|
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 |
Biomarker
|
phenotype |
BEFREE |
KIT (CD117, c-kit) is a receptor tyrosine kinase involved in the tumorigenesis of several neoplasms.
|
25634571 |
2015 |
|
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 |
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 |
Biomarker
|
phenotype |
BEFREE |
The acral/mucosal melanoma subtype is characterized by aberrant and constitutive activation of the proto-oncogene receptor tyrosine kinase C-KIT, which drives tumorigenesis.
|
29035277 |
2017 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Mutated KIT and platelet-derived growth factor alpha gene (PDGFRA) drive GI stromal tumor (GIST) oncogenesis, but the clinical significance of their single mutations is known incompletely.
|
25605837 |
2015 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Therefore, it is liable to suppose that disturbed SCF/c-KIT expression driven by (de)regulated hormone actions can be a relevant step towards carcinogenesis.
|
28751268 |
2017 |
|
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 |
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 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
ABCG2, CD133 and CD117 are pivotal markers of cancer stem cell, which are involved in carcinogenesis and cancer progression.
|
26951883 |
2017 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
KIT appears to be necessary to stabilize ETV1, and ETV1 then activates oncogenesis-associated genes.
|
25736805 |
2015 |
|
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 |
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 |
AlteredExpression
|
phenotype |
BEFREE |
PreS1 activates CD133, CD117 and CD90 expression in normal hepatocyte derived cell line (L02) and human hepatoma cell line (HepG2 and Huh-7); facilitates L02 cells migration, growth and sphere formation; and finally enhances the abilities of L02 cells and HepG2 cells to induce tumorigeneses in nude mice.
|
28455240 |
2017 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
In this review, we will discuss on the involvement of KIT gene mutations in the tumorigenesis, recurrence and chemotherapeutic resistance of GIST.
|
25961532 |
2015 |
|
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 |
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 |
The presence of mutations of BRAF, NRAS, and KIT genes is recognized as playing a role during carcinogenesis.
|
31274706 |
2020 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Our previous studies showed the colocalization of KIT with DAPI-stained nuclei in GIST cells without knowing the role of nuclear KIT in GIST tumorigenesis.
|
31363162 |
2019 |
|
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 |
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 |
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 |
The much larger fraction of melanomas that occur on sun-exposed skin is driven primarily by BRAF- or NRAS-activating mutations, but these melanomas exhibit a surprising loss of KIT expression, which raises the question of whether loss of KIT in these tumors facilitates tumorigenesis.
|
28947418 |
2017 |
|
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 |