{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tan Y"],"funding":["NCI NIH HHS"],"pagination":["580-8"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4622865"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(4)"],"pubmed_abstract":["Constitutive activation of AKT is a frequent occurrence in the development of human T-cell acute lymphocytic leukemia/lymphomas (T-ALLs), due largely to inactivation of PTEN. Up regulation of MYC is also commonly observed in human T-ALLs. We previously demonstrated that expression of a constitutively active form of Lck-Akt2 alone is sufficient to initiate T-cell lymphoma in mice, and that tumor formation typically requires up regulation of Myc or Dlx5 caused by specific chromosomal rearrangements. Furthermore, Lck-Dlx5 mice develop T-ALLs that consistently acquire overexpression of Myc and activation of Akt, the latter due to loss of Pten expression. Proliferation of T-ALL cells from Lck-Dlx5 mice was found to be highly sensitive to the Akt pathway inhibitors BEZ235 and RAD001, as well as "],"journal":["Cancer biology & therapy"],"pubmed_title":["Co-targeting of Akt and Myc inhibits viability of lymphoma cells from Lck-Dlx5 mice."],"pmcid":["PMC4622865"],"funding_grant_id":["CA06927","CA077429","CA083638","P30 CA006927"],"pubmed_authors":["Ito TK","Tan Y","Kadariya Y","Pei J","Sementino E","Testa JR"],"additional_accession":[]},"is_claimable":false,"name":"Co-targeting of Akt and Myc inhibits viability of lymphoma cells from Lck-Dlx5 mice.","description":"Constitutive activation of AKT is a frequent occurrence in the development of human T-cell acute lymphocytic leukemia/lymphomas (T-ALLs), due largely to inactivation of PTEN. Up regulation of MYC is also commonly observed in human T-ALLs. We previously demonstrated that expression of a constitutively active form of Lck-Akt2 alone is sufficient to initiate T-cell lymphoma in mice, and that tumor formation typically requires up regulation of Myc or Dlx5 caused by specific chromosomal rearrangements. Furthermore, Lck-Dlx5 mice develop T-ALLs that consistently acquire overexpression of Myc and activation of Akt, the latter due to loss of Pten expression. Proliferation of T-ALL cells from Lck-Dlx5 mice was found to be highly sensitive to the Akt pathway inhibitors BEZ235 and RAD001, as well as ","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015","modification":"2025-04-29T10:55:43.972Z","creation":"2019-03-27T02:00:52Z"},"accession":"S-EPMC4622865","cross_references":{"pubmed":["25793663"],"doi":["10.1080/15384047.2015.1018495"]}}