Esophageal cancer pathophysiology: Difference between revisions

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===Esophageal Squamous Cell Carcinoma===
===Esophageal Squamous Cell Carcinoma===
*The risk factors for esophageal [[squamous cell carcinoma]] include [[smoking]] and [[alcohol]].<ref name="pmid24834141">{{cite journal |vauthors=Napier KJ, Scheerer M, Misra S |title=Esophageal cancer: A Review of epidemiology, pathogenesis, staging workup and treatment modalities |journal=World J Gastrointest Oncol |volume=6 |issue=5 |pages=112–20 |year=2014 |pmid=24834141 |pmc=4021327 |doi=10.4251/wjgo.v6.i5.112 |url=}}</ref><ref name="pmid22320939">{{cite journal |vauthors=Mao WM, Zheng WH, Ling ZQ |title=Epidemiologic risk factors for esophageal cancer development |journal=Asian Pac. J. Cancer Prev. |volume=12 |issue=10 |pages=2461–6 |year=2011 |pmid=22320939 |doi= |url=}}</ref>
*The risk factors for esophageal [[squamous cell carcinoma]] include [[smoking]] and [[alcohol]].<ref name="pmid24834141">{{cite journal |vauthors=Napier KJ, Scheerer M, Misra S |title=Esophageal cancer: A Review of epidemiology, pathogenesis, staging workup and treatment modalities |journal=World J Gastrointest Oncol |volume=6 |issue=5 |pages=112–20 |year=2014 |pmid=24834141 |pmc=4021327 |doi=10.4251/wjgo.v6.i5.112 |url=}}</ref><ref name="pmid22320939">{{cite journal |vauthors=Mao WM, Zheng WH, Ling ZQ |title=Epidemiologic risk factors for esophageal cancer development |journal=Asian Pac. J. Cancer Prev. |volume=12 |issue=10 |pages=2461–6 |year=2011 |pmid=22320939 |doi= |url=}}</ref>
*[[Alcohol]] is able to dissolve fat soluble compounds.
*When [[alcohol]] and [[tobacco]] are combined they have a synergistic effect and the risk for esophageal squamous cell carcinoma is higher.
*When [[alcohol]] and [[tobacco]] are combined they have a synergistic effect and the risk for squamous cell esophageal cancer is higher.  
*[[Alcohol]] is able to dissolve fat soluble compounds, like that of the esophageal epithelium.
*Tobacco carcinogens such as [[Aromatic amine|aromatic amines]], [[Nitrosamine|nitrosamines]] and [[Polycyclic aromatic hydrocarbon|polycyclic hydrocarbons]] are, therefore, able to penetrate the esophageal [[epithelium]] deeper when in the presence of [[alcohol]].  
*Tobacco carcinogens such as [[Aromatic amine|aromatic amines]], [[Nitrosamine|nitrosamines]] and [[Polycyclic aromatic hydrocarbon|polycyclic hydrocarbons]] are, therefore, able to penetrate the esophageal [[epithelium]] deeper when in the presence of [[alcohol]].
*[[Alcohol]] is also able to decrease the metabolic activities of epithelial cells by damaging DNA.
*[[Alcohol]] is also able to decrease the metabolic activities of epithelial cells by damaging DNA.
*When the cellular DNA is damaged, the cell can not undergo [[detoxification]] and cannot protect itself from [[Oxidative stress|oxidative damage]].
*When the cellular DNA is damaged, the cell cannot undergo [[detoxification]] and protect itself from [[Oxidative stress|oxidative damage]].
*[[Oxidative stress|Oxidation]] leads to inflammation of the [[squamous epithelium]].
*[[Oxidative stress|Oxidation]] leads to inflammation of the [[squamous epithelium]].
*Continuous irritation of the epithelium leads to [[dysplasia]] and [[in situ]] [[malignant]] transformation.
*Continuous irritation of the epithelium leads to [[dysplasia]] and [[in situ]] [[malignant]] transformation.
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===Esophageal Adenocarcinoma===
===Esophageal Adenocarcinoma===


*The risk factors of [[adenocarcinoma]] of the esophagus include [[gastroesophageal reflux disease]] and [[obesity]].<ref name="pmid8578231">{{cite journal |vauthors=Tilanus HW |title=Changing patterns in the treatment of carcinoma of the esophagus |journal=Scand. J. Gastroenterol. Suppl. |volume=212 |issue= |pages=38–42 |year=1995 |pmid=8578231 |doi= |url=}}</ref><ref name="pmid10233832">{{cite journal |vauthors=Jankowski JA, Wright NA, Meltzer SJ, Triadafilopoulos G, Geboes K, Casson AG, Kerr D, Young LS |title=Molecular evolution of the metaplasia-dysplasia-adenocarcinoma sequence in the esophagus |journal=Am. J. Pathol. |volume=154 |issue=4 |pages=965–73 |year=1999 |pmid=10233832 |pmc=1866556 |doi=10.1016/S0002-9440(10)65346-1 |url=}}</ref><ref name="pmid16299787">{{cite journal |vauthors=Koppert LB, Wijnhoven BP, van Dekken H, Tilanus HW, Dinjens WN |title=The molecular biology of esophageal adenocarcinoma |journal=J Surg Oncol |volume=92 |issue=3 |pages=169–90 |year=2005 |pmid=16299787 |doi=10.1002/jso.20359 |url=}}</ref><ref name="pmid8998117">{{cite journal |vauthors=Ireland AP, Clark GW, DeMeester TR |title=Barrett's esophagus. The significance of p53 in clinical practice |journal=Ann. Surg. |volume=225 |issue=1 |pages=17–30 |year=1997 |pmid=8998117 |pmc=1190601 |doi= |url=}}</ref><ref name="pmid23500888">{{cite journal |vauthors=Nieman KM, Romero IL, Van Houten B, Lengyel E |title=Adipose tissue and adipocytes support tumorigenesis and metastasis |journal=Biochim. Biophys. Acta |volume=1831 |issue=10 |pages=1533–41 |year=2013 |pmid=23500888 |pmc=3742583 |doi=10.1016/j.bbalip.2013.02.010 |url=}}</ref>
*The risk factors for esophageal [[adenocarcinoma]] include [[gastroesophageal reflux disease]] and [[obesity]].<ref name="pmid8578231">{{cite journal |vauthors=Tilanus HW |title=Changing patterns in the treatment of carcinoma of the esophagus |journal=Scand. J. Gastroenterol. Suppl. |volume=212 |issue= |pages=38–42 |year=1995 |pmid=8578231 |doi= |url=}}</ref><ref name="pmid10233832">{{cite journal |vauthors=Jankowski JA, Wright NA, Meltzer SJ, Triadafilopoulos G, Geboes K, Casson AG, Kerr D, Young LS |title=Molecular evolution of the metaplasia-dysplasia-adenocarcinoma sequence in the esophagus |journal=Am. J. Pathol. |volume=154 |issue=4 |pages=965–73 |year=1999 |pmid=10233832 |pmc=1866556 |doi=10.1016/S0002-9440(10)65346-1 |url=}}</ref><ref name="pmid16299787">{{cite journal |vauthors=Koppert LB, Wijnhoven BP, van Dekken H, Tilanus HW, Dinjens WN |title=The molecular biology of esophageal adenocarcinoma |journal=J Surg Oncol |volume=92 |issue=3 |pages=169–90 |year=2005 |pmid=16299787 |doi=10.1002/jso.20359 |url=}}</ref><ref name="pmid8998117">{{cite journal |vauthors=Ireland AP, Clark GW, DeMeester TR |title=Barrett's esophagus. The significance of p53 in clinical practice |journal=Ann. Surg. |volume=225 |issue=1 |pages=17–30 |year=1997 |pmid=8998117 |pmc=1190601 |doi= |url=}}</ref><ref name="pmid23500888">{{cite journal |vauthors=Nieman KM, Romero IL, Van Houten B, Lengyel E |title=Adipose tissue and adipocytes support tumorigenesis and metastasis |journal=Biochim. Biophys. Acta |volume=1831 |issue=10 |pages=1533–41 |year=2013 |pmid=23500888 |pmc=3742583 |doi=10.1016/j.bbalip.2013.02.010 |url=}}</ref>
*The chronic [[Gastroesophageal reflux disease|reflux of gastric acid]] and [[bile]] at the gastroesophageal junction leads to the irritation of [[squamous epithelium]] lining the esophagus.
*The chronic [[Gastroesophageal reflux disease|reflux of gastric acid]] and [[bile]] at the [[Cardia|gastroesophageal junction]] leads to the irritation of [[squamous epithelium]] lining the esophagus.
*Chronic irritation leads to [[metaplasia]] of esophagus.
*Chronic irritation leads to [[metaplasia]] of esophagus.
*The lining of the esophagus changes from non-keratinized stratified [[Squamous epithelium|squamous]] [[epithelium]] to [[Columnar epithelia|columnar epithelium]].
*The lining of the esophagus changes from non-keratinized stratified [[Squamous epithelium|squamous]] [[epithelium]] to [[Columnar epithelia|columnar epithelium]].
*This condition is called [[Barrett's esophagus]].  
*This condition is called [[Barrett's esophagus]] .  
*The progression of Barrett [[metaplasia]] to [[adenocarcinoma]] is associated with several changes in gene structure, gene expression, and protein structure.
*The progression of [[Barrett's esophagus]] to [[adenocarcinoma]] is associated with changes in genetic and protein structure, as well as [[gene expression]].
*Mutations in [[P53 (protein)|PT53]] genes and [[P16 (gene)|P16]] genes along with cell cycle abnormalities and [[aneuploidy]] have all been associated with the development of esophageal [[adenocarcinoma]].  
*These mutations include:
*In addition, [[obesity]] is implicated in the development of esophageal [[adenocarcinoma]].
**Chromosomal losses (4q, 5q, 9p, and 18q)<ref name="pmid14657432">{{cite journal |vauthors=Enzinger PC, Mayer RJ |title=Esophageal cancer |journal=N. Engl. J. Med. |volume=349 |issue=23 |pages=2241–52 |year=2003 |pmid=14657432 |doi=10.1056/NEJMra035010 |url=}}</ref>
**Chromosomal gains (8q, 17q, and 20q)
**Gene amplifications (7, 8, and 17q)
**[[P53 (protein)|PT53]] genes and [[P16 (gene)|P16]] genes  
**Variants in ADH and/or ALDH2 genes<ref name="pmid21642993">{{cite journal |vauthors=Wu C, Hu Z, He Z, Jia W, Wang F, Zhou Y, Liu Z, Zhan Q, Liu Y, Yu D, Zhai K, Chang J, Qiao Y, Jin G, Liu Z, Shen Y, Guo C, Fu J, Miao X, Tan W, Shen H, Ke Y, Zeng Y, Wu T, Lin D |title=Genome-wide association study identifies three new susceptibility loci for esophageal squamous-cell carcinoma in Chinese populations |journal=Nat. Genet. |volume=43 |issue=7 |pages=679–84 |year=2011 |pmid=21642993 |doi=10.1038/ng.849 |url=}}</ref>
**'''Possibly''' Cyclin D1 (CCND1) G870A polymorphism
*In addition, [[obesity]] is implicated in the development of esophageal [[adenocarcinoma]].<ref name="pmid235008882">{{cite journal |vauthors=Nieman KM, Romero IL, Van Houten B, Lengyel E |title=Adipose tissue and adipocytes support tumorigenesis and metastasis |journal=Biochim. Biophys. Acta |volume=1831 |issue=10 |pages=1533–41 |year=2013 |pmid=23500888 |pmc=3742583 |doi=10.1016/j.bbalip.2013.02.010 |url=}}</ref>
*Patients with [[central obesity]] tend to have [[Hypertrophy (medical)|hypertrophied]] [[Adipocyte|adipocytes]] and inflammatory cells within their fat deposits.
*Patients with [[central obesity]] tend to have [[Hypertrophy (medical)|hypertrophied]] [[Adipocyte|adipocytes]] and inflammatory cells within their fat deposits.
*This creates a microenvironment within the [[adipocyte]] that promotes tumor development through the release of adipokines and [[Cytokine|cytokines]].
*This creates a microenvironment within the [[adipocyte]] that promotes tumor development through the release of [[Adipokine|adipokines]] and [[Cytokine|cytokines]].
*[[Adipocyte|Adipocytes]] are also able to supply energy to support the tumor's growth.
*[[Adipocyte|Adipocytes]] potentiate tumor expansion by supplying energy to support the tumor's growth.
 


==Pathology==
==Pathology==
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====Nuclear [[atypia]] of malignancy:====
====Nuclear [[atypia]] of malignancy:====
*Found in both types:
*Found in both types:<ref>{{Cite web | title =Squamous cell carcinoma of the esophagus| url =http://librepathology.org/wiki/index.php/Squamous_cell_carcinoma_of_the_esophagus }}</ref>
**[[Poikilocytosis|Poikilocytosis]]
**[[Poikilocytosis|Poikilocytosis]]
**[[Anisocytosis|Anisocytosis]]
**[[Anisocytosis|Anisocytosis]]
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====Squamous cell carcinoma:====
====Squamous cell carcinoma:====


*Atypical squamous cells invade the [[basement membrane]] <ref>{{Cite web | title =Squamous cell carcinoma of the esophagus| url =http://librepathology.org/wiki/index.php/Squamous_cell_carcinoma_of_the_esophagus }}</ref>
*Atypical squamous cells invade the [[basement membrane]]
**Cytology of squamous cells:
**Cytology of squamous cells:
***Eccentric [[Cell nucleus|nucleus]]
***Eccentric [[Cell nucleus|nucleus]]
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====Adenocarcinoma====
====Adenocarcinoma====


*Atypical adenomatous cells show:
*Atypical adenomatous cells show:<ref>{{Cite web | title =Esophageal adenocarcinoma| url =http://librepathology.org/wiki/index.php/Esophageal_adenocarcinoma#Microscopic }}</ref>
**Invading cell clusters or [[Gland|glands]]<ref>{{Cite web | title =Esophageal adenocarcinoma| url =http://librepathology.org/wiki/index.php/Esophageal_adenocarcinoma#Microscopic }}</ref>
**Invading cell clusters or [[Gland|glands]]
**[[Cribriform|Cribriforming]]  
**[[Cribriform|Cribriforming]]  
**[[Desmoplasia]]  
**[[Desmoplasia]]  

Latest revision as of 17:53, 11 January 2018

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

Overview

The pathophysiology of esophageal cancer depends on the histological subtype, whether squamous cell carcinoma or adenocarcinoma.

Pathophysiology

Esophageal Squamous Cell Carcinoma

Esophageal Adenocarcinoma

Pathology

Gross pathology

Squamous cell carcinoma or adenocarcinoma of the esophagus may appear as:[11]

Microscopic pathology

Nuclear atypia of malignancy:

Squamous cell carcinoma:

Esophageal squamous cell carcinoma by Nephron - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=31284085

Adenocarcinoma

Esophageal adenocarcinoma by Nephron - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=12475495

References

  1. ↑ Napier KJ, Scheerer M, Misra S (2014). "Esophageal cancer: A Review of epidemiology, pathogenesis, staging workup and treatment modalities". World J Gastrointest Oncol. 6 (5): 112–20. doi:10.4251/wjgo.v6.i5.112. PMC 4021327. PMID 24834141.
  2. ↑ Mao WM, Zheng WH, Ling ZQ (2011). "Epidemiologic risk factors for esophageal cancer development". Asian Pac. J. Cancer Prev. 12 (10): 2461–6. PMID 22320939.
  3. ↑ Tilanus HW (1995). "Changing patterns in the treatment of carcinoma of the esophagus". Scand. J. Gastroenterol. Suppl. 212: 38–42. PMID 8578231.
  4. ↑ Jankowski JA, Wright NA, Meltzer SJ, Triadafilopoulos G, Geboes K, Casson AG, Kerr D, Young LS (1999). "Molecular evolution of the metaplasia-dysplasia-adenocarcinoma sequence in the esophagus". Am. J. Pathol. 154 (4): 965–73. doi:10.1016/S0002-9440(10)65346-1. PMC 1866556. PMID 10233832.
  5. ↑ Koppert LB, Wijnhoven BP, van Dekken H, Tilanus HW, Dinjens WN (2005). "The molecular biology of esophageal adenocarcinoma". J Surg Oncol. 92 (3): 169–90. doi:10.1002/jso.20359. PMID 16299787.
  6. ↑ Ireland AP, Clark GW, DeMeester TR (1997). "Barrett's esophagus. The significance of p53 in clinical practice". Ann. Surg. 225 (1): 17–30. PMC 1190601. PMID 8998117.
  7. ↑ Nieman KM, Romero IL, Van Houten B, Lengyel E (2013). "Adipose tissue and adipocytes support tumorigenesis and metastasis". Biochim. Biophys. Acta. 1831 (10): 1533–41. doi:10.1016/j.bbalip.2013.02.010. PMC 3742583. PMID 23500888.
  8. ↑ Enzinger PC, Mayer RJ (2003). "Esophageal cancer". N. Engl. J. Med. 349 (23): 2241–52. doi:10.1056/NEJMra035010. PMID 14657432.
  9. ↑ Wu C, Hu Z, He Z, Jia W, Wang F, Zhou Y, Liu Z, Zhan Q, Liu Y, Yu D, Zhai K, Chang J, Qiao Y, Jin G, Liu Z, Shen Y, Guo C, Fu J, Miao X, Tan W, Shen H, Ke Y, Zeng Y, Wu T, Lin D (2011). "Genome-wide association study identifies three new susceptibility loci for esophageal squamous-cell carcinoma in Chinese populations". Nat. Genet. 43 (7): 679–84. doi:10.1038/ng.849. PMID 21642993.
  10. ↑ Nieman KM, Romero IL, Van Houten B, Lengyel E (2013). "Adipose tissue and adipocytes support tumorigenesis and metastasis". Biochim. Biophys. Acta. 1831 (10): 1533–41. doi:10.1016/j.bbalip.2013.02.010. PMC 3742583. PMID 23500888.
  11. ↑ Sugarbaker, David (2015). Adult chest surgery. New York: McGraw-Hill Education. ISBN 0071781897.
  12. ↑ "Squamous cell carcinoma of the esophagus".
  13. ↑ "Esophageal adenocarcinoma".


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