| The expression of the proto-oncogene C-kit in the blast cells of acute myeloblastic leukemia. | leukemia, |
| The overexpression of KIT proto-oncogene in acute leukemic cells is not necessarily caused by the gene mutation. | leukemia, |
| Unusual c-KIT+ squamous cell carcinoma of the uterine cervix showing paradoxical hypermethylation of the c-KIT proto-oncogene. | uterine, |
| Neutralization of KIT Oncogenic Signaling in Leukemia with Antibodies Targeting KIT Membrane Proximal Domain 5. | leukemia, |
| low level of MITF cooperates with oncogenic KIT to transform melanocytes. Activation of the cAMP pathway in transformed (L576P)KIT melanocytes stimulated MITF expression, and reduced cellular proliferation and sphere formation. These findings highlight the essential role of MITF in revealing the oncogenic activity of KIT in melanocytes and suggest that the cAMP pathway is a therapeutic target in KIT-mutated melanoma. | skin, |
| Study demonstrates that an oncogenic tyrosine kinase mutant, KIT(D816V), can alter the transcriptional program of the transcription factor MITF in melanoma. | skin, |
| Data indicate two cases of acute myeloid leukemia (AML) t(8;21) associated systemic mastocytosis (SM) that proto-oncogene c-Kit (KIT) mutation occurred in exon 8 (T417_D419delinsY). | leukemia, |
| Given the regulatory roles that c-Kit plays in cell proliferation and migration, and the realization that c-Kit is an important oncogene in Colorectal cancer (CRC), it is likely that some of the biological effects of TIMP-1 overexpression in CRC may be exerted through its effect on c-Kit signaling. | colorectal, |
| Translocated c-myc oncogene of Burkitt lymphoma is transcribed in plasma cells and repressed in lymphoblastoid cells. | lymphoma, |
| Granulocyte-macrophage colony-stimulating factor (GM-CSF) reduces the density of stem cell factor receptors (c-kit oncogene product) on a GM-CSF-dependent human myeloid cell line. | colorectal, |
| Activating mutations of the c-kit proto-oncogene in a human mast cell leukemia cell line. | leukemia, |
| Tumor necrosis factor alpha (TNF alpha) downregulates c-kit proto-oncogene product expression in normal and acute myeloid leukemia CD34+ cells via p55 TNF alpha receptors. | leukemia, |
| Expression of the c-kit proto-oncogene and its ligand stem cell factor (SCF) in normal and malignant human testicular tissue. | testicular, |
| Transforming growth factor-beta 1 interferes with the proliferation-inducing activity of stem cell factor in myelogenous leukemia blasts through functional down-regulation of the c-kit proto-oncogene product. | leukemia, |
| Expression, function and activation of the proto-oncogene c-kit product in human leukemia cells. | leukemia, |
| Identification of mutations in the coding sequence of the proto-oncogene c-kit in a human mast cell leukemia cell line causing ligand-independent activation of c-kit product. | leukemia, |
| Transfection of the c-myc oncogene into normal Epstein-Barr virus-harboring B cells results in new phenotypic and functional features resembling those of Burkitt lymphoma cells and normal centroblasts. | lymphoma, |
| Absence of point mutations in a functionally important part of the extracellular domain of the c-kit proto-oncogene in a series of patients with acute myeloid leukemia (AML). | leukemia, |
| [Proto-oncogene C-kit expression in human cell lines of malignant melanoma]. | skin, |
| c-Kit proto-oncogene is more likely to lose expression in differentiated thyroid carcinoma than three thyroid-specific genes: thyroid peroxidase, thyroglobulin, and thyroid stimulating hormone receptor. | thyroid, |