| The anti-apoptotic and growth stimulatory actions of leptin in human colon cancer cells involves activation of JNK mitogen activated protein kinase, JAK2 and PI3 kinase/Akt. | colorectal, |
| A new potential oncogenic mutation in the FERM domain of JAK2 in BCR/ABL1-negative and V617F-negative chronic myeloproliferative neoplasms revealed by a comprehensive screening of 17 tyrosine kinase coding genes. | neoplasm, |
| STAT3 is activated by JAK2 independent of key oncogenic driver mutations in non-small cell lung carcinoma. | lung, |
| Differences in signaling through the B-cell leukemia oncoprotein CRLF2 in response to TSLP and through mutant JAK2. | leukemia, |
| the JAK2 46/1 haplotype, represented in this study by the presence of the G allele, is an important predisposing factor in the oncogenetic development of these neoplasms in our population. | neoplasm, |
| Oncogenic Drivers in Myeloproliferative Neoplasms: From JAK2 to Calreticulin Mutations. | neoplasm, |
| In this context, we investigated in vivo study using the nitrosodiethyl amine (NDEA)-induced HCC model, which strengthened our previous findings by showing the blockade of the IL-6 mediated JAK2/STAT3 oncogenic signaling pathway. | liver, |
| JAK2 ex13InDel drives oncogenic transformation and is associated with chronic eosinophilic leukemia and polycythemia vera. | leukemia, |
| The TEL-Jak2 oncoprotein induces Socs1 expression and altered cytokine response in Ba/F3 cells. | None |
| Hematopoietic perturbation in zebrafish expressing a tel-jak2a fusion. | None |
| Bioluminometric assay for relative quantification of mutant allele burden: application to the oncogenic somatic point mutation JAK2 V617F. | None |
| Using both cell lines as well as a murine bone marrow transplantation model, the authors show evidence for a SH2-dependent mechanism required for oncogenic activation of Jak2. | None |
| Oncogenic JAK2V617F requires an intact SH2-like domain for constitutive activation and induction of a myeloproliferative disease in mice. | None |
| The phosphorylation of EpoR at Y479 is required for oncogenic signaling of JAK2 V617F mutant and that targeted disruption of this pathway has therapeutic utility. | None |
| Oncogenic JAK1 and JAK2-activating mutations resistant to ATP-competitive inhibitors. | None |
| [Analysis of the mechanism of polycythemia vera by studying JAK2 mutant-induced signaling pathway]. | None |
| show that JAK2 V617F mutant was constitutively active and exhibited tumorigenesis activity as a potent oncogene when erythropoietin receptor (EpoR) was co-expressed (review) | None |
| constitutively active JAK2 enhances anchorage-independent cell growth in the presence of a co-operating oncogene and accelerates tumourigenesis | None |
| The cell cycle regulator CDC25A is a target for JAK2V617F oncogene. | None |
| JAK2 V617F mutant causes aberrant activation of a transcription factor c-Myc,which is critical for the KAK2 V617F mutant-caused oncogenic activities. | None |