeVita, Vincent (2011). DeVita, Hellman, and Rosenberg’s cancer : principles & practice of oncology. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 978-1-4511-0545-2.

[IJRSR-2] 2.0 ^2.1 ^2.2 ^2.3 ^2.4 International Journal of Recent Scientific Research. doi:10.24327/IJRSR. ISSN 0976-3031. Missing or empty |title= (help)

[bbb-3] Hypopharyngeal cancer epidemiology and treatment. http://www.cancer.gov/types/head-and-neck/hp/hypopharyngeal-treatment-pdq

[4] Barnes, Leon (2001). Surgical pathology of the head and neck. New York: M. Dekker. ISBN 0-8247-0109-7.

[5] Barnes, Leon (2001). Surgical pathology of the head and neck. New York: M. Dekker. ISBN 0-8247-0109-7.

[Maaslandvan_den_Brandt2014-1] Maasland, Denise HE; van den Brandt, Piet A; Kremer, Bernd; Goldbohm, R Alexandra; Schouten, Leo J (2014). “Alcohol consumption, cigarette smoking and the risk of subtypes of head-neck cancer: results from the Netherlands Cohort Study”. BMC Cancer. 14 (1). doi:10.1186/1471-2407-14-187. ISSN 1471-2407.

[Novacek2006-2] Novacek, Gottfried (2006). Orphanet Journal of Rare Diseases. 1 (1): 36. doi:10.1186/1750-1172-1-36. ISSN 1750-1172. Missing or empty |title= (help)

[TolandJoo2013-3] Toland, Amanda Ewart; Joo, Young-Hoon; Lee, Youn-Soo; Cho, Kwang-Jae; Park, Jun-Ook; Nam, In-Chul; Kim, Chung-Soo; Kim, Sang-Yeon; Kim, Min-Sik (2013). “Characteristics and Prognostic Implications of High-Risk HPV-Associated Hypopharyngeal Cancers”. PLoS ONE. 8 (11): e78718. doi:10.1371/journal.pone.0078718. ISSN 1932-6203.

[GuhaWarnakulasuriya2014-4] Guha, Neela; Warnakulasuriya, Saman; Vlaanderen, Jelle; Straif, Kurt (2014). “Betel quid chewing and the risk of oral and oropharyngeal cancers: A meta-analysis with implications for cancer control”. International Journal of Cancer. 135 (6): 1433–1443. doi:10.1002/ijc.28643. ISSN 0020-7136.

[pmid19445556-5] Auluck A, Hislop G, Poh C, Zhang L, Rosin MP (2009). “Areca nut and betel quid chewing among South Asian immigrants to Western countries and its implications for oral cancer screening”. Rural Remote Health. 9 (2): 1118. PMC 2726113. PMID 19445556.

[pmid24142981-6] Langevin SM, O’Sullivan MH, Valerio JL, Pawlita M, Applebaum KM, Eliot M, McClean MD, Kelsey KT (December 2013). “Occupational asbestos exposure is associated with pharyngeal squamous cell carcinoma in men from the greater Boston area”. Occup Environ Med. 70 (12): 858–63. doi:10.1136/oemed-2013-101528. PMC 4227396. PMID 24142981.

[1]

[2]

[1]

[2]

[3]

[4]

[1]

[2]

[1]

[1]

[2]

[3]

[4]

[5]

[6]

[7]

[8]

[9]

[10]

[11]

[12]

[13]

[14]

[15]

[16]

[17]

[18]

[19]

[20]

[21]

[22]

[23]

[24]

[25]

[26]

[27]

[28]

[29]

[30]

[31]

[32]

[33]

[34]

[35]

[36]

[37]

[38]

[39]

[40]

[41]

[42]

[43]

[44]

[45]

[46]

[47]

[48]

[49]

[50]

[51]

[52]

[53]

[54]

[55]

[56]

[57]

[58]

[59]

[60]

[61]

[62]

[63]

[64]

[65]

[66]

[67]

[68]

[69]

[70]

[71]

[72]

[73]

[74]

[75]

[76]

[77]

[78]

[79]

[80]

[81]

[82]

[83]

[84]

[85]

[86]

[87]

[88]

[89]

[90]

[91]

Hypopharyngeal cancer

Overview

Historical Prospective

Classification

Pathophysiology

Causes

Differentiating Hypopharyngeal Cancer from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnostic Study of Choice and Staging

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Chest X Ray

CT

MRI

Other Imaging Findings

Other Diagnostic Studies

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

References

Overview

Historical Perspective

Discovery

References

Overview

Classification

References

Overview

Pathophysiology

Genetics

Associated Diseases

Gross Pathology

Microscopic Pathology

Immunohistochemistry

References

Overview

Causes

References

Overview

Differentiating Hypopharyngeal Cancer From other Diseases

References

Overview

Epidemiology and Demographics

Prevalence

Incidence

Age

Gender

Region

References

Overview

Risk Factors

Common Risk Factors

Less Common Risk Factors

References

Overview

Screening

References

References

Treatment

Case Studies

Looking for the patient version?