IMPACT OF LEUKEMIA STEM CELLS PHENOTYPE EXPRESSION ON RESPONSE TO INDUCTION THERAPY IN ACUTE MYELOID LEUKEMIA PATIENTS
(Abstract release date: 05/19/16)
EHA Library. almohsen f. 06/09/16; 132687; E1138
faez almohsen
Contributions
Contributions
Abstract
Abstract: E1138
Type: Eposter Presentation
Background
Laboratory data suggest that acute myeloid leukemia AML originates from a rare population of cells, termed leukemic stem cells (LSCs) or leukemia-initiating cells, which are capable of self-renewal, proliferation and differentiation into malignant blasts. There's a universal agreement that LSCs lie within the CD34+ compartment of hemopoietic cells and most of leukemic stem cells express the interleukin-3 alpha chain receptor, CD123 and lack CD38. The standard model of leukemogenesis posits the stepwise acquisition of genetic mutations in a susceptible cell and its progeny, leading to the development of an autonomous clone that expands enough to cause a clinical syndrome.The genetic events occur in susceptible cells that are either hemopoietic stem cells or its progeny. The resultant leukemic cell has the properties of a stem cell in terms of self-renewal, but with persistent uncontrolled division and resistance to chemotherapy. This leukemia stem cell theory has been proved by proliferation of proposed leukemic stem cell after its injection into lethally irradiated mice. This finding inspired scientists and researchers to explore new fields for leukemia treatments because with the current regimes, the relapse rate is high and death frequently happens due to treatment failure or consequences of bone marrow blast invasion. In the same perspective, researchers began to assess the prognostic value of leukemic stem cells at diagnosis and to weigh its significance with other known prognostic factors of AML.
Aims
This study aimed to estimate the expression of LSC phenotype in AML patients and to correlate it with response to induction therapy.
Methods
A cohort of 41 patients older than 15 years with newly diagnosed de novo AML were enrolled in this study. They were obtained from the National center of hematology in Baghdad and Baghdad teaching hospital between February and July 2013. The expression of CD34, CD38 and CD123 was assessed by multi-color flow cytometry. LSC positive (LSC+) samples must express CD34 and CD123 and lack the expression of CD38 in >1% of cells. French American British (FAB) classification system was used in this study.After four weeks of induction therapy; three groups were found: those who reached the complete morphological remission (CR), those who failed to reach CR and those who died before assessment of morphological remission. The last two groups were merged for statistical purposes.All statistical operations were done by Microsoft excel 2010 and SPSS programs. The p-value for significance was calculated from Chi square test and Fisher Exact test for 2X2 contingency tables when the Chi square test was not applicable.The percentage of LSCs was calculated as the percentage of cells in CD34+CD123+ quadrant X the percentage of CD38- cells X the blast% of the individual patient
Results
The mean expression of CD34+CD38-CD123+ cells at diagnosis was 3.85+7.14 (mean+SD), range=0% to 42.05%, median=2.15%.A cut off value of 1.0% was designed to separate two groups of patients; those with LSCs of less than or equal to 1.0% and those with more than 1.0%.In the first group (LSCs <1.0%), the CR rate was 53.33%, while it was 34.61% in the second group. Percentage of cases who sustained NR was 46.67% in the first group and 65.39% in the second age group.Regarding gender, LSC+ male patients were more (70.83%) than LSC+ females (52.94%).Patients with a low (<1%) percentage of CD123+CD34+ cells had a CR rate of 50% and an NR rate of 50%. On the other side, in patients who had a higher expression (>1%) of CD123+CD34+ cells, the CR rate was less (7 of 21, 33.33%) and NR was higher than the other group (14 of 21, 66.67%).
Conclusion
1. LSCs were expressed in 63.41% of AML cases and were distributed among FAB subtypes without preference to any FAB subtype.2. The expression of LSC phenotype was associated with poor response to induction therapy in AML patients.
Session topic: E-poster
Keyword(s): AML, Leukemic stem cell
Type: Eposter Presentation
Background
Laboratory data suggest that acute myeloid leukemia AML originates from a rare population of cells, termed leukemic stem cells (LSCs) or leukemia-initiating cells, which are capable of self-renewal, proliferation and differentiation into malignant blasts. There's a universal agreement that LSCs lie within the CD34+ compartment of hemopoietic cells and most of leukemic stem cells express the interleukin-3 alpha chain receptor, CD123 and lack CD38. The standard model of leukemogenesis posits the stepwise acquisition of genetic mutations in a susceptible cell and its progeny, leading to the development of an autonomous clone that expands enough to cause a clinical syndrome.The genetic events occur in susceptible cells that are either hemopoietic stem cells or its progeny. The resultant leukemic cell has the properties of a stem cell in terms of self-renewal, but with persistent uncontrolled division and resistance to chemotherapy. This leukemia stem cell theory has been proved by proliferation of proposed leukemic stem cell after its injection into lethally irradiated mice. This finding inspired scientists and researchers to explore new fields for leukemia treatments because with the current regimes, the relapse rate is high and death frequently happens due to treatment failure or consequences of bone marrow blast invasion. In the same perspective, researchers began to assess the prognostic value of leukemic stem cells at diagnosis and to weigh its significance with other known prognostic factors of AML.
Aims
This study aimed to estimate the expression of LSC phenotype in AML patients and to correlate it with response to induction therapy.
Methods
A cohort of 41 patients older than 15 years with newly diagnosed de novo AML were enrolled in this study. They were obtained from the National center of hematology in Baghdad and Baghdad teaching hospital between February and July 2013. The expression of CD34, CD38 and CD123 was assessed by multi-color flow cytometry. LSC positive (LSC+) samples must express CD34 and CD123 and lack the expression of CD38 in >1% of cells. French American British (FAB) classification system was used in this study.After four weeks of induction therapy; three groups were found: those who reached the complete morphological remission (CR), those who failed to reach CR and those who died before assessment of morphological remission. The last two groups were merged for statistical purposes.All statistical operations were done by Microsoft excel 2010 and SPSS programs. The p-value for significance was calculated from Chi square test and Fisher Exact test for 2X2 contingency tables when the Chi square test was not applicable.The percentage of LSCs was calculated as the percentage of cells in CD34+CD123+ quadrant X the percentage of CD38- cells X the blast% of the individual patient
Results
The mean expression of CD34+CD38-CD123+ cells at diagnosis was 3.85+7.14 (mean+SD), range=0% to 42.05%, median=2.15%.A cut off value of 1.0% was designed to separate two groups of patients; those with LSCs of less than or equal to 1.0% and those with more than 1.0%.In the first group (LSCs <1.0%), the CR rate was 53.33%, while it was 34.61% in the second group. Percentage of cases who sustained NR was 46.67% in the first group and 65.39% in the second age group.Regarding gender, LSC+ male patients were more (70.83%) than LSC+ females (52.94%).Patients with a low (<1%) percentage of CD123+CD34+ cells had a CR rate of 50% and an NR rate of 50%. On the other side, in patients who had a higher expression (>1%) of CD123+CD34+ cells, the CR rate was less (7 of 21, 33.33%) and NR was higher than the other group (14 of 21, 66.67%).
Conclusion
1. LSCs were expressed in 63.41% of AML cases and were distributed among FAB subtypes without preference to any FAB subtype.2. The expression of LSC phenotype was associated with poor response to induction therapy in AML patients.
Session topic: E-poster
Keyword(s): AML, Leukemic stem cell
Abstract: E1138
Type: Eposter Presentation
Background
Laboratory data suggest that acute myeloid leukemia AML originates from a rare population of cells, termed leukemic stem cells (LSCs) or leukemia-initiating cells, which are capable of self-renewal, proliferation and differentiation into malignant blasts. There's a universal agreement that LSCs lie within the CD34+ compartment of hemopoietic cells and most of leukemic stem cells express the interleukin-3 alpha chain receptor, CD123 and lack CD38. The standard model of leukemogenesis posits the stepwise acquisition of genetic mutations in a susceptible cell and its progeny, leading to the development of an autonomous clone that expands enough to cause a clinical syndrome.The genetic events occur in susceptible cells that are either hemopoietic stem cells or its progeny. The resultant leukemic cell has the properties of a stem cell in terms of self-renewal, but with persistent uncontrolled division and resistance to chemotherapy. This leukemia stem cell theory has been proved by proliferation of proposed leukemic stem cell after its injection into lethally irradiated mice. This finding inspired scientists and researchers to explore new fields for leukemia treatments because with the current regimes, the relapse rate is high and death frequently happens due to treatment failure or consequences of bone marrow blast invasion. In the same perspective, researchers began to assess the prognostic value of leukemic stem cells at diagnosis and to weigh its significance with other known prognostic factors of AML.
Aims
This study aimed to estimate the expression of LSC phenotype in AML patients and to correlate it with response to induction therapy.
Methods
A cohort of 41 patients older than 15 years with newly diagnosed de novo AML were enrolled in this study. They were obtained from the National center of hematology in Baghdad and Baghdad teaching hospital between February and July 2013. The expression of CD34, CD38 and CD123 was assessed by multi-color flow cytometry. LSC positive (LSC+) samples must express CD34 and CD123 and lack the expression of CD38 in >1% of cells. French American British (FAB) classification system was used in this study.After four weeks of induction therapy; three groups were found: those who reached the complete morphological remission (CR), those who failed to reach CR and those who died before assessment of morphological remission. The last two groups were merged for statistical purposes.All statistical operations were done by Microsoft excel 2010 and SPSS programs. The p-value for significance was calculated from Chi square test and Fisher Exact test for 2X2 contingency tables when the Chi square test was not applicable.The percentage of LSCs was calculated as the percentage of cells in CD34+CD123+ quadrant X the percentage of CD38- cells X the blast% of the individual patient
Results
The mean expression of CD34+CD38-CD123+ cells at diagnosis was 3.85+7.14 (mean+SD), range=0% to 42.05%, median=2.15%.A cut off value of 1.0% was designed to separate two groups of patients; those with LSCs of less than or equal to 1.0% and those with more than 1.0%.In the first group (LSCs <1.0%), the CR rate was 53.33%, while it was 34.61% in the second group. Percentage of cases who sustained NR was 46.67% in the first group and 65.39% in the second age group.Regarding gender, LSC+ male patients were more (70.83%) than LSC+ females (52.94%).Patients with a low (<1%) percentage of CD123+CD34+ cells had a CR rate of 50% and an NR rate of 50%. On the other side, in patients who had a higher expression (>1%) of CD123+CD34+ cells, the CR rate was less (7 of 21, 33.33%) and NR was higher than the other group (14 of 21, 66.67%).
Conclusion
1. LSCs were expressed in 63.41% of AML cases and were distributed among FAB subtypes without preference to any FAB subtype.2. The expression of LSC phenotype was associated with poor response to induction therapy in AML patients.
Session topic: E-poster
Keyword(s): AML, Leukemic stem cell
Type: Eposter Presentation
Background
Laboratory data suggest that acute myeloid leukemia AML originates from a rare population of cells, termed leukemic stem cells (LSCs) or leukemia-initiating cells, which are capable of self-renewal, proliferation and differentiation into malignant blasts. There's a universal agreement that LSCs lie within the CD34+ compartment of hemopoietic cells and most of leukemic stem cells express the interleukin-3 alpha chain receptor, CD123 and lack CD38. The standard model of leukemogenesis posits the stepwise acquisition of genetic mutations in a susceptible cell and its progeny, leading to the development of an autonomous clone that expands enough to cause a clinical syndrome.The genetic events occur in susceptible cells that are either hemopoietic stem cells or its progeny. The resultant leukemic cell has the properties of a stem cell in terms of self-renewal, but with persistent uncontrolled division and resistance to chemotherapy. This leukemia stem cell theory has been proved by proliferation of proposed leukemic stem cell after its injection into lethally irradiated mice. This finding inspired scientists and researchers to explore new fields for leukemia treatments because with the current regimes, the relapse rate is high and death frequently happens due to treatment failure or consequences of bone marrow blast invasion. In the same perspective, researchers began to assess the prognostic value of leukemic stem cells at diagnosis and to weigh its significance with other known prognostic factors of AML.
Aims
This study aimed to estimate the expression of LSC phenotype in AML patients and to correlate it with response to induction therapy.
Methods
A cohort of 41 patients older than 15 years with newly diagnosed de novo AML were enrolled in this study. They were obtained from the National center of hematology in Baghdad and Baghdad teaching hospital between February and July 2013. The expression of CD34, CD38 and CD123 was assessed by multi-color flow cytometry. LSC positive (LSC+) samples must express CD34 and CD123 and lack the expression of CD38 in >1% of cells. French American British (FAB) classification system was used in this study.After four weeks of induction therapy; three groups were found: those who reached the complete morphological remission (CR), those who failed to reach CR and those who died before assessment of morphological remission. The last two groups were merged for statistical purposes.All statistical operations were done by Microsoft excel 2010 and SPSS programs. The p-value for significance was calculated from Chi square test and Fisher Exact test for 2X2 contingency tables when the Chi square test was not applicable.The percentage of LSCs was calculated as the percentage of cells in CD34+CD123+ quadrant X the percentage of CD38- cells X the blast% of the individual patient
Results
The mean expression of CD34+CD38-CD123+ cells at diagnosis was 3.85+7.14 (mean+SD), range=0% to 42.05%, median=2.15%.A cut off value of 1.0% was designed to separate two groups of patients; those with LSCs of less than or equal to 1.0% and those with more than 1.0%.In the first group (LSCs <1.0%), the CR rate was 53.33%, while it was 34.61% in the second group. Percentage of cases who sustained NR was 46.67% in the first group and 65.39% in the second age group.Regarding gender, LSC+ male patients were more (70.83%) than LSC+ females (52.94%).Patients with a low (<1%) percentage of CD123+CD34+ cells had a CR rate of 50% and an NR rate of 50%. On the other side, in patients who had a higher expression (>1%) of CD123+CD34+ cells, the CR rate was less (7 of 21, 33.33%) and NR was higher than the other group (14 of 21, 66.67%).
Conclusion
1. LSCs were expressed in 63.41% of AML cases and were distributed among FAB subtypes without preference to any FAB subtype.2. The expression of LSC phenotype was associated with poor response to induction therapy in AML patients.
Session topic: E-poster
Keyword(s): AML, Leukemic stem cell
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