{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhao Y"],"funding":["Science, Technology and Innovation Commission of Shenzhen Municipality","Guangdong Basic and Applied Basic Research Foundation","National Natural Science Foundation of China","Sanming Project of Medicine in Shenzhen","Guangdong Provincial Key Laboratory of Reproductive Medicine"],"pagination":["20"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9940371"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(1)"],"pubmed_abstract":["Leukemogenic SHP2 mutations occur in 35% of patients with juvenile myelomonocytic leukemia (JMML), a rare but fatal hematopoietic malignancy without representative cell models, which are urgently needed to investigate the pathogenesis and to develop novel therapeutic strategies. In this study, we established stable cell lines with aberrant signaling resembling SHP2-mutant JMML through retroviral expression of SHP2-D61Y/E76K in HCD-57 cells, a murine erythroleukemia cell line that depends on erythropoietin (EPO) for survival. SHP2-D61Y/E76K drives the survival and proliferation of HCD-57 cells in the absence of EPO, but not in Ba/F3 cells in the absence of IL-3. Transformed HCD-57 cells showed activated MAPK signaling that is consistent with SHP2-mutant JMML. Transformed HCD-57 cells were s"],"journal":["Experimental hematology & oncology"],"pubmed_title":["Leukemogenic SHP2 mutations lead to erythropoietin independency of HCD-57 cells: a novel model for preclinical research of SHP2-mutant JMML."],"pmcid":["PMC9940371"],"funding_grant_id":["JCYJ20220530144814032","2021B1212040006","JCYJ20190814164601648","82000150","82202579","SZSM202011004","2019A1515110121","JCYJ20210324123003009","JCYJ20210324123210028"],"pubmed_authors":["He C","Yu L","Zhang D","Guo Y","Zhao ZJ","Chen Y","Chen C","Zhao Y","Peng Z","Li N"],"additional_accession":[]},"is_claimable":false,"name":"Leukemogenic SHP2 mutations lead to erythropoietin independency of HCD-57 cells: a novel model for preclinical research of SHP2-mutant JMML.","description":"Leukemogenic SHP2 mutations occur in 35% of patients with juvenile myelomonocytic leukemia (JMML), a rare but fatal hematopoietic malignancy without representative cell models, which are urgently needed to investigate the pathogenesis and to develop novel therapeutic strategies. In this study, we established stable cell lines with aberrant signaling resembling SHP2-mutant JMML through retroviral expression of SHP2-D61Y/E76K in HCD-57 cells, a murine erythroleukemia cell line that depends on erythropoietin (EPO) for survival. SHP2-D61Y/E76K drives the survival and proliferation of HCD-57 cells in the absence of EPO, but not in Ba/F3 cells in the absence of IL-3. Transformed HCD-57 cells showed activated MAPK signaling that is consistent with SHP2-mutant JMML. Transformed HCD-57 cells were s","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Feb","modification":"2026-07-14T22:12:42.219Z","creation":"2024-12-03T21:47:36.722Z"},"accession":"S-EPMC9940371","cross_references":{"pubmed":["36805832"],"doi":["10.1186/s40164-023-00379-1"]}}