Sarcomatoid carcinoma of the lung pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
*The pathogenesis of sarcomatoid carcinoma of the lung is characterized by a rare epithelial origin and morphologic features suggestive of a malignant [[Mesenchyme|mesenchymal]] tumor.<ref name="BrambillaTravis2001" /><ref name="pmid20073605">{{cite journal |vauthors=Franks TJ, Galvin JR |title=Sarcomatoid carcinoma of the lung: histologic criteria and common lesions in the differential diagnosis |journal=Arch. Pathol. Lab. Med. |volume=134 |issue=1 |pages=49–54 |year=2010 |pmid=20073605 |doi=10.1043/2008-0547-RAR.1 |url=}}</ref> | *The pathogenesis of sarcomatoid carcinoma of the lung is characterized by a rare epithelial origin and morphologic features suggestive of a malignant [[Mesenchyme|mesenchymal]] tumor.<ref name="BrambillaTravis2001" /><ref name="pmid20073605">{{cite journal |vauthors=Franks TJ, Galvin JR |title=Sarcomatoid carcinoma of the lung: histologic criteria and common lesions in the differential diagnosis |journal=Arch. Pathol. Lab. Med. |volume=134 |issue=1 |pages=49–54 |year=2010 |pmid=20073605 |doi=10.1043/2008-0547-RAR.1 |url=}}</ref> | ||
*Four major hypotheses may explain sarcomatoid neoplasms:<ref name="pmid8772780">{{cite journal |vauthors=Thompson L, Chang B, Barsky SH |title=Monoclonal origins of malignant mixed tumors (carcinosarcomas). Evidence for a divergent histogenesis |journal=Am. J. Surg. Pathol. |volume=20 |issue=3 |pages=277–85 |date=March 1996 |pmid=8772780 |doi= |url=}}</ref><ref name="pmid200736052">{{cite journal |vauthors=Franks TJ, Galvin JR |title=Sarcomatoid carcinoma of the lung: histologic criteria and common lesions in the differential diagnosis |journal=Arch. Pathol. Lab. Med. |volume=134 |issue=1 |pages=49–54 |date=January 2010 |pmid=20073605 |doi=10.1043/2008-0547-RAR.1 |url=}}</ref> | *Four major hypotheses may explain sarcomatoid neoplasms:<ref name="pmid8772780">{{cite journal |vauthors=Thompson L, Chang B, Barsky SH |title=Monoclonal origins of malignant mixed tumors (carcinosarcomas). Evidence for a divergent histogenesis |journal=Am. J. Surg. Pathol. |volume=20 |issue=3 |pages=277–85 |date=March 1996 |pmid=8772780 |doi= |url=}}</ref><ref name="pmid200736052">{{cite journal |vauthors=Franks TJ, Galvin JR |title=Sarcomatoid carcinoma of the lung: histologic criteria and common lesions in the differential diagnosis |journal=Arch. Pathol. Lab. Med. |volume=134 |issue=1 |pages=49–54 |date=January 2010 |pmid=20073605 |doi=10.1043/2008-0547-RAR.1 |url=}}</ref> | ||
**'''The embryonic rest hypothesis:''' This theory suggests that sarcomatoid tumors are the result of misplaced “mini-organs” that has epithelial and stromal component. | **'''The embryonic rest hypothesis:''' This theory suggests that sarcomatoid tumors are the result of misplaced “mini-organs” that has epithelial and stromal component. | ||
Revision as of 16:33, 31 December 2018
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Trusha Tank, M.D.[2]
Overview
The exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Physiology
The normal physiology of [name of process] can be understood as follows:
Pathogenesis
- The pathogenesis of sarcomatoid carcinoma of the lung is characterized by a rare epithelial origin and morphologic features suggestive of a malignant mesenchymal tumor.[1][2]
- Four major hypotheses may explain sarcomatoid neoplasms:[3][4]
- The embryonic rest hypothesis: This theory suggests that sarcomatoid tumors are the result of misplaced “mini-organs” that has epithelial and stromal component.
- The collision hypothesis: This theory implies separate but concomitant malignant proliferation of epithelium and mesenchyme.
- The stromal induction/metaplasia hypothesis: This theory suggests that sarcomatous elements are an atypical response to the growth of a carcinoma.
- Totipotential hypothesis: This hypothesis proposes an origin from a single totipotential stem cell that differentiates into epithelial and mesenchymal components.
Genetics
[Disease name] is transmitted in [mode of genetic transmission] pattern.
OR
Genes involved in the pathogenesis of [disease name] include:
- [Gene1]
- [Gene2]
- [Gene3]
OR
The development of [disease name] is the result of multiple genetic mutations such as:
- [Mutation 1]
- [Mutation 2]
- [Mutation 3]
Associated Conditions
Conditions associated with [disease name] include:
- [Condition 1]
- [Condition 2]
- [Condition 3]
Gross Pathology
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑
- ↑ Franks TJ, Galvin JR (2010). "Sarcomatoid carcinoma of the lung: histologic criteria and common lesions in the differential diagnosis". Arch. Pathol. Lab. Med. 134 (1): 49–54. doi:10.1043/2008-0547-RAR.1. PMID 20073605.
- ↑ Thompson L, Chang B, Barsky SH (March 1996). "Monoclonal origins of malignant mixed tumors (carcinosarcomas). Evidence for a divergent histogenesis". Am. J. Surg. Pathol. 20 (3): 277–85. PMID 8772780.
- ↑ Franks TJ, Galvin JR (January 2010). "Sarcomatoid carcinoma of the lung: histologic criteria and common lesions in the differential diagnosis". Arch. Pathol. Lab. Med. 134 (1): 49–54. doi:10.1043/2008-0547-RAR.1. PMID 20073605.