scholarly journals Hematopoietic Graft Detected by a Change in ABO Group

Blood ◽  
1964 ◽  
Vol 23 (2) ◽  
pp. 239-249 ◽  
Author(s):  
WILLIAM R. BRONSON ◽  
MARY H. MCGINNISS ◽  
EDWARD E. MORSE
Keyword(s):  
Blood Group ◽  
Chronic Myelogenous Leukemia ◽  
Peripheral Blood ◽  
Acute Lymphocytic Leukemia ◽  
Hematopoietic Cells ◽  
White Cell ◽  
Lymphocytic Leukemia ◽  
Red Cells ◽  
Myelogenous Leukemia

Abstract A change in blood group was discovered in a group O boy with acute lymphocytic leukemia. Fifty-six per cent of his red cells were of group AB 6 weeks after he received white cell-rich plasma from a group AB donor with chronic myelogenous leukemia. It is concluded that hematopoietic cells in the peripheral blood of the donor survived and divided in the recipient, and were then rejected 6 weeks after transfusion. Factors favoring the acceptance of the graft, consideration of the type of cell or cells that proliferated, and the relation of this finding to recently published reports of survival of cells containing the Ph1 chromosome are discussed.

Cardiovascular involvement in blood cancers: ALL, AML, CLL, and CML

2021 ◽  
Author(s):  
Amer Yazdanparast ◽  
Gholamreza Fathpour ◽  
Shirin Saberianpour
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Chronic Myelogenous Leukemia ◽  
Acute Myelogenous Leukemia ◽  
Acute Lymphocytic Leukemia ◽  
The Body ◽  
Lymphocytic Leukemia ◽  
Myelogenous Leukemia ◽  
Primary Tumors ◽  
Secondary Tumors ◽  
Acute Myelogenous

Global cancer statistics will continue to grow in the coming years. Leukemia is the fifth leading cause of death in the world and the second one in Iran; therefore, it is very important to study the affected areas, including the cardiovascular system in this disease. In heart cancer, tumors whose primary origin is the heart are called primary tumors, which are very rare. Tumors that originate in other parts of the body and spread to the heart are called secondary tumors. Although heart cancer is still rare, most cancers found in the heart come from other parts of the body and are considered as secondary tumors. The symptoms of metastatic heart cancer vary and depend on the location and extent of the lesion. Cancer can also affect the heart in other ways. One of these ways is the effect of the treatments used, which is reported among acute lymphocytic leukemia, acute myelogenous leukemia, chronic lymphocytic leukemia, and chronic myelogenous leukemia due to the use of tyrosine kinase inhibitors as the main drug in reducing mortality among these patients. Pericardial involvement is reported to be the most common cardiovascular complication of drug use among different kinds of leukemias. In this article, we try to collect cardiovascular evidence related to acute lymphocytic leukemia, acute myelogenous leukemia, chronic lymphocytic leukemia, and chronic myelogenous leukemia, separately.

Alternative forms of the BCR-ABL oncogene have quantitatively different potencies for stimulation of immature lymphoid cells

1989 ◽  
Vol 9 (5) ◽  
pp. 1866-1874
Author(s):  
J McLaughlin ◽  
E Chianese ◽  
O N Witte
Keyword(s):  
Gene Product ◽  
Chronic Myelogenous Leukemia ◽  
Acute Lymphocytic Leukemia ◽  
Structural Changes ◽  
Philadelphia Chromosome ◽  
Lymphocytic Leukemia ◽  
Lymphoid Cells ◽  
Chromosome 9 ◽  
Myelogenous Leukemia ◽  
Cdna Clones

The Philadelphia chromosome (t9:22;q34:q11) is found in more than 90% of patients with chronic myelogenous leukemia, in 10 to 20% of patients with acute lymphocytic leukemia, and in 1 to 2% of patients with acute myelogenous leukemia. Alternative chimeric oncogenes are formed by splicing different sets of BCR gene exons on chromosome 22 across the translocation breakpoint to a common set of ABL oncogene sequences on chromosome 9. This results in an 8.7-kilobase mRNA that encodes the P210 BCR-ABL gene product commonly found in patients with chronic myelogenous leukemia or a 7.0-kilobase mRNA that produces the P185 BCR-ABL gene product found in most Philadelphia chromosome-positive patients with acute lymphocytic leukemia. To compare the efficiency of growth stimulation by these two proteins, we derived cDNA clones for each with identical 5' and 3' untranslated regions and expressed them from retrovirus vectors. Matched stocks were compared for potency to transform immature B-lymphoid lineage precursors. The growth-stimulating effects of P185 for this cell type were found to be significantly greater than those of P210. Structural changes in BCR may regulate the effectiveness of the ABL tyrosine kinase function, as monitored by lymphocyte growth response. Changes in mitogenic potency may help to explain the more acute leukemic presentation usually associated with expression of the P185 BCR-ABL oncogene.

scholarly journals Alternative forms of the BCR-ABL oncogene have quantitatively different potencies for stimulation of immature lymphoid cells.

1989 ◽  
Vol 9 (5) ◽  
pp. 1866-1874 ◽  
Author(s):  
J McLaughlin ◽  
E Chianese ◽  
O N Witte
Keyword(s):  
Gene Product ◽  
Chronic Myelogenous Leukemia ◽  
Acute Lymphocytic Leukemia ◽  
Structural Changes ◽  
Philadelphia Chromosome ◽  
Lymphocytic Leukemia ◽  
Lymphoid Cells ◽  
Chromosome 9 ◽  
Myelogenous Leukemia ◽  
Cdna Clones

The Philadelphia chromosome (t9:22;q34:q11) is found in more than 90% of patients with chronic myelogenous leukemia, in 10 to 20% of patients with acute lymphocytic leukemia, and in 1 to 2% of patients with acute myelogenous leukemia. Alternative chimeric oncogenes are formed by splicing different sets of BCR gene exons on chromosome 22 across the translocation breakpoint to a common set of ABL oncogene sequences on chromosome 9. This results in an 8.7-kilobase mRNA that encodes the P210 BCR-ABL gene product commonly found in patients with chronic myelogenous leukemia or a 7.0-kilobase mRNA that produces the P185 BCR-ABL gene product found in most Philadelphia chromosome-positive patients with acute lymphocytic leukemia. To compare the efficiency of growth stimulation by these two proteins, we derived cDNA clones for each with identical 5' and 3' untranslated regions and expressed them from retrovirus vectors. Matched stocks were compared for potency to transform immature B-lymphoid lineage precursors. The growth-stimulating effects of P185 for this cell type were found to be significantly greater than those of P210. Structural changes in BCR may regulate the effectiveness of the ABL tyrosine kinase function, as monitored by lymphocyte growth response. Changes in mitogenic potency may help to explain the more acute leukemic presentation usually associated with expression of the P185 BCR-ABL oncogene.

Congenital Juvenile Chronic Myelogenous Leukemia: Case Report and Review

PEDIATRICS ◽  
1984 ◽  
Vol 73 (3) ◽  
pp. 324-326
Author(s):  
Reese H. Clark ◽  
Leslie L. Taylor ◽  
Robert J. Wells
Keyword(s):  
Bone Marrow ◽  
Case Report ◽  
Chronic Myelogenous Leukemia ◽  
Peripheral Blood ◽  
Blast Crisis ◽  
Myelogenous Leukemia ◽  
Juvenile Form

The case of a patient with ecchymosis, hepatomegaly, leukocytosis, thrombocytopenia, and anemia at birth is presented. Throughout his course, thrombocytopenia, anemia, and leukocytosis without a marked increase in the number of blast forms in either peripheral blood or bone marrow persisted until the patient developed a blast crisis shortly before his death at age 4 months. This patient is the youngest reported to have the juvenile form of chronic myelogenous leukemia and the first that in the present era can be considered congenital in origin.

Immunophenotypic Study of Basophils by Multiparameter Flow Cytometry

2008 ◽  
Vol 132 (5) ◽  
pp. 813-819
Author(s):  
Xiaohong Han ◽  
Jeffrey L. Jorgensen ◽  
Archana Brahmandam ◽  
Ellen Schlette ◽  
Yang O. Huh ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Flow Cytometry ◽  
Chronic Myelogenous Leukemia ◽  
Peripheral Blood ◽  
Myelogenous Leukemia ◽  
Multiparameter Flow Cytometry ◽  
Color Flow ◽  
Aberrant Expression ◽  
Flow Cytometric ◽  
Hla Dr

Abstract Context.—The immunophenotypic profile of basophils is not yet fully established, and the immunophenotypic changes in chronic myelogenous leukemia are not fully characterized. Objective.—To establish a comprehensive immunophenotypic spectrum of normal basophils and to assess the range of immunophenotypic aberrations of basophils in chronic myelogenous leukemia. Design.—Using 4-color flow cytometry, we compared the immunophenotypic profile of basophils in peripheral blood or bone marrow samples from 20 patients with no evidence of neoplasia to basophils from 15 patients with chronic myelogenous leukemia. Results.—Basophils in control cases were all positive for CD9, CD13, CD22, CD25 (dim), CD33, CD36, CD38 (bright), CD45 (dimmer than lymphocytes and brighter than myeloblasts), and CD123 (bright), and were negative for CD19, CD34, CD64, CD117, and HLA-DR. Basophils in all chronic myelogenous leukemia patients possessed 1 to 5 immunophenotypic aberrancies. The most common aberrancies were underexpression of CD38, followed by aberrant expression of CD64 and underexpression of CD123. CD34 and CD117 were present in cases with basophilic precursors. Myeloblasts showed a distinct immunophenotypic profile, as they typically expressed CD34 and CD117, showed dimmer expression (compared with basophils) of CD38, CD45, and CD123, and lacked expression of CD22. Conclusions.—Flow cytometric immunophenotyping can identify immunophenotypic aberrations of basophils in chronic myelogenous leukemia, and discriminate basophils from myeloblasts.

scholarly journals A two-color flow cytometry assay for detection of hairy cells using monoclonal antibodies

Blood ◽  
1987 ◽  
Vol 70 (4) ◽  
pp. 1063-1068
Author(s):  
JS Kristensen ◽  
J Ellegaard ◽  
P Hokland
Keyword(s):  
Flow Cytometry ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Cell Suspensions ◽  
Lymphocytic Leukemia ◽  
Myelogenous Leukemia ◽  
Morphological Evidence ◽  
Acute Leukemias ◽  
Color Flow ◽  
Hairy Cells

We have developed a simple two-color immunofluorescence assay equally suited for microscopy and flow cytometry detecting hairy cells (HCs) in single cell suspensions, based on the concomitant reactivities with the B cell-specific monoclonal antibody B1 (CD20) and the monocyte/HC- associated antibody SHCL-3 (CD11c). Thus, HCs can be demonstrated in peripheral blood, bone marrow, and spleen specimens from hairy cell leukemia (HCL) patients even when they constitute less than 1% of the cell suspension. Likewise, admixture experiments with normal mononuclear cells and the MOLT-4 T-acute lymphocytic leukemia (ALL) cell line demonstrated that HCs could be detected in amounts as low as 1%. The validity of this assay has been ascertained by the lack of double marker positivity in cell suspensions from B-chronic lymphocytic leukemia (CLL) and acute myelogenous leukemia (AML) patients that only expressed B1 or SHCL-3, respectively. Furthermore, other malignant blood diseases, including malignant lymphomas, acute leukemias, and chronic leukemias disclosed no double marker positive cells. In a clinical setting, this assay was used for purifying HCs (by flow cytometry) from the peripheral blood from patients with no apparent morphological evidence of circulating HC infiltration and for monitoring the effect of interferon therapy. In conclusion, this assay should be of value for both diagnosis and monitoring patients with HCL.

scholarly journals A unique surface marker profile in T-cell acute lymphocytic leukemia

Blood ◽  
1980 ◽  
Vol 55 (4) ◽  
pp. 702-705
Author(s):  
ER Richie ◽  
MP Sullivan ◽  
J van Eys
Keyword(s):  
T Cell ◽  
Peripheral Blood ◽  
Acute Lymphocytic Leukemia ◽  
Early Stage ◽  
Mixed Lymphocyte Culture ◽  
Lymphocyte Culture ◽  
Surface Marker ◽  
Lymphocytic Leukemia ◽  
Leukemic Cells ◽  
Surface Marker Analysis

A 5-yr-old girl with acute lymphocytic leukemia presented with moderate hepatomegaly, marked splenomegaly, but no evidence of a mediastinal mass. The peripheral blood white count was 270 x 10(9)/liter with 99% leukemic cells. Surface marker analysis showed the lymphoblasts to be E- rosette negative and complement receptor positive. The patient's leukemic cells were unreactive with anti-p23,30, which detects Ia-like antigens, and strongly reactive with A99 anti-T-cell serum, which reacts with normal human thymocytes and peripheral blood T cells. The percentage of leukemic cells bearing complement receptors diminished during relapse. The leukemic cells obtained at diagnosis and during relapse were nonreactive to mitogens and alloantigens and failed to stimulate proliferation of normal lymphocytes in mixed lymphocyte culture. There was no evidence for active suppression of normal lymphocyte reactivity mediated by the leukemic cells. The surface marker and functional profile of these leukemic cells is consistent with that of an early stage in T-cell maturation.

scholarly journals STUDIES ON CHARCOT-LEYDEN CRYSTALS

Blood ◽  
1950 ◽  
Vol 5 (3) ◽  
pp. 254-266 ◽  
Author(s):  
WILLIAM W. AYRES ◽  
N. M. STARKEY
Keyword(s):  
Chronic Myelogenous Leukemia ◽  
Red Cells ◽  
Wetting Agent ◽  
Myelogenous Leukemia ◽  
Appreciable Effect ◽  
Polarizing Microscopy ◽  
Sudan Black B ◽  
Wetting Agents

Abstract 1. Synthetic detergents of the anionic, cationic and nonionic types result in the rapid and constant formation of Charcot-Leyden crystals from eosinophils. 2. Charcot-Leyden crystals have a negative crystalline birefringence and form penetration twins. 3. The changes taking place in the eosinophil in the formation of Charcot-Leyden crystals under the influence of wetting agents, utilizing phase and polarizing microscopy, are described. 4. In the formation of Charcot-Leyden crystals with wetting agents, the nucleus of the eosinophil lyses with no appreciable effect on the granules. 5. In the formation of Charcot-Leyden crystals with a wetting agent, there is no change in the lipoid cortex of the eosinophil as demonstrated by staining with sudan black B. 6. Charcot-Leyden crystals undergo changes on standing that affect their solubilities. 7. The staining reactions and solubilities of Charcot-Leyden crystals are described. 8. Oxyhemoglobin crystals constantly form from red cells on exposure to Aerosol MA; on two occasions, tyrosine crystals formed from the blood of a patient with chronic myelogenous leukemia. 9. Evidence is offered that Charcot-Leyden crystals are crystalline proteins derived only from the nucleus of the eosinophil.

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