Gastrointestinal stromal tumor pathophysiology: Difference between revisions
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{{Gastrointestinal stromal tumor}} | {{Gastrointestinal stromal tumor}} | ||
{{CMG}} | {{CMG}} | ||
==Pathophysiology== | |||
GISTs are thought to arise from [[interstitial cells of Cajal]] (ICC),<ref name=miettinen>{{cite journal |author=Miettinen M, Lasota J |title=Gastrointestinal stromal tumors: review on morphology, molecular pathology, prognosis, and differential diagnosis |journal=Arch Pathol Lab Med |volume=130 |issue=10 |pages=1466-78 |year=2006 |id=PMID 17090188}}</ref> that are normally part of the [[autonomic nervous system]] of the intestine. They serve a pacemaker function in controlling [[motility]]. | |||
Most (50-80%) GISTs arise because of a mutation in a [[gene]] called ''[[c-kit]]''. This gene encodes a [[transmembrane receptor]] for a growth factor termed ''scf'' (stem cell factor). The ''c-kit''/CD117 receptor is expressed on ICCs and a large number of other cells, mainly [[bone marrow]] cells, [[mast cell]]s, [[melanocyte]]s and several others. In the gut, however, a mass staining positive for [[CD117]] is likely to be a GIST, arising from ICC cells. | |||
The ''c-kit'' [[molecule]] comprises a long [[Membrane protein|extracellular domain]], a [[Membrane protein|transmembrane segment]], and an intracellular part. Mutations generally occur in the [[deoxyribonucleic acid|DNA]] encoding the intracellular part (exon 11), which acts as a [[tyrosine kinase]] to activate other [[enzyme]]s. Mutations make ''c-kit'' function independent of activation by ''scf'', leading to a high cell division rate and possibly genomic instability. It is likely that additional mutations are "required" for a cell with a ''c-kit'' mutation to develop into a GIST, but the ''c-kit'' mutation is probably the first step of this process. | |||
The [[tyrosine kinase]] function of ''c-kit'' is vital in the therapy for GISTs. | |||
==Histopathology== | ==Histopathology== | ||
Revision as of 02:14, 18 January 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
GISTs are thought to arise from interstitial cells of Cajal (ICC),[1] that are normally part of the autonomic nervous system of the intestine. They serve a pacemaker function in controlling motility.
Most (50-80%) GISTs arise because of a mutation in a gene called c-kit. This gene encodes a transmembrane receptor for a growth factor termed scf (stem cell factor). The c-kit/CD117 receptor is expressed on ICCs and a large number of other cells, mainly bone marrow cells, mast cells, melanocytes and several others. In the gut, however, a mass staining positive for CD117 is likely to be a GIST, arising from ICC cells.
The c-kit molecule comprises a long extracellular domain, a transmembrane segment, and an intracellular part. Mutations generally occur in the DNA encoding the intracellular part (exon 11), which acts as a tyrosine kinase to activate other enzymes. Mutations make c-kit function independent of activation by scf, leading to a high cell division rate and possibly genomic instability. It is likely that additional mutations are "required" for a cell with a c-kit mutation to develop into a GIST, but the c-kit mutation is probably the first step of this process.
The tyrosine kinase function of c-kit is vital in the therapy for GISTs.
Histopathology
References
- ↑ Miettinen M, Lasota J (2006). "Gastrointestinal stromal tumors: review on morphology, molecular pathology, prognosis, and differential diagnosis". Arch Pathol Lab Med. 130 (10): 1466–78. PMID 17090188.