Contributions
Abstract: EP935
Type: E-Poster Presentation
Session title: Myelodysplastic syndromes - Clinical
Background
Myelodysplastic syndrome (MDS) belongs to a clinically, morphologically, genetically heterogeneous group of diseases characterized by clonality and arising from mutations in the hematopoietic progenitor cell, moreover, the disease has a progressively unfavorable course and a high probability of transformation into acute leukemia.
CD33+ expression is known to occur mainly on myeloid progenitor and hematopoietic stem cells and maturing granulocytes. At the same time, CD33+ has been shown to constitutionally inhibit the production of proinflammatory cytokines such as IL-1 and TNF-a. There are isolated pieces of evidence of increased cytokine secretion and cytokine-induced hematopoietic cell proliferation with decreased CD33+ expression.
Aims
The study aimed to establish the relationship between TNF-a and CD33+ cells in the bone marrow of patients with MDS RAEB I depending on the level of response to Lenalidomide therapy.
Methods
The object of the study was 25 patients with MDS RAEB I aged 36 to 81 years (mean age 58 years). The diagnosis was made based on clinical data and mandatory laboratory tests. Verification of the diagnosis of MDS RAEB I was carried out in accordance with the WHO criteria for myeloid neoplasms and acute leukemias, 2008. The duration of the disease at the time of inclusion of patients in the examination varied from 4 to 9 months. All patients included in the study corresponded to the functional state of ECOG-1 ECOG-2.
The immunophenotypic profile of tumor cells was established by flow laser cytometry. Determination of TNF-a concentration was performed by enzyme-linked immunosorbent assay using standard kits using an enzyme-linked immunosorbent assay 'MultiScan EX' at a wavelength of 430 nm. The control was the plasma of healthy individuals. Student's test was used for statistical processing of the received data.
Results
Analysis of the obtained data shows an increase in the number of CD33+ cells in the bone marrow of patients with MDS RAEB I 1.4 times before treatment 13.9±1.7%, with an improvement of 19.8±1.3% (p<0, 05). The level of TNF-a with improvement decreased to 8.9±0.3 pg /ml at the pre-treatment rate of 11.3±0.5 pg/ml (7.9±0.5 pg/ml healthy individuals). In the group of 11 people (40.7%) with stabilization of the disease, the indicators of CD33+ and TNF-a remained at the pre-therapeutic level. Progression of the pathological process occurred in 33.3% (9 people) with reduced CD33+ cells in the bone marrow to 9.5±0.5%, which is 1.5 times lower than in patients before treatment and 2.08 times less, than in the period of improvement (19.8±1.3%). At the same time, there was an increase in the concentration of TNF-a in 1.4 times, compared with the improvement group (12.9±0.2 pg / ml and 8.9±0.3 pg / ml), respectively (p <0.05). The level of TNF-a in the groups before treatment and in the period of stabilization of the process did not differ significantly.
Conclusion
Thus there is an inverse relationship between TNF-a and CD33+ in different responses to treatment with Lenalidomide in patients with MDS RAEB I.
Keyword(s): CD33, Clonality, MDS/AML
Abstract: EP935
Type: E-Poster Presentation
Session title: Myelodysplastic syndromes - Clinical
Background
Myelodysplastic syndrome (MDS) belongs to a clinically, morphologically, genetically heterogeneous group of diseases characterized by clonality and arising from mutations in the hematopoietic progenitor cell, moreover, the disease has a progressively unfavorable course and a high probability of transformation into acute leukemia.
CD33+ expression is known to occur mainly on myeloid progenitor and hematopoietic stem cells and maturing granulocytes. At the same time, CD33+ has been shown to constitutionally inhibit the production of proinflammatory cytokines such as IL-1 and TNF-a. There are isolated pieces of evidence of increased cytokine secretion and cytokine-induced hematopoietic cell proliferation with decreased CD33+ expression.
Aims
The study aimed to establish the relationship between TNF-a and CD33+ cells in the bone marrow of patients with MDS RAEB I depending on the level of response to Lenalidomide therapy.
Methods
The object of the study was 25 patients with MDS RAEB I aged 36 to 81 years (mean age 58 years). The diagnosis was made based on clinical data and mandatory laboratory tests. Verification of the diagnosis of MDS RAEB I was carried out in accordance with the WHO criteria for myeloid neoplasms and acute leukemias, 2008. The duration of the disease at the time of inclusion of patients in the examination varied from 4 to 9 months. All patients included in the study corresponded to the functional state of ECOG-1 ECOG-2.
The immunophenotypic profile of tumor cells was established by flow laser cytometry. Determination of TNF-a concentration was performed by enzyme-linked immunosorbent assay using standard kits using an enzyme-linked immunosorbent assay 'MultiScan EX' at a wavelength of 430 nm. The control was the plasma of healthy individuals. Student's test was used for statistical processing of the received data.
Results
Analysis of the obtained data shows an increase in the number of CD33+ cells in the bone marrow of patients with MDS RAEB I 1.4 times before treatment 13.9±1.7%, with an improvement of 19.8±1.3% (p<0, 05). The level of TNF-a with improvement decreased to 8.9±0.3 pg /ml at the pre-treatment rate of 11.3±0.5 pg/ml (7.9±0.5 pg/ml healthy individuals). In the group of 11 people (40.7%) with stabilization of the disease, the indicators of CD33+ and TNF-a remained at the pre-therapeutic level. Progression of the pathological process occurred in 33.3% (9 people) with reduced CD33+ cells in the bone marrow to 9.5±0.5%, which is 1.5 times lower than in patients before treatment and 2.08 times less, than in the period of improvement (19.8±1.3%). At the same time, there was an increase in the concentration of TNF-a in 1.4 times, compared with the improvement group (12.9±0.2 pg / ml and 8.9±0.3 pg / ml), respectively (p <0.05). The level of TNF-a in the groups before treatment and in the period of stabilization of the process did not differ significantly.
Conclusion
Thus there is an inverse relationship between TNF-a and CD33+ in different responses to treatment with Lenalidomide in patients with MDS RAEB I.
Keyword(s): CD33, Clonality, MDS/AML