scholarly journals Evaluation of the FAB classification of acute leukemia with special reference to differential diagnosis between acute lymphoblastic leukemia cells and acute myeloid leukemia cells.

1986 ◽  
Vol 25 (6) ◽  
pp. 1003-1009
Author(s):  
Shinobu NAKAMURA ◽  
Jin NAKANISHI ◽  
Takashi YOSHIDA ◽  
Shigeki OHTAKE ◽  
Keiko ITOH ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Differential Diagnosis ◽  
Acute Lymphoblastic Leukemia ◽  
Myeloid Leukemia ◽  
Lymphoblastic Leukemia ◽  
Leukemia Cells ◽  
Fab Classification ◽  
Acute Myeloid Leukemia Cells ◽  
Acute Myeloid

Acute Leukemia

2016 ◽  
Author(s):  
Richard A. Larson ◽  
Roland B Walter
Keyword(s):  
Acute Myeloid Leukemia ◽  
Acute Lymphoblastic Leukemia ◽  
Acute Leukemia ◽  
Myeloid Leukemia ◽  
Who Classification ◽  
Lymphoblastic Leukemia ◽  
World Health ◽  
Acute Leukemias ◽  
Acute Myeloid

The acute leukemias are malignant clonal disorders characterized by aberrant differentiation and proliferation of transformed hematopoietic progenitor cells. These cells accumulate within the bone marrow and lead to suppression of the production of normal blood cells, with resulting symptoms from varying degrees of anemia, neutropenia, and thrombocytopenia or from infiltration into tissues. They are currently classified by their presumed cell of origin, although the field is moving rapidly to genetic subclassification. This review covers epidemiology; etiology; classification of leukemia by morphology, immunophenotyping, and cytogenetic/molecular abnormalities; cytogenetics of acute leukemia; general principles of therapy; acute myeloid leukemia; acute lymphoblastic leukemia; and future possibilities. The figure shows the incidence of acute leukemias in the United States. Tables list World Health Organization (WHO) classification of acute myeloid leukemia and related neoplasms, expression of cell surface and cytoplasmic markers for the diagnosis of acute myeloid leukemia and mixed-phenotype acute leukemia, WHO classification of acute lymphoblastic leukemia, WHO classification of acute leukemias of ambiguous lineage, WHO classification of myelodysplastic syndromes, European LeukemiaNet cytogenetic and molecular genetic subsets in acute myeloid leukemia with prognostic importance, cytogenetic and molecular subtypes of acute lymphoblastic leukemia, terminology used in leukemia treatment, and treatment outcome for adults with acute leukemia. This review contains 1 highly rendered figure, 9 tables, and 117 references.

Acute Myeloid Leukemia Cells Contain Constitutively Activated STAT3 and Require STAT3 for Survival.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3368-3368
Author(s):  
Tae Kon Kim ◽  
Martin Carroll ◽  
Alan M. Gewirtz
Keyword(s):  
Cell Proliferation ◽  
Acute Myeloid Leukemia ◽  
Gene Silencing ◽  
Myeloid Leukemia ◽  
Target Gene ◽  
Leukemia Cells ◽  
Specific Cell ◽  
Fab Classification ◽  
Acute Myeloid Leukemia Cells ◽  
Acute Myeloid

Abstract Signal transducer and activator of transcription (STAT) family proteins play crucial roles in the cytokine signaling pathways which regulate survival and proliferation of normal and malignant hematopoietic cells. The STAT proteins which regulate myeloid leukemia cell survival and proliferation remain ill defined. STAT3, for example, has been reported to be constitutively activated in acute myeloid leukemia (AML) cells but its function in these cells is not clear. In order to better understand the role of STAT3 in AML biology, we studied its expression, activation, and requirement for cell growth in several AML cell lines, and in primary patient material. We first confirmed the activation of STAT3 in primary AML cells by western blotting. An analysis of 5 AML patient samples revealed elevated levels of constitutive STAT3 phosphorylation in 4 of 5 samples. In addition, two AML cell lines (MOLM-14, KG-1) displayed constitutive STAT3 activation. In order to evalute the functional significance of STAT3 overexpression in AML cells, we synthesized a siRNA that had been reported effective in silencing STAT3 expression. The siRNA were delivered to MOLM-14 cells using an amaxa nucleoporation device (amaxa, Inc. Gaithersburg, MD) (Program O-17/Solution V). In treated cells, STAT3 expression decreased 72%±1% [n=5] but in a non-dose related manner suggesting that “off-target” gene silencing, or other mechanisms unrelated to target gene silencing might have played a role squelching STAT3 expression. In contrast, nucleofection of MOLM-14 cells with an antisense oligodeoxynucleotide (AS ODN) corresponding to the antisense sequence of the siRNA duplex, decreased STAT3 expression 96%±1% [n=5] compared to control treated cells. Importantly, inhibition was dose dependent and sequence specific. Cell proliferation was also inhibited in the AS ODN treated cells (82%±7% at 24 hour, 92%±2% at 48 hour, 91%±4% at 72 hour [n=3]) in comparison to control treated cells. To determine if these results were unique to a specific cell line, we nucleofected AS ODN into KG-1 cells (amaxa, Program T-27/Solution V). Again, the AS ODN decreased STAT3 expression 90% compared to control treated cells and inhibited cell proliferation in a manner similar to that obtained for MOLM-14 cells (72% at 24 hour, 78% at 48 hour, 79% at 72 hour) in comparison to control treated cells. To determine if STAT3 is necessary for survival of primary AML cells, cells from 5 patients (four frozen leukapheresis samples-FAB Classification M1, M4, M4, M5, one fresh peripheral blood sample-FAB Classification M5) were nucleofected (amaxa, Program U-15/Solution V) with the STAT3 AS or control ODN and incubated on the EBM-2(Endothelial Basal Medium, CABREX®) for 72 hours. Primary AML cells treated with STAT3 AS ODN showed a ~50–80% decrease in survival compared to control ODN treated cells. These results demonstrate that STAT3 plays an important role in the survival and proliferation of acute myeloid leukemia cells. Accordingly, STAT3 appears to be a legitimate target for the treatment of AML. These results also demonstrate that an effectively delivered, appropriately targeted, AS ODN has the ability to silence its targeted gene’s expression with a specificity and an efficiency equivalent to, or in some cases better, than any highly active siRNA.

Acute Leukemia

2021 ◽  
Author(s):  
Richard A. Larson ◽  
Roland B Walter
Keyword(s):  
Acute Myeloid Leukemia ◽  
Acute Lymphoblastic Leukemia ◽  
Acute Leukemia ◽  
Myeloid Leukemia ◽  
Who Classification ◽  
Lymphoblastic Leukemia ◽  
World Health ◽  
Acute Leukemias ◽  
Acute Myeloid

The acute leukemias are malignant clonal disorders characterized by aberrant differentiation and proliferation of transformed hematopoietic progenitor cells. These cells accumulate within the bone marrow and lead to suppression of the production of normal blood cells, with resulting symptoms from varying degrees of anemia, neutropenia, and thrombocytopenia or from infiltration into tissues. They are currently classified by their presumed cell of origin, although the field is moving rapidly to genetic subclassification. This review covers epidemiology; etiology; classification of leukemia by morphology, immunophenotyping, and cytogenetic/molecular abnormalities; cytogenetics of acute leukemia; general principles of therapy; acute myeloid leukemia; acute lymphoblastic leukemia; and future possibilities. The figure shows the incidence of acute leukemias in the United States. Tables list World Health Organization (WHO) classification of acute myeloid leukemia and related neoplasms, expression of cell surface and cytoplasmic markers for the diagnosis of acute myeloid leukemia and mixed-phenotype acute leukemia, WHO classification of acute lymphoblastic leukemia, WHO classification of acute leukemias of ambiguous lineage, WHO classification of myelodysplastic syndromes, European LeukemiaNet cytogenetic and molecular genetic subsets in acute myeloid leukemia with prognostic importance, cytogenetic and molecular subtypes of acute lymphoblastic leukemia, terminology used in leukemia treatment, and treatment outcome for adults with acute leukemia. This review contains 2 figures, 15 tables, and 119 references. Keywords: Acute leukemia, acute myeloid leukemia, acute lymphoblastic leukemia, cancer, cytogenetics, chromosomal abnormality

Acute Leukemia

2018 ◽  
Author(s):  
Richard A. Larson ◽  
Roland B Walter
Keyword(s):  
Acute Myeloid Leukemia ◽  
Acute Lymphoblastic Leukemia ◽  
Acute Leukemia ◽  
Myeloid Leukemia ◽  
Who Classification ◽  
Lymphoblastic Leukemia ◽  
World Health ◽  
Acute Leukemias ◽  
Acute Myeloid

The acute leukemias are malignant clonal disorders characterized by aberrant differentiation and proliferation of transformed hematopoietic progenitor cells. These cells accumulate within the bone marrow and lead to suppression of the production of normal blood cells, with resulting symptoms from varying degrees of anemia, neutropenia, and thrombocytopenia or from infiltration into tissues. They are currently classified by their presumed cell of origin, although the field is moving rapidly to genetic subclassification. This review covers epidemiology; etiology; classification of leukemia by morphology, immunophenotyping, and cytogenetic/molecular abnormalities; cytogenetics of acute leukemia; general principles of therapy; acute myeloid leukemia; acute lymphoblastic leukemia; and future possibilities. The figure shows the incidence of acute leukemias in the United States. Tables list World Health Organization (WHO) classification of acute myeloid leukemia and related neoplasms, expression of cell surface and cytoplasmic markers for the diagnosis of acute myeloid leukemia and mixed-phenotype acute leukemia, WHO classification of acute lymphoblastic leukemia, WHO classification of acute leukemias of ambiguous lineage, WHO classification of myelodysplastic syndromes, European LeukemiaNet cytogenetic and molecular genetic subsets in acute myeloid leukemia with prognostic importance, cytogenetic and molecular subtypes of acute lymphoblastic leukemia, terminology used in leukemia treatment, and treatment outcome for adults with acute leukemia. This review contains 1 highly rendered figure, 9 tables, and 117 references.

Effect of miR-128 in DNA Damage of HL-60 Acute Myeloid Leukemia Cells

2014 ◽  
Vol 15 (5) ◽  
pp. 492-502 ◽  
Author(s):  
Hugo Seca ◽  
Raquel Lima ◽  
Gabriela Almeida ◽  
Manuel Sobrinho-Simoes ◽  
Rui Bergantim ◽  
...  
Keyword(s):  
Dna Damage ◽  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Leukemia Cells ◽  
Acute Myeloid Leukemia Cells ◽  
Acute Myeloid
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