Ewing's sarcoma pathophysiology: Difference between revisions
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{{Ewing's sarcoma}} | {{Ewing's sarcoma}} | ||
{{CMG}}; {{MJM}} | {{CMG}}; {{MJM}} | ||
==Pathophysiology== | ==Pathophysiology== | ||
Revision as of 13:58, 13 August 2015
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Ewing's sarcoma Microchapters |
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Diagnosis |
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Treatment |
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Ewing's sarcoma pathophysiology On the Web |
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Risk calculators and risk factors for Ewing's sarcoma pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Michael Maddaleni, B.S.
Pathophysiology
Microscopic pathology
- The composition of Ewing's sarcoma consists of a homogeneous population of small round cells that have a high nuclear to cytoplasmic ratio. Also, the population of small round cells are arrayed in sheets. There is a presence of scant cytoplasms which are pale, vacuolated, and are characterized by their faded boundaries.[1] The nuclei have intense color which make them easily visible. Mitotic activity is usually low within these cells, and cytoplasmic glycogen is also usually present.
Genetics
- Ewing's sarcoma is the result of a translocation between chromosomes 11 and 22, which fuses the EWS gene of chromosome 22 to the FLI1 gene of chromosome 11. This abnormal gene caused by the translocation can in fact be found using DNA testing. This abnormality does not appear to be genetically linked, and it is exceedingly rare to have two cases of Ewing's Sarcoma within the same family.
References
- ↑ Iwamoto Y (2007). "Diagnosis and treatment of Ewing's sarcoma". Japanese Journal of Clinical Oncology. 37 (2): 79–89. doi:10.1093/jjco/hyl142. PMID 17272319. Retrieved 2012-01-04. Unknown parameter
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