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Paper Details

A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1.
Cancer Discov
51
2019
AML, CK, CK-AML, FOXH1, GOF, HSPC, Myeloid Leukemia, Pluripotency Factor FOXH1, TP53, TP53 tumor suppressor gene, Trp53, Trp53 mutation, acute myeloid leukemia, bona fide oncogene, cancer, complex karyotype AML, hematopoietic stem, hematopoietic stem and progenitor cells, humans, leukemic, leukemic cells, mutant, mutant Trp53, mutant p53, myeloid leukemia, oncogene, p53, p53 mutant, p53-Mutant Oncogene, stem, stem cell-associated genes, tumor
Author NameAffiliation
Richard KocheCenter for Epigenetics Research, Memorial Sloan Kettering Cancer Center
Richard KocheCenter for Epigenetics Research, Memorial Sloan Kettering Cancer Center
Frederik Otzen BaggerCenter for Genomic Medicine, University of Copenhagen
Frederik Otzen BaggerUKBB Universitats-Kinderspital
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Release 1.2