Additional Chromosomal Abnormalities to Ph during the Clinical Course in Patients with Acute Lymphoblastic Leukemia

1986 ◽  
Vol 76 (2-3) ◽  
pp. 130-135
Author(s):  
P. Carbone ◽  
G. Barbata ◽  
F. Bellanca ◽  
F. Fabbiano ◽  
G. Granata
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Chromosomal Abnormalities ◽  
Clinical Course ◽  
Lymphoblastic Leukemia ◽  
Additional Chromosomal Abnormalities

scholarly journals Clonal identification in acute lymphoblastic leukemia

Blood ◽  
1979 ◽  
Vol 53 (5) ◽  
pp. 892-898 ◽  
Author(s):  
AH Goldstone ◽  
BA McVerry ◽  
G Janossy ◽  
H Walker
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Chromosomal Abnormalities ◽  
Lymphoblastic Leukemia ◽  
Surface Membrane ◽  
Cell Types ◽  
Drug Resistant ◽  
Dominant Type ◽  
Blast Cells ◽  
Clonal Origin ◽  
Additional Chromosomal Abnormalities

Abstract In a case of acute lymphoblastic leukemia, two distinct types of leukemia blast cells could be identified throughout the course of the disease. The initially dominant type of blast cell was sensitive to chemotherapy; the other was drug-resistant, gradually becoming dominant as the disease progressed. The cell types could be clearly separated by their morphologic and surface membrane marker characteristics. The same chromosomal constitution was present in both types of blast cells, indicating a common clonal origin. Additional chromosomal abnormalities were present in the later stages of the disease, demonstrating that a distinct subclone had proliferated. This study illustrates that in some cases of acute leukemia, disease relapse is caused by growth of drug- resistant subclones that may be clearly identified by changes in morphology and surface membrane marker characteristics.

CD15+ Acute Lymphoblastic Leukemia and Subsequent Monoblastic Leukemia

2001 ◽  
Vol 125 (9) ◽  
pp. 1227-1230
Author(s):  
Cherie H. Dunphy ◽  
Laura J. Gardner ◽  
H. Lance Evans ◽  
Nader Javadi
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
B Cell ◽  
Progenitor Cell ◽  
Gene Rearrangement ◽  
Chromosomal Abnormalities ◽  
Lymphoblastic Leukemia ◽  
Enzyme Cytochemistry ◽  
Flow Cytometric ◽  
Additional Chromosomal Abnormalities ◽  
Cell Gene

Abstract The abnormality in the translocation of chromosomes 4 and 11 (t[4;11]) has been characteristically associated with calla-negative CD15+ acute lymphoblastic leukemia (ALL) of early pre–B-cell origin. Transformation of a lymphoblastoid to a monoblastoid morphologic structure has rarely been described at relapse in these cases; however, these cases have lacked flow cytometric immunophenotyping (FCI) and genotypic studies (GS) to define the immunophenotype of and the presence of a B-cell gene rearrangement in the monoblastoid component. We report a case of CD15+, CD10− ALL of early pre–B-cell origin defined by morphologic testing and FCI with the t(4;11) abnormality. At relapse, the morphologic testing, enzyme cytochemistry, and FCI data were characteristic of monoblastic leukemia. The t(4;11) abnormality persisted with associated additional chromosomal abnormalities, and the monoblasts contained a B-cell gene rearrangement by GS. These findings support the concept that both processes arose from a multipotential progenitor cell.

scholarly journals Clonal identification in acute lymphoblastic leukemia

Blood ◽  
1979 ◽  
Vol 53 (5) ◽  
pp. 892-898
Author(s):  
AH Goldstone ◽  
BA McVerry ◽  
G Janossy ◽  
H Walker
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Chromosomal Abnormalities ◽  
Lymphoblastic Leukemia ◽  
Surface Membrane ◽  
Cell Types ◽  
Drug Resistant ◽  
Dominant Type ◽  
Blast Cells ◽  
Clonal Origin ◽  
Additional Chromosomal Abnormalities

In a case of acute lymphoblastic leukemia, two distinct types of leukemia blast cells could be identified throughout the course of the disease. The initially dominant type of blast cell was sensitive to chemotherapy; the other was drug-resistant, gradually becoming dominant as the disease progressed. The cell types could be clearly separated by their morphologic and surface membrane marker characteristics. The same chromosomal constitution was present in both types of blast cells, indicating a common clonal origin. Additional chromosomal abnormalities were present in the later stages of the disease, demonstrating that a distinct subclone had proliferated. This study illustrates that in some cases of acute leukemia, disease relapse is caused by growth of drug- resistant subclones that may be clearly identified by changes in morphology and surface membrane marker characteristics.

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