New publication in Oncogene
One of respectable research journals Oncogene, a member of Nature Publishing Group, recently published in its online version the article by Petra Bašová, Vít Pospíšil and co-authors from Dr. Tomáš Stopka’s research group at the Pathophysiology department, First Medical Faculty, Charles University in Prague. This research group is one of new incoming teams in the project BioCev – Division Functional Genomics.
Research article entitled: „Aggressive acute myeloid leukaemia in PU.1/p53 double-mutant mice” describes yet-unknown molecular mechanism that is responsible for development of aggressive acute myeloid leukemia (AML). As publicly well known, AML represents a rapidly-appearing deadly disease characterized by accumulation of tumor cells of bone marrow origin that result in failure of blood cell production as well as other organ infiltration. The work by Ms. Bašová at al. is based on highly sophisticated mouse models and translates these findings into human hematology.
Specifically, the article documents that aggressive AML is coincidently caused by loss of two major tumor suppressors PU.1 and p53 leading to pronounced tumor cell expansion, failure of hematopoiesis and shortened overall survival. These two tumor suppressor genes (PU.1 and p53) require, and are interconnected by, deregulation of additional two oncogenes: MYB and miR-155. The newly defined axis of the four genetic AML-associates can be manipulated so the aggressive AML phenotype is replaced by normal hematopoietic regulation. Lastly, mechanisms observed in mouse are observable in tumor cells derived from AML patients with aggressive course of this disease.