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Lack of p73 expression in mature B-ALL and identification of three new splicing variants restricted to pre B and C-ALL indicate a role of p73 in B cell ALL differentiation

Leukemia volume 14, pages 518–519 (2000)Cite this article

p73 is a newly identified member of the p53 family, which was originally considered a candidate tumor suppressor gene. Unlike p53, p73 codes for several splicing variants (p73α, β, γ, δ, ε, ζ and Δexon2) which are differently expressed in normal cells and tumor cells.12 DNA damage induces p73 expression through the c-abl tyrosine kinase pathway. Interestingly, activation of c-abl oncogene is associated with chronic myelogenous and acute leukemias in humans. p73 might contribute to the development and progression of lymphoid neoplasms, since its expression is down-regulated by DNA methylation in acute lymphoblastic leukemia (ALL) and non-Hodgkin's lymphoma.34

In an attempt to understand the role of p73 expression in leukemias, we have determined the pattern of expression of this gene in 91 B-ALLs (7 pre-pre B-ALLs, 40 C-ALLs, 40 pre B-ALLs and 4 B-ALLs) and 39 T-ALLs. In the group of patients included in the study, overall p73 expression was approximately 60% with similar frequency in B-ALLs (61.5%) and T-ALLs (56.4%). The event-free survival among homogeneous subgroups of patients with p73 positive and negative leukemic cells was similar, which indicates that p73 expression is not of prognostic value. However, p73 may be a marker of differentiation in the leukemic process of child B cell ALL. Indeed, we detected the p73 transcript in 7/7 samples with a pre-pre B phenotype (CD10 negative) and in 49/80 cases of early B cells (CD10-positive C-ALL and pre-B-ALL), whereas p73 mRNA was not detectable in 4/4 mature B-ALLs (surface immunoglobulins positive, κ or λ restricted). These results indicate that p73 expression is significantly associated with early B-ALL (P = 0.005, Fisher's exact test).

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Acknowledgements

This work was partially supported by Associazione Italiana per la Ricerca sul Cancro (AIRC), Associazione Italiana per la Lotta al Neuroblastoma, Associazione Città della Speranza. PS is supported by a FIRC (Fondazione Italiana Ricerca sul Cancro) fellowship.

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  1. P Scaruffi and I Casciano: The first two authors contributed equally to the work

Authors and Affiliations

  1. Solid Tumour Biology Unit, Advanced Biotechnology Centre, Genoa, Italy

    P Scaruffi & GP Tonini

  2. Laboratory of Oncology, G Gaslini Children's Hospital, Genoa, Italy

    P Scaruffi

  3. Laboratory of Population Genetics, Istituto Nazionale per la Ricerca, sul Cancro, Genoa, Italy

    I Casciano, M Romani & GP Tonini

  4. University of Padua, Padua, Italy

    L Masiero

  5. University of Turin, Italy

    G Basso

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  1. P Scaruffi
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Scaruffi, P., Casciano, I., Masiero, L. et al. Lack of p73 expression in mature B-ALL and identification of three new splicing variants restricted to pre B and C-ALL indicate a role of p73 in B cell ALL differentiation. Leukemia 14, 518–519 (2000). https://doi.org/10.1038/sj.leu.2401698

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