Hypopharyngeal cancer pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
Hypopharyngeal cancer arises from [[squamous cell]]s, which are cells that are normally involved in protection of aerodigestive tract. Genes involved in the pathogenesis of hypopharyngeal cancer include ''[[P16 (gene)|p16]]'', ''[[NOTCH1]]'', ''[[cyclin D1]]'', and ''[[TP53]]''. 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 characteristic findings of hypopharyngeal cancer. On microscopic histopathological analysis, [[spindle cell]]s, basaloid cells, and nuclear atypia are characteristic findings of hypopharyngeal cancer. | Hypopharyngeal cancer arises from [[squamous cell]]s, which are cells that are normally involved in protection of aerodigestive tract. Genes involved in the pathogenesis of hypopharyngeal cancer include ''[[P16 (gene)|p16]]'', ''[[NOTCH1]]'', ''[[cyclin D1]]'', and ''[[TP53]]''. 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 characteristic findings of hypopharyngeal cancer. On microscopic histopathological analysis, [[spindle cell]]s, basaloid cells, and nuclear atypia are characteristic findings of hypopharyngeal cancer. | ||
==Pathophysiology== | ==Pathophysiology== | ||
Hypopharyngeal cancer arises from [[squamous cell]]s, which are cells that are normally involved in protection of aerodigestive tract. 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. | Hypopharyngeal cancer arises from [[squamous cell]]s, which are cells that are normally involved in protection of aerodigestive tract. 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. | ||
Revision as of 19:49, 3 January 2019
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Faizan Sheraz, M.D. [2]
Overview
Hypopharyngeal cancer arises from squamous cells, which are cells that are normally involved in protection of aerodigestive tract. Genes involved in the pathogenesis of hypopharyngeal cancer include p16, NOTCH1, cyclin D1, and TP53. 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 characteristic findings of hypopharyngeal cancer. On microscopic histopathological analysis, spindle cells, basaloid cells, and nuclear atypia are characteristic findings of hypopharyngeal cancer.
Pathophysiology
Hypopharyngeal cancer arises from squamous cells, which are cells that are normally involved in protection of aerodigestive tract. 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.
Genetics
Genes involved in the pathogenesis of hypopharyngeal cancer include:
Associated Diseases
Hypopharyngeal carcinoma is associated with:[1]
Gross Pathology
On gross pathology, hypopharyngeal cancer is characterized by:[1]
- Flattened plaques
- Raised margins of the lesion
- Mucosal ulceration
- Tumor spread to piriform sinus
Microscopic Pathology
On microscopic histopathological analysis, hypopharyngeal carcinoma is characterized by:[1]
- Spindle cells
- Basaloid cells
- Nuclear atypia
- Abundant chromatin