HEMATOPOIESIS FEATURES OF APLASTIC ANEMIA PATIENTS WITH PNH CLONES
(Abstract release date: 05/19/16)
EHA Library. Semenova N. 06/09/16; 134663; PB1763

Ms. Natalya Semenova
Contributions
Contributions
Abstract
Abstract: PB1763
Type: Publication Only
Background
One of the reasons for the development of aplastic anemia (AA) is considered immunopositive inhibition of hematopoiesis – cytotoxicity of antigen-specific T lymphocytes and over-production of inflammatory cytokines type I. In addition, AA may be associated with defective hematopoietic stem cells (HSC) and a violation of the regulatory effect of stromal microenvironment. It is known that colony-forming units (CFU) HSC of AA patients drastically reduced and may be absent at all. At the same time in AA patients often recorded the emergence of PNH clones. However, the functional potential of HSCs of the indicated category of patients is characterized by little
Aims
Study of CFU HSC bone marrow of AA patients depending on the presence of PNH clones.
Methods
The research is based on the bone marrow aspirates of 55 AA patients with no PNH clone and 25 patients with PNH clones. CFU HSC was studied using the method of culturing cells in complete nutrient medium Metho-Cult HYY35 on the basis of methyl cellulose. This environment contains all the necessary growth factors and is able to support the growth of erythroid, granulocyte-monocyte and multilinear colonies. The cultivation was carried out in CO2-incubator at t – 37 ° C for 14 days in Petri dishes with a diameter of 40 mm.
Results
Revealed a sharp decline CFU HSC of AA patients with primarily established diagnosis prior to treatment. The total number of colonies in patients without PNH clones amounted to 57,0 (0-252) 1х105 of myelokaryocytes. At the same time, the number of colonies in PNH patients amounted to 130,0 (8-293) for the same volume of myelokaryocytes. The results suggest that CFU bone marrow HSC in AA patients with PNH clones is significantly higher than in patients without PNH clones. On this basis we can conclude about the relative safety of the proliferative potential of HSC in AA patients with PNH clones.
Conclusion
Analysis of CFU HSC confirms a defect in the development of progenitor hematopoietic cells in AA. However, in patients with AA with PNH clones the level of violations of the proliferative activity of HSC is expressed to a lesser extent. It is known that the effectiveness of therapy significantly higher in AA patients with PNH clones. Given our data on the functional status of HSC, it is possible to conclude that higher efficiency of treatment of AA patients with PNH clones may be associated with relative preservation of proliferative potential of HSC in this category of patients.
Session topic: E-poster
Keyword(s): Aplastic anemia, Hematopoiesis
Type: Publication Only
Background
One of the reasons for the development of aplastic anemia (AA) is considered immunopositive inhibition of hematopoiesis – cytotoxicity of antigen-specific T lymphocytes and over-production of inflammatory cytokines type I. In addition, AA may be associated with defective hematopoietic stem cells (HSC) and a violation of the regulatory effect of stromal microenvironment. It is known that colony-forming units (CFU) HSC of AA patients drastically reduced and may be absent at all. At the same time in AA patients often recorded the emergence of PNH clones. However, the functional potential of HSCs of the indicated category of patients is characterized by little
Aims
Study of CFU HSC bone marrow of AA patients depending on the presence of PNH clones.
Methods
The research is based on the bone marrow aspirates of 55 AA patients with no PNH clone and 25 patients with PNH clones. CFU HSC was studied using the method of culturing cells in complete nutrient medium Metho-Cult HYY35 on the basis of methyl cellulose. This environment contains all the necessary growth factors and is able to support the growth of erythroid, granulocyte-monocyte and multilinear colonies. The cultivation was carried out in CO2-incubator at t – 37 ° C for 14 days in Petri dishes with a diameter of 40 mm.
Results
Revealed a sharp decline CFU HSC of AA patients with primarily established diagnosis prior to treatment. The total number of colonies in patients without PNH clones amounted to 57,0 (0-252) 1х105 of myelokaryocytes. At the same time, the number of colonies in PNH patients amounted to 130,0 (8-293) for the same volume of myelokaryocytes. The results suggest that CFU bone marrow HSC in AA patients with PNH clones is significantly higher than in patients without PNH clones. On this basis we can conclude about the relative safety of the proliferative potential of HSC in AA patients with PNH clones.
Conclusion
Analysis of CFU HSC confirms a defect in the development of progenitor hematopoietic cells in AA. However, in patients with AA with PNH clones the level of violations of the proliferative activity of HSC is expressed to a lesser extent. It is known that the effectiveness of therapy significantly higher in AA patients with PNH clones. Given our data on the functional status of HSC, it is possible to conclude that higher efficiency of treatment of AA patients with PNH clones may be associated with relative preservation of proliferative potential of HSC in this category of patients.
Session topic: E-poster
Keyword(s): Aplastic anemia, Hematopoiesis
Abstract: PB1763
Type: Publication Only
Background
One of the reasons for the development of aplastic anemia (AA) is considered immunopositive inhibition of hematopoiesis – cytotoxicity of antigen-specific T lymphocytes and over-production of inflammatory cytokines type I. In addition, AA may be associated with defective hematopoietic stem cells (HSC) and a violation of the regulatory effect of stromal microenvironment. It is known that colony-forming units (CFU) HSC of AA patients drastically reduced and may be absent at all. At the same time in AA patients often recorded the emergence of PNH clones. However, the functional potential of HSCs of the indicated category of patients is characterized by little
Aims
Study of CFU HSC bone marrow of AA patients depending on the presence of PNH clones.
Methods
The research is based on the bone marrow aspirates of 55 AA patients with no PNH clone and 25 patients with PNH clones. CFU HSC was studied using the method of culturing cells in complete nutrient medium Metho-Cult HYY35 on the basis of methyl cellulose. This environment contains all the necessary growth factors and is able to support the growth of erythroid, granulocyte-monocyte and multilinear colonies. The cultivation was carried out in CO2-incubator at t – 37 ° C for 14 days in Petri dishes with a diameter of 40 mm.
Results
Revealed a sharp decline CFU HSC of AA patients with primarily established diagnosis prior to treatment. The total number of colonies in patients without PNH clones amounted to 57,0 (0-252) 1х105 of myelokaryocytes. At the same time, the number of colonies in PNH patients amounted to 130,0 (8-293) for the same volume of myelokaryocytes. The results suggest that CFU bone marrow HSC in AA patients with PNH clones is significantly higher than in patients without PNH clones. On this basis we can conclude about the relative safety of the proliferative potential of HSC in AA patients with PNH clones.
Conclusion
Analysis of CFU HSC confirms a defect in the development of progenitor hematopoietic cells in AA. However, in patients with AA with PNH clones the level of violations of the proliferative activity of HSC is expressed to a lesser extent. It is known that the effectiveness of therapy significantly higher in AA patients with PNH clones. Given our data on the functional status of HSC, it is possible to conclude that higher efficiency of treatment of AA patients with PNH clones may be associated with relative preservation of proliferative potential of HSC in this category of patients.
Session topic: E-poster
Keyword(s): Aplastic anemia, Hematopoiesis
Type: Publication Only
Background
One of the reasons for the development of aplastic anemia (AA) is considered immunopositive inhibition of hematopoiesis – cytotoxicity of antigen-specific T lymphocytes and over-production of inflammatory cytokines type I. In addition, AA may be associated with defective hematopoietic stem cells (HSC) and a violation of the regulatory effect of stromal microenvironment. It is known that colony-forming units (CFU) HSC of AA patients drastically reduced and may be absent at all. At the same time in AA patients often recorded the emergence of PNH clones. However, the functional potential of HSCs of the indicated category of patients is characterized by little
Aims
Study of CFU HSC bone marrow of AA patients depending on the presence of PNH clones.
Methods
The research is based on the bone marrow aspirates of 55 AA patients with no PNH clone and 25 patients with PNH clones. CFU HSC was studied using the method of culturing cells in complete nutrient medium Metho-Cult HYY35 on the basis of methyl cellulose. This environment contains all the necessary growth factors and is able to support the growth of erythroid, granulocyte-monocyte and multilinear colonies. The cultivation was carried out in CO2-incubator at t – 37 ° C for 14 days in Petri dishes with a diameter of 40 mm.
Results
Revealed a sharp decline CFU HSC of AA patients with primarily established diagnosis prior to treatment. The total number of colonies in patients without PNH clones amounted to 57,0 (0-252) 1х105 of myelokaryocytes. At the same time, the number of colonies in PNH patients amounted to 130,0 (8-293) for the same volume of myelokaryocytes. The results suggest that CFU bone marrow HSC in AA patients with PNH clones is significantly higher than in patients without PNH clones. On this basis we can conclude about the relative safety of the proliferative potential of HSC in AA patients with PNH clones.
Conclusion
Analysis of CFU HSC confirms a defect in the development of progenitor hematopoietic cells in AA. However, in patients with AA with PNH clones the level of violations of the proliferative activity of HSC is expressed to a lesser extent. It is known that the effectiveness of therapy significantly higher in AA patients with PNH clones. Given our data on the functional status of HSC, it is possible to conclude that higher efficiency of treatment of AA patients with PNH clones may be associated with relative preservation of proliferative potential of HSC in this category of patients.
Session topic: E-poster
Keyword(s): Aplastic anemia, Hematopoiesis
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