|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
These results suggest that constitutive activation of KitR in HMC-1 results from the activating mutations of c-kit gene, and raise the possibility that the activating mutations, particularly at codon 814 of murine c-kit or at codon 816 of human c-kit, may participate in oncogenesis of mast cells.
|
7512180 |
1994 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Our data suggest (a) a possible relationship between estrogen and CD117 expression in benign endometrium and (b) potential involvement of this growth factor receptor in endometrial carcinogenesis.
|
11151069 |
2001 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Our results indicate that the overexpression of HMGB1 is common in GISTs and is related to the KIT mutation, and that this may play a role in the tumorigenesis of GISTs because overexpressed HMGB1 could accelerate genes related to tumor growth and invasion.
|
12727838 |
2003 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Recently we reported the different frequencies of p53 and c-kit gene mutations among sinonasal NK/T cell lymphoma (NKTCL) in Korea, north China (Beijing), and Japan, suggesting some racial, environmental, or life-style differences as a possible cause of nasal tumorigenesis.
|
12824925 |
2003 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
These findings suggest that activating KIT mutations may contribute to tumorigenesis in a subset of seminomas, but are not involved in NSGCT.
|
14695343 |
2004 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The high expression level of both mutated and wild-type allele transcripts of c-kit suggests that interactions between spontaneously activated and normal c-kit receptors are important in GIST tumorigenesis.
|
15062876 |
2004 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
We investigated the possible roles of activating mutations in c-KIT, the overexpression of this gene, and ligand-dependent c-Kit overactivation in uveal melanoma cell tumorigenesis.
|
15145934 |
2004 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The tyrosine kinase receptor KIT plays a major role in gastrointestinal stromal tumors (GISTs) oncogenesis.
|
15869870 |
2005 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Furthermore, we have found tumors that are both KIT and PDGFRalpha mutation negative, suggesting that additional, yet unidentified, abnormalities may contribute to GIST tumorigenesis.
|
15897563 |
2005 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Mutations of proto-oncogene c-kit in gastrointestinal stromal tumors (GISTs) are considered to cause a constitutive activation of KIT responsible for their oncogenesis.
|
16077968 |
2005 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
A novel gain of function mutant in C-kit gene and its tumorigenesis in nude mice.
|
16437655 |
2005 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
It seems that KIT may have a significant role in the oncogenesis of mesenchymal tumours of the uterus and ovary.
|
17367465 |
2007 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
However, some therapeutic inhibitors of KIT have efficacy in pediatric GIST, suggesting that KIT may, nevertheless, play an important role in oncogenesis.
|
17909012 |
2007 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
C-kit protein expression correlated with activating mutations indicating the pertinent role of the proto-oncogene KIT in the tumorigenesis of OMM.
|
18066592 |
2008 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Silent mutations in KIT and PDGFRA and coexpression of receptors with SCF and PDGFA in Merkel cell carcinoma: implications for tyrosine kinase-based tumorigenesis.
|
18084259 |
2008 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
These results indicate that LOH of the PTEN region is one of the molecular alterations of an ovarian mature cystic teratoma and a KIT mutation is an additional promotional event associated with the oncogenesis of a melanoma arising from an ovarian mature cystic teratoma.
|
19264228 |
2009 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Moreover, the expression profiling of GISTs may be used as a basic reference to better understand the molecular basis of GISTs tumorigenesis and to identify a novel target molecule for replacing KIT and PDGFRA for a complementary diagnosis and effective curative treatments.
|
20108043 |
2010 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Our findings show that PP2A inhibition is essential for c-KIT-mediated tumorigenesis, and that reactivating PP2A may offer an attractive strategy to treat drug-resistant c-KIT(+) cancers.
|
20551067 |
2010 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
During tumorigenesis of gastrointestinal stromal tumors (GISTs), the most frequent changes are reported to be gain-of-function mutations in the C-KIT proto-oncogene.
|
20683002 |
2010 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The ETV1 transcriptional program is further regulated by activated KIT, which prolongs ETV1 protein stability and cooperates with ETV1 to promote tumorigenesis.
|
20927104 |
2010 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Gain-of-function mutations and KIT overexpression are well-known tumorigenesis mechanisms in gastrointestinal stromal tumors (GIST).
|
22042971 |
2011 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
The importance of KIT and PDGFRA mutations in the oncogenesis of gastrointestinal stromal tumors (GIST) is well established, but the genetic basis of GIST metastasis is poorly understood.
|
22167411 |
2012 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Therefore, despite expression of CD117 and PDGFRA, the absence of activating mutations in these tyrosine kinases makes KIT and PDGFRA unlikely candidates of MCC oncogenesis.
|
23621836 |
2013 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
The mutation of KIT is considered as an early event in tumorigenesis of GIST.
|
24119563 |
2013 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
On the other hand, the fine regulation of tissue homeostasis by mechanisms that control cell fate is a factor that can prevent carcinogenesis. c-KIT is a type III receptor tyrosine kinase activated by its ligand, stem cell factor (SCF). c-KIT signaling plays a crucial role in cell fate decisions, specifically controlling cell proliferation, differentiation, survival, and apoptosis.
|
25359157 |
2014 |