TP53 mutations are frequent in adult acute lymphoblastic leukemia cases negative for recurrent fusion genes and correlate with poor response to induction therapy

Simona Sica, Sabina Chiaretti, Fulvia Brugnoletti, Simona Tavolaro, Silvia Bonina, Francesca Paoloni, Marilisa Marinelli, Nancy Patten, Massimiliano Bonifacio, Maria Grazia Kropp, Anna Guarini, Robin Foà

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

Acute lymphoblastic leukemia (ALL) is a disease of either B-cell (80–85%) or T-cell (20–25%) derivation. Several molecular aberrations (i.e. BCR-ABL1, MLL/AFF1, SIL/TAL1 and E2A/PBX1) confer an overall poor outcome.1,2 However, a proportion of patients do not carry known genetic abnormalities and have a heterogeneous clinical course. P53 plays a crucial role in cell cycle regulation and apoptosis after DNA damage, and its role in tumorigenesis is well-recognized in solid and hematologic malignancies, particularly acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL), in which its deregulation represents an important predictor of poor outcome.3–10
Original languageEnglish
Pages (from-to)e59-e59-61
JournalHaematologica
Volume98
DOIs
Publication statusPublished - 2013

Keywords

  • Adult
  • Humans
  • Mutation
  • Oncogene Proteins, Fusion
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma
  • Remission Induction
  • TP53 mutations
  • Treatment Outcome
  • Tumor Suppressor Protein p53
  • adult acute lymphoblastic leukemia
  • response to induction chemotherapy

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