Quantification of -chain excess in erythrocytes in -thalassaemia by microinterferometry.
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Biomedical subjects
Publications and source records attributed to X Yataganas.
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BACKGROUND: Activating mutations of the FLT3 receptor tyrosine kinase are common in acute promyelocytic leukemia (APL) but have uncertain prognostic significance. Information regarding FLT3 expression levels in APL without FLT3 mutations is lacking. MATERIALS AND METHODS: Using RT-PCR, mutation analysis of the FLT3 gene, regarding internal tandem duplications (ITDs) and codon 835-836 point mutations, was performed and real-time PCR was carried out to determine the level of FLT3 expression in 11 APL patients at diagnosis and 5 in haematological remission with molecularly detectable disease. RESULTS: High levels of FLT3 transcript, at least a 10-fold increase compared to the normal controls, were found at diagnosis in all 3 mutated cases and in 2 patients without detectable FLT3 mutations. CONCLUSION: FLT3 overexpression can be documented in patients without FLT3 mutations. These patients might benefit from treatment using specific FLT3 tyrosine kinase inhibitors. Larger studies are needed to evaluate the clinical and biological significance of FLT3 overexpression in the absence of FLT3 mutations.
Peripheral blood mitogen - induced cellular cytotoxicity (MICC) and natural killer- cell cytotoxicity (NKCC) were assessed in 25 patients with myelodysplastic syndromes (MDS). Both MICC and NKCC were examined under the same experimental conditions using the 18 hr chromium release assay, except that cultures for MICC were stimulated in vitro by the addition of phytohemagglutinin (PHA). Patients' MICC was found significantly reduced, in relation to controls (p less than 0.001), but significantly higher than patients' NKCC (p less than 0.001). Furthermore, patients CD3+ cells and CD4+ cells, as well as the CD4+/CD8+ ratio, were significantly decreased (p less than 0.01, p less than 0.001 and p less than 0.001, respectively), while CD8+ cells and CD16+ cells were within normal limits. No relationship was noted between patients' MICC and total lymphocyte count or any lymphocyte subpopulation. In eleven patients who were subsequently subjected to a-interferon (a-IFN) administration, MICC values were found within normal range one month after the cessation of alpha-IFN, while NKCC values were significantly increased (p less than 0.01), but they still remained below the lower limit of the control (p less than 0.001). Percentages of CD3+, CD4+ and CD8+ cells, as well as the CD4+/CD8+ ratio, did not change after alpha-IFN, but the absolute numbers of CD3+ cells and CD8+ cells were significantly reduced. A statistically significant rise was noted in CD16+ cells. Post- IFN rises in MICC did not correlate with lymphocyte subpopulations. The findings indicate that MDS patients display very low MICC, which can be restored by alpha-IFN administration. The cause of this disturbance and the mechanism of its restoration by alpha-IFN remain unclear.
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A 56 year old female patient treated with carbimazole for hyperthyroidism developed agranulocytosis complicated by pneumonia. She was treated by sc administration of 6 micrograms/kg rhGM-CSF for 10 days. The first neutrophils appeared in the peripheral blood on the 4th day and normal numbers are reached on the 7th day of treatment. This was accompanied by a rapid resolution of fever. The use of growth factors may be justified in cases of drug-induced agranulocytosis.