INT91891
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Kit expression was detected in a large number of cells in the liver from 0.5 to 2.5 dpp, as a reminiscence of fetal hematopoiesis (Figure 5A). | |||||||||||||||
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Consistent with the phenotype, Kit gene expression was detected during post-natal development in the liver by using the lacZ reporter gene inserted in the first exon of Kit from the Kittm1Alf/+ mouse [8]. | |||||||||||||||
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Based on several features, including KIT expression and KIT dependence, ICC-like cells were identified in nongastrointestinal tissues. | |||||||||||||||
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These tumors are identified by expression of CD117 or CD34 antigen. | |||||||||||||||
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After stem cell kinase receptor CD117 (c-Kit) was introduced, the GISTs presumed to derive from stem cells differentiating to the GI pacemaker cells, known as interstitial cells of Cajal (ICC), because nearly all GISTs are implicated with c-Kit gene abnormality and CD117 (c-Kit) overexpression (1). | |||||||||||||||
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After stem cell kinase receptor CD117 (c-Kit) was introduced, the GISTs presumed to derive from stem cells differentiating to the GI pacemaker cells, known as interstitial cells of Cajal (ICC), because nearly all GISTs are implicated with c-Kit gene abnormality and CD117 (c-Kit) overexpression (1). | |||||||||||||||
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The exceptions were very clearly described in the paper of Christopher et al.; including fixation artifact, technical error of immunostaining, sampling error, cessation of Kit expression perhaps following STI-571 therapy and very rare cases (2%) with real lack of Kit mutation and/or Kit expression (15). | |||||||||||||||
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Tumors of our cases also showed variable histology, but immunohistochemically, our cases were compatible with GISTs or GANTs based on expression of vimentin (100%), CD117 (100%), and CD34 (66.7%). | |||||||||||||||
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g of total RNA were subsequently used to synthesize cDNA using the First Strand cDNA synthesis kit (Roche, Switzerland). | |||||||||||||||
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The proliferation of the KIT-expressing and imatinib-sensitive and KIT-expressing but imatinib-resistant cell lines was inhibited by 17-AAG, but that of the KIT-non-expressing and imatinib-resistant cell line was not. | |||||||||||||||
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The proliferation of the KIT-expressing and imatinib-sensitive and KIT-expressing but imatinib-resistant cell lines was inhibited by 17-AAG, but that of the KIT-non-expressing and imatinib-resistant cell line was not. | |||||||||||||||
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Gastrointestinal stromal tumors of the small intestine that expressed c-kit protein. | |||||||||||||||
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We report two patients with gastrointestinal stromal tumors (GISTs) of the small intestine that expressed c-kit protein (CD117). | |||||||||||||||
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We report two patients with gastrointestinal stromal tumors (GISTs) of the small intestine that expressed c-kit protein (CD117). | |||||||||||||||
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The immunohistochemical detection of the protein CD 117 (c-kit) is an important diagnostic tool. | |||||||||||||||
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point mutation and protein activation, superimposed on the original mutation in that gene. 2) KIT genomic amplification with overexpression of the KIT oncoprotein, without a new point mutation. 3) Target modulation activation of an alternate receptor tyrosine kinase protein, accompanied by loss of KIT oncoprotein expression. 4) Functional resistance KIT or PDGFR? | |||||||||||||||
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KIT overexpression is common in a variety of tumor types including GISTs, seminomas, adenoid cystic carcinomas, malignant melanomas, and lung carcinomas (non-small cell and small cell types) (Takahashi et al 1995; Went et al 2004). | |||||||||||||||
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The KIT proto-oncogene on chromosome 4 (4q11q12) encodes for the KIT protein, which is also expressed on mast cells, germ cells, and hemopoietic cells. | |||||||||||||||
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Thereafter, Kit expression was confined to a few cells located in the hepatic parenchyma and was also found in the epithelial cells of the biliary canals at later stages and in adults. | |||||||||||||||
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Consistently, KIT and KITL were found to be expressed in the rat cholangiocytes [9] and several mouse mutants of Kitl displayed comparable low post-natal viability [46,47].
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General Comments
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