Leukemia research
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Comparative Study
Hypermethylation of p16 and p15 genes and RB protein expression in acute leukemia.
Both p16 and p15, encoded by genes located on chromosome 9p21, are inhibitors of cyclin-dependent kinases 4/6 (CDK4/6) and upstream regulators of RB function, and set up the RB/p16 tumor suppressive pathway, which is abrogated frequently in human neoplasms, either through inactivation of the RB or p16 tumor-suppressor protein, or alteration of the cyclin D1 or CDK4 oncoproteins. In hematological malignancies, deletion of p16/p15 locus has been shown to be highly specific to lymphoid malignancies, and more particularly to T-cell acute lymphoblastic leukemia (T-ALL). However, in the other subsets of ALL, deletions of p16 and p15 are relatively rare events. ⋯ Inactivation of the p16 gene was found in all the cell lines with expression of RB. Neither amplification nor rearrangement of cyclin D1 gene was found in any cell lines. These results suggest that inactivation of p16 and p15 genes is one of the most common genetic events in acute leukemia, and plays an important role for the RB/p16 pathway in the pathogenesis of acute leukemia.
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The role of G-CSF, GM-CSF and M-CSF in the treatment of AML and ALL was reviewed. These CSFs significantly accelerate the neutrophil recovery after intensive chemotherapy, and reduce febrile neutropenia and documented infections. ⋯ Patients who have received CSFs tend to have a higher CR rate, which does not seem to be translated into definite survival benefit. There has been no prospective randomized study showing any beneficial priming effect of CSFs on AML cells with better clinical outcomes.
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Patients with extreme leukocytosis or thrombocytosis who have hypoxemia on arterial blood gas analysis may demonstrate normal oxygen saturation using pulse oximetry. The most commonly invoked explanation for this phenomenon is oxygen consumption in the blood gas sample prior to analysis. However, others have challenged the premise that the hypoxemia is spurious. We describe a patient with extreme leukocytosis and hypoxemia in whom normoxia was confirmed by continuous blood gas analysis.
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It has been suggested that in asymptomatic patients with leukaemias and very high white blood cell counts, the apparent hypoxaemia found using routine blood gas analysis is spurious, the result of excessive O2 metabolism by leukocytes. Pulse oximetry has been suggested as a means of overcoming the shortcomings of blood gas analysis in the assessment of these patients. ⋯ We also showed that pulse oximetry was completely unreliable in our patients due to the elevated met-haemoglobin levels. We recommend that all patients with markedly elevated white cell counts should undergo blood gas analysis with no delay between sampling and processing and that patients with low PaO2 should undergo urgent cytoreduction.