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
Lingua originale | English |
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pagine (da-a) | e59-e59-61 |
Rivista | Haematologica |
Volume | 98 |
DOI | |
Stato di pubblicazione | Pubblicato - 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