Chronic myeloid leukemia (CML) is caused by the BCR-ABL hybrid gene. The molecular mechanisms leading from chronic phase (CP) to blast crisis (BC) are not understood. However, both the presence and the levels of BCR-ABL seem to be important for CML progression. BCR-ABL is under the transcriptional control of BCR promoter. Here we focused on the gene expression control of BCR and BCR-ABL upon myeloid differentiation in healthy donors (HDs), CP and BC patients. As previously reported, BCR-ABL is downregulated during myeloid maturation in CP patients. A similar pattern was detected for BCR (but not for ABL) in CP-CML and in HD, thus suggesting that the two genes may be under a similar transcriptional control. In BC this mechanism is similarly impaired for both BCR-ABL and BCR. These data indicate the presence of an 'in trans' deregulated transcription of both BCR and BCR-ABL promoters, associated with CML progression.

Marega, M., Piazza, R., Pirola, A., Redaelli, S., Mogavero, A., Iacobucci, I., et al. (2010). BCR and BCR-ABL regulation during myeloid differentiation in healthy donors and in chronic phase/blast crisis CML patients. LEUKEMIA, 24(8), 1445-1449 [10.1038/leu.2010.101].

BCR and BCR-ABL regulation during myeloid differentiation in healthy donors and in chronic phase/blast crisis CML patients

MAREGA, MANUELA;PIAZZA, ROCCO GIOVANNI;PIROLA, ALESSANDRA;REDAELLI, SARA;MOGAVERO, ANGELA;POGLIANI, ENRICO MARIA;GAMBACORTI PASSERINI, CARLO
2010

Abstract

Chronic myeloid leukemia (CML) is caused by the BCR-ABL hybrid gene. The molecular mechanisms leading from chronic phase (CP) to blast crisis (BC) are not understood. However, both the presence and the levels of BCR-ABL seem to be important for CML progression. BCR-ABL is under the transcriptional control of BCR promoter. Here we focused on the gene expression control of BCR and BCR-ABL upon myeloid differentiation in healthy donors (HDs), CP and BC patients. As previously reported, BCR-ABL is downregulated during myeloid maturation in CP patients. A similar pattern was detected for BCR (but not for ABL) in CP-CML and in HD, thus suggesting that the two genes may be under a similar transcriptional control. In BC this mechanism is similarly impaired for both BCR-ABL and BCR. These data indicate the presence of an 'in trans' deregulated transcription of both BCR and BCR-ABL promoters, associated with CML progression.
Articolo in rivista - Articolo scientifico
K562 Cells; Fusion Proteins, bcr-abl; Polymerase Chain Reaction; Cell Differentiation; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; DNA Primers; Base Sequence; Proto-Oncogene Proteins c-bcr; Blast Crisis; Humans
English
1445
1449
Marega, M., Piazza, R., Pirola, A., Redaelli, S., Mogavero, A., Iacobucci, I., et al. (2010). BCR and BCR-ABL regulation during myeloid differentiation in healthy donors and in chronic phase/blast crisis CML patients. LEUKEMIA, 24(8), 1445-1449 [10.1038/leu.2010.101].
Marega, M; Piazza, R; Pirola, A; Redaelli, S; Mogavero, A; Iacobucci, I; Meneghetti, I; Parma, M; Pogliani, E; GAMBACORTI PASSERINI, C
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/20867
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