| We found that VPA induced proliferation suppression, cell apoptosis and cell cycle arrest in all tested cell lines, with an increase of Notch1 active form ICN1 as a tumor suppressor | None |
| Notch1 pathway role in the mutant p53 regulation of p63/p73 transcriptional program during tumor suppression. | None |
| more than 50% of T cell acute lymphoblastic leukemias, including tumors from all major molecular oncogenic subtypes, have activating mutations involving the extracellular heterodimerization domain and/or the C-terminal PEST domain of NOTCH1 | leukemia, |
| Transgenic intracellular Notch1 and C-terminal-deleted Notch1 mutant molecules behave collaboratively as oncogenes for T cells; these mice may represent relevant models of human T-cell leukemias. | leukemia, |
| Oncogenic NOTCH1 control of MYC and PI3K: challenges and opportunities for anti-NOTCH1 therapy in T-cell acute lymphoblastic leukemias and lymphomas. | lymphoma,leukemia, |
| The oncogenic roles of Notch1 in astrocytic gliomas in vitro and in vivo. | glioma, |
| These results suggest that Notch1 plays an important oncogenic role in the development and progression of astrocytic gliomas. | glioma, |
| RhoC is an effector of Notch1 in cervical carcinoma cells. There is a pro-oncogenic role of Notch signalling in human cervical cancers. | cervical, |
| Oncogenic activation of the Notch1 gene by deletion of its promoter in Ikaros-deficient mice is associated with T-cell acute lymphoblastic leukemias. | leukemia, |
| This review is an update on the current understanding of the molecular basis of T-cell acute lymphoblastic leukemia, with a particular focus on the role of the NOTCH1 oncogene. | leukemia, |
| NOTCH-1 and NOTCH-4 are novel gene targets of PEA3 in breast cancer: novel therapeutic implications. | breast, |
| identified mutations in FBXW7 and NOTCH in head and neck squamous cell carcinoma; nearly 40% of mutations in NOTCH1 predicted to truncate the gene product, suggesting NOTCH1 may function as tumor suppressor gene rather than oncogene in this tumor type | HNSC, |
| study reports presence of loss-of-function mutations and deletions of the EZH2 and SUZ12 genes, which encode components of the Polycomb repressive complex 2 (PRC2), in 25% of T cell acute lymphoblastic leukemias; study suggesst tumor suppressor role for PRC2 in leukemia and suggest a gnized dynamic interplay between oncogenic NOTCH1 and PRC2 | leukemia, |
| Aberrant and constitutively active NOTCH1 signaling triggered by activating mutations in the NOTCH1 gene contributes to oncogenic transformation and is a hallmark of T-cell acute lymphoblastic leukemia. (Review) | leukemia, |
| NOTCH1 gene may function as an oncogene by regulating HES1/PTEN in invasive bladder transitional cell carcinoma, and its aberrant activation promotes cell proliferation. | bladder, |
| Notch1 signaling contributes to the oncogenic effect of HBx on human hepatic cells. | liver, |
| DDX5 is a positive regulator of oncogenic NOTCH1 signaling in T cell acute lymphoblastic leukemia. | leukemia, |
| The viral oncogene Np9 acts as a critical molecular switch for co-activating beta-catenin, ERK, Akt and Notch1 and promoting the growth of human leukemia stem/progenitor cells. | leukemia, |
| Missense FBXW7 mutations are prevalent in various tumors, including T cell acute lymphoblastic leukemia; study shows that these mutations specifically bolster cancer-initiating cell activity in collaboration with Notch1 oncogenes but spare normal hematopoietic stem cell function. | leukemia, |
| The ubiquitin ligase FBXW7 modulates leukemia-initiating cell activity by regulating MYC stability. | leukemia, |