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An international group of researchers from the German University of Ulm and the University of Padua published their most recent work in Blood, the flagship journal of the American Society of Hematology entitled MicroRNA-497/195 is tumor-suppressive and cooperates with CDKN2A/B in pediatric acute lymphoblastic leukemia. The work is the result of over five years of research, revealing new factors underling the aggressiveness of B-cell precursor pediatric acute lymphoblastic leukemia (BCP-ALL).
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An international group of researchers from the German University of Ulm and the University of Padua published their most recent work in Blood, the flagship journal of the American Society of Hematology entitled MicroRNA-497/195 is tumor-suppressive and cooperates with CDKN2A/B in pediatric acute lymphoblastic leukemia. The work is the result of over five years of research, revealing new factors underling the aggressiveness of B-cell precursor pediatric acute lymphoblastic leukemia (BCP-ALL).
Prof Stefania Bortoluzzi of the University of Padua Department of Molecular Medicine explains, “Our work has shown that an increase in the expression of miR-497/195 can counteract the activity of CDK4, which is a key gene for cell cycle control that hinders the proliferation of cancer cells in patients. In healthy subjects, CDK4 is controlled by the CDKN2A and CDKN2B genes that are often compromised in this type of leukemia. We were able to find the cooperative loss between CDKN2A / B and microRNA-497/195, leaving "free rein" in cancer cell growth. This work demonstrates a new prognostic factor, and more importantly, a potential new target for therapy. The research began by observing how leukemia cells took root and grew more effectively in a mouse model the same way as when patients were found to have a high probability rate of early relapse after therapy. We asked ourselves which molecular characteristics were at the root of the diseases’ aggressiveness, and from there we began to study the expression of microRNAs during the first cohort of cases.
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Prof Stefania Bortoluzzi of the University of Padua Department of Molecular Medicine explains, “Our work has shown that an increase in the expression of miR-497/195 can counteract the activity of CDK4, which is a key gene for cell cycle control that hinders the proliferation of cancer cells in patients. In healthy subjects, CDK4 is controlled by the CDKN2A and CDKN2B genes that are often compromised in this type of leukemia. We were able to find the cooperative loss between CDKN2A / B and microRNA-497/195, leaving "free rein" in cancer cell growth. This work demonstrates a new prognostic factor, and more importantly, a potential new target for therapy. The research began by observing how leukemia cells took root and grew more effectively in a mouse model the same way as when patients were found to have a high probability rate of early relapse after therapy. We asked ourselves which molecular characteristics were at the root of the diseases’ aggressiveness, and from there we began to study the expression of microRNAs during the first cohort of cases.
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Prof Stefania Bortoluzzi of the University of Padua Department of Molecular Medicine explains, “Our work has shown that an increase in the expression of miR-497/195 can counteract the activity of CDK4, which is a key gene for cell cycle control that hinders the proliferation of cancer cells in patients. In healthy subjects, CDK4 is controlled by the CDKN2A and CDKN2B genes that are often compromised in this type of leukemia. We were able to find the cooperative loss between CDKN2A / B and microRNA-497/195, leaving "free rein" in cancer cell growth. This work demonstrates a new prognostic factor, and more importantly, a potential new target for therapy. The research began by observing how leukemia cells took root and grew more effectively in a mouse model the same way as when patients were found to have a high probability rate of early relapse after therapy. We asked ourselves which molecular characteristics were at the root of the diseases’ aggressiveness, and from there we began to study the expression of microRNAs during the first cohort of cases.
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