Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
While the deregulated activation of DNMT1 or KIT has been implicated in lung cancer pathogenesis, whether and how DNMT1 and KIT orchestrate lung tumorigenesis are unclear.
|
28869603 |
2017 |
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 |
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 |
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 |
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 |
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 |
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 |
Biomarker
|
phenotype |
BEFREE |
The tyrosine kinase receptor KIT plays a major role in gastrointestinal stromal tumors (GISTs) oncogenesis.
|
15869870 |
2005 |
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 |
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 |
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 |
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 |
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 |
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 |
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 |
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 |
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 |
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 |
Permanently active KIT mutations lead these host cells to tumorigenesis, and to such diseases as mast cell leukemia (MCL), gastrointestinal stromal tumor (GIST), and acute myeloid leukemia (AML).
|
31484543 |
2019 |
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 |
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 |
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 |
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 |
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 |
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 |