|
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 |
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 |
Activating alterations of KIT-a transmembrane receptor tyrosine kinase important for cell development, growth, and differentiation-have been shown to be critical to oncogenesis across many tumor subtypes.
|
30707374 |
2019 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Dysregulation in miRNA expression may lead to KIT overexpression and tumorigenesis.
|
29661252 |
2018 |
|
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 |
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 |
ABCG2, CD133 and CD117 are pivotal markers of cancer stem cell, which are involved in carcinogenesis and cancer progression.
|
26951883 |
2017 |
|
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 |
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 |
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 |
In KIT/PDGFRA wild-type gastrointestinal stromal tumors (wt-GISTs), BRAF mutations are regarded as alternative pathogenic events driving tumorigenesis.
|
28159677 |
2017 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Mutation of KIT and PDGFRA genes is implicated in the tumorigenesis.
|
27427238 |
2016 |
|
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 |
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 |
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 |
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 |
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 |
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 |
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 |
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 |
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 |
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 |