| Identification of multiple SNT-binding sites on NPM-ALK oncoprotein and their involvement in cell transformation. | None |
| Oncogenic kinase NPM/ALK induces through STAT3 expression of immunosuppressive protein CD274 (PD-L1, B7-H1).( | None |
| Results support the notion that the tumor suppressor effects of SHP1 on NPM-ALK are dependent on its ability to bind to this oncogenic protein. | None |
| Serine phosphorylation of NPM-ALK, contributes to its oncogenic potential. | None |
| Oncogenic kinase NPM/ALK induces expression of HIF1alpha mRNA. | None |
| Oncogenic tyrosine kinase NPM-ALK induces expression of the growth-promoting receptor ICOS. | None |
| novel ALK point mutations possessed tumorigenic effects mainly through hyperphosphorylation of Y1604 and activation of downstream oncogenic signaling. | None |
| KLC1-ALK is the first novel oncogenic fusion identified using only formalin-fixed paraffin-embedded tissue tissues | None |
| Global genomic comparison with SNP arrays showed tumours with ALK fusion to have fewer alterations in oncogenes and suppressor genes despite a similar overall aberration frequency, suggesting strong oncogenic potency of ALK activation by gene fusion | None |
| The pathobiology of the oncogenic tyrosine kinase NPM-ALK: a brief update. | None |
| ALK activation in cancer can arise from translocations creating oncogenic fusion proteins or through overexpression & mutation of full-length ALK. Review. | None |
| The potent oncogene NPM-ALK mediates malignant transformation of normal human CD4(+) T lymphocytes. | None |
| Hsp90-sensitive EML4-ALK variants are exceptions to the rule that oncogenic fusion proteins involve breakpoints in disordered regions of both partners | None |
| Results suggested that chromothripsis may be a mechanism of oncogenic rearrangement of EML4-ALK. | None |
| Microtubule association of EML proteins and the EML4-ALK variant 3 oncoprotein require an N-terminal trimerization domain. | None |
| our findings indicate that LADCs with ALK, RET, and ROS1 fusions develop exclusively via their dependence on these oncogene fusions. | None |
| findings suggest a novel mechanism of oncogene activation in cancer through de novo alternative transcription initiation, such as for ALK | None |
| ALK was the most commonly mutated gene in this cohort, and we observed a higher frequency of suspected oncogenic ALK mutations in relapsed disease than at diagnosis. | None |