scholarly journals Differences in the expression of alkaline phosphatase mRNA in chronic myelogenous leukemia and paroxysmal nocturnal hemoglobinuria polymorphonuclear leukocytes

Blood ◽  
1989 ◽  
Vol 73 (5) ◽  
pp. 1113-1115 ◽  
Author(s):  
A Rambaldi ◽  
M Terao ◽  
S Bettoni ◽  
R Bassan ◽  
R Battista ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Chronic Myelogenous Leukemia ◽  
Polymorphonuclear Leukocytes ◽  
Paroxysmal Nocturnal Hemoglobinuria ◽  
Myelogenous Leukemia ◽  
Stable Phase ◽  
Polymorphonuclear Cells ◽  
Mrna Levels ◽  
Leukocyte Alkaline Phosphatase ◽  
Low Levels

Abstract Paroxysmal nocturnal hemoglobinuria (PNH) and the stable phase of chronic myelogenous leukemia (CML) are the two hematological conditions known to be associated with low levels of leukocyte alkaline phosphatase (LAP) activity in peripheral blood polymorphonuclear cells (PMN). LAP mRNA levels were determined in PMN from PNH and CML patients by RNA blotting analysis. In CML, LAP mRNA is undetectable, suggesting either decreased transcription or rapid degradation of the message. Contrarily, in PNH normal or high levels of LAP mRNA are present. This latter finding supports the concept of a deficit in the anchorage of the protein to the plasma membrane through the glycolipid pathway, even though other post-transcriptional mechanisms could be involved.

scholarly journals Differences in the expression of alkaline phosphatase mRNA in chronic myelogenous leukemia and paroxysmal nocturnal hemoglobinuria polymorphonuclear leukocytes

Blood ◽  
1989 ◽  
Vol 73 (5) ◽  
pp. 1113-1115
Author(s):  
A Rambaldi ◽  
M Terao ◽  
S Bettoni ◽  
R Bassan ◽  
R Battista ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Chronic Myelogenous Leukemia ◽  
Polymorphonuclear Leukocytes ◽  
Paroxysmal Nocturnal Hemoglobinuria ◽  
Myelogenous Leukemia ◽  
Stable Phase ◽  
Polymorphonuclear Cells ◽  
Mrna Levels ◽  
Leukocyte Alkaline Phosphatase ◽  
Low Levels

Paroxysmal nocturnal hemoglobinuria (PNH) and the stable phase of chronic myelogenous leukemia (CML) are the two hematological conditions known to be associated with low levels of leukocyte alkaline phosphatase (LAP) activity in peripheral blood polymorphonuclear cells (PMN). LAP mRNA levels were determined in PMN from PNH and CML patients by RNA blotting analysis. In CML, LAP mRNA is undetectable, suggesting either decreased transcription or rapid degradation of the message. Contrarily, in PNH normal or high levels of LAP mRNA are present. This latter finding supports the concept of a deficit in the anchorage of the protein to the plasma membrane through the glycolipid pathway, even though other post-transcriptional mechanisms could be involved.

scholarly journals Expression of leukocyte alkaline phosphatase gene in normal and leukemic cells: regulation of the transcript by granulocyte colony- stimulating factor

Blood ◽  
1990 ◽  
Vol 76 (12) ◽  
pp. 2565-2571 ◽  
Author(s):  
A Rambaldi ◽  
M Terao ◽  
S Bettoni ◽  
ML Tini ◽  
R Bassan ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Lymphoblastic Leukemia ◽  
Lymphocytic Leukemia ◽  
Myelogenous Leukemia ◽  
Leukemic Cells ◽  
Polymorphonuclear Cells ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Leukocyte Alkaline Phosphatase ◽  
Stimulating Factor

Abstract The levels of leukocyte alkaline phosphatase (LAP) messenger RNA (mRNA) are evaluated in B and T lymphocytes, monocytes, and polymorphonuclear cells (PMNs), and this transcript is found to be present only in PMNs. Precursors of the myelomonocytic pathway, represented by leukemic cells isolated from several cases of chronic myelogenous leukemia (CML) in its stable and blastic phase and acute myelogenous leukemia (AML), are devoid of LAP transcript. These data support the notion that LAP is a marker of the granulocyte terminal differentiation. Despite the absence of LAP mRNA in both the myeloid and the lymphoid precursors, nuclear run-on experiments show constitutive transcription of the LAP gene in leukemic cells obtained from AML, CML, as well as acute lymphoblastic leukemia (ALL) and B-cell chronic lymphocytic leukemia (B-CLL). In CML and in chronic myelo-monocytic leukemia (CMML) PMNs, granulocyte colony- stimulating factor (G-CSF) specifically accumulates LAP mRNA without showing a substantial increase in the rate of transcription of the LAP gene. Once increased by G-CSF, LAP mRNA is very stable, showing a half- life of more than 4 hours in the presence of actinomycin-D. G-CSF is suggested to play a pivotal role in the modulation of LAP transcript in PMNs.

scholarly journals Expression of leukocyte alkaline phosphatase gene in normal and leukemic cells: regulation of the transcript by granulocyte colony- stimulating factor

Blood ◽  
1990 ◽  
Vol 76 (12) ◽  
pp. 2565-2571 ◽  
Author(s):  
A Rambaldi ◽  
M Terao ◽  
S Bettoni ◽  
ML Tini ◽  
R Bassan ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Lymphoblastic Leukemia ◽  
Lymphocytic Leukemia ◽  
Myelogenous Leukemia ◽  
Leukemic Cells ◽  
Polymorphonuclear Cells ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Leukocyte Alkaline Phosphatase ◽  
Stimulating Factor

The levels of leukocyte alkaline phosphatase (LAP) messenger RNA (mRNA) are evaluated in B and T lymphocytes, monocytes, and polymorphonuclear cells (PMNs), and this transcript is found to be present only in PMNs. Precursors of the myelomonocytic pathway, represented by leukemic cells isolated from several cases of chronic myelogenous leukemia (CML) in its stable and blastic phase and acute myelogenous leukemia (AML), are devoid of LAP transcript. These data support the notion that LAP is a marker of the granulocyte terminal differentiation. Despite the absence of LAP mRNA in both the myeloid and the lymphoid precursors, nuclear run-on experiments show constitutive transcription of the LAP gene in leukemic cells obtained from AML, CML, as well as acute lymphoblastic leukemia (ALL) and B-cell chronic lymphocytic leukemia (B-CLL). In CML and in chronic myelo-monocytic leukemia (CMML) PMNs, granulocyte colony- stimulating factor (G-CSF) specifically accumulates LAP mRNA without showing a substantial increase in the rate of transcription of the LAP gene. Once increased by G-CSF, LAP mRNA is very stable, showing a half- life of more than 4 hours in the presence of actinomycin-D. G-CSF is suggested to play a pivotal role in the modulation of LAP transcript in PMNs.

Azurophil and specific granules of blood neutrophils in chronic myelogenous leukemia: an ultrastructural and cytochemical analysis

Blood ◽  
1975 ◽  
Vol 45 (4) ◽  
pp. 469-482
Author(s):  
JL Ullyot ◽  
DF Bainton
Keyword(s):  
Electron Microscopy ◽  
Alkaline Phosphatase ◽  
Chronic Myelogenous Leukemia ◽  
Chronic Phase ◽  
Myelogenous Leukemia ◽  
Terminal Phase ◽  
Leukocyte Alkaline Phosphatase ◽  
Specific Granules ◽  
Blood Neutrophils ◽  
Specific Granule

That most patients with chronic myelogenous leukemia (CML) have either very low levels or no leukocyte alkaline phosphatase activity (LAP) is an established fact. In view of our new findings7 that normal mature human polymorphonuclear leukocytes (PMN) contain two types of granules, azurophils (1/3) and specifics (2/3), and that alkaline phosphatase is present only in specific granules, we undertook the present studies to determine whether these neoplastic PMN lack a specific granule population or simply lack the enzyme. The cellular buffy coats of five patients with CML (Ph1 plus, LAP minus) were fixed in glutaraldehyde, incubated for peroxidase to identify the azurophil population, and examined by electron microscopy. It was found that the specific granule population was present in all mature PMN. Counts of both azurophil and specific granules per cell were slightly lower than normal but were within an 80%-90% overlap of the normal range. We therefore conclude that the low level of LAP in patients with CML reflects a deficiency of the enzyme rather than a missing granule population. Although the mature PMN appeared relatively normal (with few exceptions), circulating myeloblasts and promyelocytes revealed several abnormalities, the most notable being the presence of large bundles of cytoplasmic microfilaments. The blood of two patients in the terminal phase of disease was reexamined. Most of their cells were immature, with aberrations similar to those in myeloblasts and promyelocytes in the chronic phase of the disorder. In addition, however, we discovered three adnormal populations of mature PMN: (1) PMN containing both populations of granules but lacking peroxidase, (2) PMN lacking specific granules, and (3) PMN lacking azurophil granules. Our findings emphasize the value of electron microscopy and cytochemistry in detecting abnormalities of maturation in the cytoplasm of leukemic PMN.

scholarly journals Azurophil and Specific Granules of Blood Neutrophils in Chronic Myelogenous Leukemia: An Ultrastructural and Cytochemical Analysis

Blood ◽  
1974 ◽  
Vol 44 (4) ◽  
pp. 469-482 ◽  
Author(s):  
Joan L. Ullyot ◽  
Dorothy F. Bainton
Keyword(s):  
Electron Microscopy ◽  
Alkaline Phosphatase ◽  
Chronic Myelogenous Leukemia ◽  
Chronic Phase ◽  
Myelogenous Leukemia ◽  
Terminal Phase ◽  
Leukocyte Alkaline Phosphatase ◽  
Specific Granules ◽  
Blood Neutrophils ◽  
Specific Granule

Abstract That most patients with chronic myelogenous leukemia (CML) have either very low levels or no leukocyte alkaline phosphatase activity (LAP) is an established fact. In view of our new findings7 that normal mature human polymorphonuclear leukocytes (PMN) contain two types of granules, azurophils (1/3) and specifics (2/3), and that alkaline phosphatase is present only in specific granules, we undertook the present studies to determine whether these neoplastic PMN lack a specific granule population or simply lack the enzyme. The cellular buffy coats of five patients with CML (Ph1+, LAP-) were fixed in glutaraldehyde, incubated for peroxidase to identify the azurophil population, and examined by electron microscopy. It was found that the specific granule population was present in all mature PMN. Counts of both azurophil and specific granules per cell were slightly lower than normal but were within an 80%-90% overlap of the normal range. We therefore conclude that the low level of LAP in patients with CML reflects a deficiency of the enzyme rather than a missing granule population. Although the mature PMN appeared relatively normal (with few exceptions), circulating myeloblasts and promyelocytes revealed several abnormalities, the most notable being the presence of large bundles of cytoplasmic microfilaments. The blood of two patients in the terminal phase of disease was reexamined. Most of their cells were immature, with aberrations similar to those in myeloblasts and promyelocytes in the chronic phase of the disorder. In addition, however, we discovered three adnormal populations of mature PMN: (1) PMN containing both populations of granules but lacking peroxidase, (2) PMN lacking specific granules, and (3) PMN lacking azurophil granules. Our findings emphasize the value of electron microscopy and cytochemistry in detecting abnormalities of maturation in the cytoplasm of leukemic PMN.

Azurophil and specific granules of blood neutrophils in chronic myelogenous leukemia: an ultrastructural and cytochemical analysis

Blood ◽  
1975 ◽  
Vol 45 (4) ◽  
pp. 469-482
Author(s):  
JL Ullyot ◽  
DF Bainton
Keyword(s):  
Electron Microscopy ◽  
Alkaline Phosphatase ◽  
Chronic Myelogenous Leukemia ◽  
Chronic Phase ◽  
Myelogenous Leukemia ◽  
Terminal Phase ◽  
Leukocyte Alkaline Phosphatase ◽  
Specific Granules ◽  
Blood Neutrophils ◽  
Specific Granule

Abstract That most patients with chronic myelogenous leukemia (CML) have either very low levels or no leukocyte alkaline phosphatase activity (LAP) is an established fact. In view of our new findings7 that normal mature human polymorphonuclear leukocytes (PMN) contain two types of granules, azurophils (1/3) and specifics (2/3), and that alkaline phosphatase is present only in specific granules, we undertook the present studies to determine whether these neoplastic PMN lack a specific granule population or simply lack the enzyme. The cellular buffy coats of five patients with CML (Ph1 plus, LAP minus) were fixed in glutaraldehyde, incubated for peroxidase to identify the azurophil population, and examined by electron microscopy. It was found that the specific granule population was present in all mature PMN. Counts of both azurophil and specific granules per cell were slightly lower than normal but were within an 80%-90% overlap of the normal range. We therefore conclude that the low level of LAP in patients with CML reflects a deficiency of the enzyme rather than a missing granule population. Although the mature PMN appeared relatively normal (with few exceptions), circulating myeloblasts and promyelocytes revealed several abnormalities, the most notable being the presence of large bundles of cytoplasmic microfilaments. The blood of two patients in the terminal phase of disease was reexamined. Most of their cells were immature, with aberrations similar to those in myeloblasts and promyelocytes in the chronic phase of the disorder. In addition, however, we discovered three adnormal populations of mature PMN: (1) PMN containing both populations of granules but lacking peroxidase, (2) PMN lacking specific granules, and (3) PMN lacking azurophil granules. Our findings emphasize the value of electron microscopy and cytochemistry in detecting abnormalities of maturation in the cytoplasm of leukemic PMN.

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