TP53 Mutations and its Consequences: Insight into Leukemia and Lymphoma Cases

Mohamed Magdy¹, Ola Gaber², Ihab Eldessouki², Mohamed Rahouma^3*, Mohamed Kamel³, Abdelrahman Mohamed³ & John Morris²

¹Pediatric Oncology Department, 57357 Hospital, Cairo, Egypt
²Vontz Center for Molecular Studies, Hematology-Oncology Department, University of Cincinnati, Ohio, USA
³Surgical Oncology Department, National Cancer Institute, Cairo University, Egypt

Dr. Mohamed Rahouma, Surgical Oncology Department, National Cancer Institute, Cairo University, Egypt (email: <a

Keywords: Leukemia; Lymphoma; Myeloid Leukemia

Abstract

TP53 mutations are among the most common genetic alterations observed in human cancers and its product p53 has a major role in protection of the genome. In acute lymphoblastic leukemia (ALL), around 16.2% had normal karyotype by chromosome banding techniques, while 93% showed a TP53 mutation. Chromosome 17 showed monosomy in the majority of them. In chronic lymphoblastic leukemia (CLL), with median follow up of 8.1 years, 14.8% had TP53 mutations. Subclonal TP53 mutations were mostly missense substitutions in the DNA binding domain (78%). In acute myeloid leukemia (AML), TP53 mutations were frequently detected in patients with therapy related AML with its adverse effect on overall survival in those with complex karyotype. In pediatric ALL [1], TP53 mutations occurred in 11.3%. In B cell precursor ALL cases, 12.4% of cases showed TP53 mutation, commonly missense mutations. TP53 mutations were significant predictors of event free survival and time to relapse (hazard ratio (HR), 2.28; 95%CI, 1.41-3.69).
In Conclusion
TP53 mutations are common that are associated with adverse survival. Drugs targeting these mutations should be explored thoroughly.

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