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Unquestionably, this differentiation process is occurring in a malignant cell, where, despite some remaining functional pathways, various abnormal proteins may disorganize or completely impede either the differentiation process or other potential targeted therapies. This may be generalized to specific APL subtypes or be specific of a given patient's clone. These altered pathways may explain some of the clinical symptoms of APL, the side effects observed with ATRA and/or differences in ATRA sensitivity of the APL cells. Though these abnormalities may be multiple and not frequent, their knowledge is directly implicated in the understanding of the leukemogenesis of APL, and the management of ATRA therapy. To date different features have been listed, with as yet no apparent link, despite multiple correlation studies. Interestingly, most of these features, which are reviewed below, have been identified as prognostic parameters for the APL patients.
In vitro differentiation of the APL blasts has on the other hand always been exquisitely correlated with the in vivo efficacy in terms of achievement of complete remission (Chomienne et al., 1990; Warrel et al., 1993). We have, however, recently evidenced that a poor in vitro sensitivity to ATRA at diagnosis is correlated to Event Free Survival, relapse rate and long term survival (Cassinat et al., 2001). We had previously reported in small cohorts, a great heterogeneity in ATRA sensitivity from one patient to another, evidenced on the oxydo reduction function, cytokine expression and intracellular ATRA concentrations (Agadir et al., 1995a; Dubois et al., 1991) suggesting that some APL clones can not achieve terminal differentiation. Likewise ATRA differentiated APL cells in vitro and in vivo have been reported to be deficient for secondary granules (Miyauchi et al., 1997). These inter patient differences in differentiation achievement may reflect the presence of distinct altered pathways. Our study did not allow to correlate the in vitro sensitivity with biological features of the APL cell such as CD2, CD13 expression or high WBC count, though a trend with PML subtype and the AML cytological variant may be interesting to pursue in a bigger cohort. Gallagher et al. (1995) had previously reported a weaker differentiating response of the BCR2 PML subtype. This novel prognostic factor underlines the importance of defining these various altered pathways and optimizing ATRA's mechanism of action in the APL cell in the hope that it may still by pass most of these altered pathways.
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