scholarly journals Detection by enzymatic amplification of bcr-abl mRNA in peripheral blood and bone marrow cells of patients with chronic myelogenous leukemia

Blood ◽  
1989 ◽  
Vol 73 (6) ◽  
pp. 1735-1741 ◽  
Author(s):  
W Lange ◽  
DS Snyder ◽  
R Castro ◽  
JJ Rossi ◽  
KG Blume
Keyword(s):  
Bone Marrow ◽  
Chronic Myelogenous Leukemia ◽  
Peripheral Blood ◽  
Bone Marrow Cells ◽  
Philadelphia Chromosome ◽  
Chromosome 9 ◽  
Myelogenous Leukemia ◽  
Enzymatic Amplification ◽  
Polymerase Chain ◽  
Marrow Cells

Abstract The Philadelphia chromosome of chronic myelogenous leukemia (CML) patients is caused by a translocation of the c-abl gene from chromosome 9 to the breakpoint cluster region (bcr) on chromosome 22. A new bcr- abl mRNA is expressed in these cases. We have developed a modified polymerase chain reaction (PCR) for the detection of this mRNA. The method is extremely sensitive, reliable, and relatively fast. The analysis of peripheral blood or bone marrow cells from CML patients treated with chemotherapy shows that the two possible mRNAs are expressed in various combinations. Our results show that even after myeloablative therapy for bone marrow transplantation bcr-abl mRNAs are still expressed. Further studies, however, are necessary to determine the clinical relevance of a small number of persisting cells expressing the bcr-abl mRNA.

scholarly journals Detection by enzymatic amplification of bcr-abl mRNA in peripheral blood and bone marrow cells of patients with chronic myelogenous leukemia

Blood ◽  
1989 ◽  
Vol 73 (6) ◽  
pp. 1735-1741
Author(s):  
W Lange ◽  
DS Snyder ◽  
R Castro ◽  
JJ Rossi ◽  
KG Blume
Keyword(s):  
Bone Marrow ◽  
Chronic Myelogenous Leukemia ◽  
Peripheral Blood ◽  
Bone Marrow Cells ◽  
Philadelphia Chromosome ◽  
Chromosome 9 ◽  
Myelogenous Leukemia ◽  
Enzymatic Amplification ◽  
Polymerase Chain ◽  
Marrow Cells

The Philadelphia chromosome of chronic myelogenous leukemia (CML) patients is caused by a translocation of the c-abl gene from chromosome 9 to the breakpoint cluster region (bcr) on chromosome 22. A new bcr- abl mRNA is expressed in these cases. We have developed a modified polymerase chain reaction (PCR) for the detection of this mRNA. The method is extremely sensitive, reliable, and relatively fast. The analysis of peripheral blood or bone marrow cells from CML patients treated with chemotherapy shows that the two possible mRNAs are expressed in various combinations. Our results show that even after myeloablative therapy for bone marrow transplantation bcr-abl mRNAs are still expressed. Further studies, however, are necessary to determine the clinical relevance of a small number of persisting cells expressing the bcr-abl mRNA.

scholarly journals Late-appearing Philadelphia chromosome in two patients with chronic myelogenous leukemia

Blood ◽  
1980 ◽  
Vol 56 (5) ◽  
pp. 812-814 ◽  
Author(s):  
R Lisker ◽  
L Casas ◽  
O Mutchinick ◽  
F Perez-Chavez ◽  
J Labardini
Keyword(s):  
Bone Marrow ◽  
Chronic Myelogenous Leukemia ◽  
Bone Marrow Cells ◽  
Philadelphia Chromosome ◽  
Rapid Change ◽  
Selective Advantage ◽  
Myelogenous Leukemia ◽  
Leukemic Cells ◽  
Marrow Cells

Abstract We describe two patients with typical myelogenous leukemia, who at the beginning of the disease lacked the Philadelphia chromosome in bone marrow cells, and 90 and 42 days later, respectively, its presence was shown in all cells analyzed from that tissue. These findings are compatible with the possibility that at least occasionally Ph1 occurs secondarily in already leukemic cells. The rapid change form Ph1- to Ph1+ CML in one of the patients (42 days), suggests the possibility that in addition to Ph1+ cells enjoying marked selective advantage, this change is induced simultaneously in multiple bone marrow cells.

scholarly journals Late-appearing Philadelphia chromosome in two patients with chronic myelogenous leukemia

Blood ◽  
1980 ◽  
Vol 56 (5) ◽  
pp. 812-814 ◽  
Author(s):  
R Lisker ◽  
L Casas ◽  
O Mutchinick ◽  
F Perez-Chavez ◽  
J Labardini
Keyword(s):  
Bone Marrow ◽  
Chronic Myelogenous Leukemia ◽  
Bone Marrow Cells ◽  
Philadelphia Chromosome ◽  
Rapid Change ◽  
Selective Advantage ◽  
Myelogenous Leukemia ◽  
Leukemic Cells ◽  
Marrow Cells

We describe two patients with typical myelogenous leukemia, who at the beginning of the disease lacked the Philadelphia chromosome in bone marrow cells, and 90 and 42 days later, respectively, its presence was shown in all cells analyzed from that tissue. These findings are compatible with the possibility that at least occasionally Ph1 occurs secondarily in already leukemic cells. The rapid change form Ph1- to Ph1+ CML in one of the patients (42 days), suggests the possibility that in addition to Ph1+ cells enjoying marked selective advantage, this change is induced simultaneously in multiple bone marrow cells.

scholarly journals Association of the translocation (15;17) with malignant proliferation of promyelocytes in acute leukemia and chronic myelogenous leukemia at blastic crisis

Blood ◽  
1986 ◽  
Vol 67 (2) ◽  
pp. 270-274 ◽  
Author(s):  
S Misawa ◽  
E Lee ◽  
CA Schiffer ◽  
Z Liu ◽  
JR Testa
Keyword(s):  
Bone Marrow ◽  
Chronic Myelogenous Leukemia ◽  
Bone Marrow Cells ◽  
Chronic Phase ◽  
Myelogenous Leukemia ◽  
Blastic Crisis ◽  
Cytogenetic Studies ◽  
Chromosomal Breakpoints ◽  
Variant Translocation ◽  
Marrow Cells

Abstract Cytogenetic studies were performed on nine patients with acute promyelocytic leukemia. Every patient had an identical translocation (15;17) or, in one case, a variant three-way rearrangement between chromosomes 7, 15, and 17. Another patient with chronic myelogenous leukemia was examined at the time of blastic crisis when the patient's bone marrow was infiltrated by hypergranular promyelocytes and blasts. Bone marrow cells contained a t(15;17) as well as a Ph1 chromosome. Only the latter abnormality was observed in the chronic phase of the disease. The translocation (15;17) was detected in all ten patients when bone marrow or peripheral blood cells were cultured for 24 hours prior to making chromosome preparations. However, the t(15;17) was not seen in three of these same cases when bone marrow cells were processed directly. These findings indicate that the t(15;17) is closely associated with acute proliferation of leukemic promyelocytes and that detection of this karyotypic defect may be influenced by the particular cytogenetic processing method used in different laboratories. An analysis of the banding pattern in the variant translocation provided additional evidence favoring chromosomal breakpoints at or very near the junction between bands 17q12 and 17q21 and at 15q22.

scholarly journals In vitro restoration of polyclonal hematopoiesis in a chronic myelogenous leukemia after in vitro treatment with 4- hydroperoxycyclophosphamide

Blood ◽  
1985 ◽  
Vol 65 (3) ◽  
pp. 753-757 ◽  
Author(s):  
G Degliantoni ◽  
L Mangoni ◽  
V Rizzoli
Keyword(s):  
Bone Marrow ◽  
Chronic Myelogenous Leukemia ◽  
Early Phase ◽  
Bone Marrow Cells ◽  
Type A ◽  
G6pd Activity ◽  
Myelogenous Leukemia ◽  
Stem Cell Population ◽  
Marrow Cells

Bone marrow cells of a 45-year-old female with Philadelphia chromosome (Ph1)-positive, early-phase chronic myelogenous leukemia (CML), who was heterozygous for the glucose-6-phosphate dehydrogenase (G6PD) locus, were pretreated in vitro with 4-hydroperoxycyclophosphamide (4-HC) and tested for G6PD activity in several colony formation assays and for karyotypic abnormalities. All cells within the mixed (CFU-GEMM), the erythroid burst (BFU-E), and the granulocyte-macrophage (CFU-GM) colonies expressed type A and type B G6PD activity and a normal karyotype, whereas untreated cells expressed type A G6PD and the Ph1 chromosome. This reversal of G6PD activity type and the disappearance of the Ph1 chromosome in colonies grown from 4-HC-treated cells indicate that this cytotoxic agent spares a residual normal stem cell population in bone marrow cells of early-phase CML patients. This finding, in turn, suggests a therapeutic approach in CML based on in vitro chemotherapy of autologous bone marrow grafts.

scholarly journals Efficient and Rapid Induction of a Chronic Myelogenous Leukemia-Like Myeloproliferative Disease in Mice Receiving P210 bcr/abl-Transduced Bone Marrow

Blood ◽  
1998 ◽  
Vol 92 (10) ◽  
pp. 3780-3792 ◽  
Author(s):  
Warren S. Pear ◽  
Juli P. Miller ◽  
Lanwei Xu ◽  
John C. Pui ◽  
Benny Soffer ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Chronic Myelogenous Leukemia ◽  
Fluorescent Protein ◽  
Bone Marrow Cells ◽  
Blast Crisis ◽  
Extramedullary Hematopoiesis ◽  
Myelogenous Leukemia ◽  
Myeloproliferative Disease ◽  
Cell Counts ◽  
Marrow Cells

Expression of the 210-kD bcr/abl fusion oncoprotein can cause a chronic myelogenous leukemia (CML)-like disease in mice receiving bone marrow cells transduced by bcr/abl-encoding retroviruses. However, previous methods failed to yield this disease at a frequency sufficient enough to allow for its use in the study of CML pathogenesis. To overcome this limitation, we have developed an efficient and reproducible method for inducing a CML-like disease in mice receiving P210 bcr/abl-transduced bone marrow cells. All mice receiving P210 bcr/abl-transduced bone marrow cells succumb to a myeloproliferative disease between 3 and 5 weeks after bone marrow transplantation. The myeloproliferative disease recapitulates many of the hallmarks of human CML and is characterized by high white blood cell counts and extensive extramedullary hematopoiesis in the spleen, liver, bone marrow, and lungs. Use of a retroviral vector coexpressing P210 bcr/abl and green fluorescent protein shows that the vast majority of bcr/abl-expressing cells are myeloid. Analysis of the proviral integration pattern shows that, in some mice, the myeloproliferative disease is clonal. In multiple mice, the CML-like disease has been transplantable, inducing a similar myeloproliferative syndrome within 1 month of transfer to sublethally irradiated syngeneic recipients. The disease in many of these mice has progressed to the development of acute lymphoma/leukemia resembling blast crisis. These results demonstrate that murine CML recapitulates important features of human CML. As such, it should be an excellent model for addressing specific issues relating to the pathogenesis and treatment of this disease.

Trisomy D in Bone Marrow Cells in a Patient with Chronic Myelogenous Leukemia

1974 ◽  
Vol 52 (1) ◽  
pp. 61-64 ◽  
Author(s):  
Lillian Y. F. Hsu ◽  
Peter Papenhausen ◽  
Michael L. Greenberg ◽  
Kurt Hirschhorn
Keyword(s):  
Bone Marrow ◽  
Chronic Myelogenous Leukemia ◽  
Bone Marrow Cells ◽  
Myelogenous Leukemia ◽  
Marrow Cells

scholarly journals Association of the translocation (15;17) with malignant proliferation of promyelocytes in acute leukemia and chronic myelogenous leukemia at blastic crisis

Blood ◽  
1986 ◽  
Vol 67 (2) ◽  
pp. 270-274 ◽  
Author(s):  
S Misawa ◽  
E Lee ◽  
CA Schiffer ◽  
Z Liu ◽  
JR Testa
Keyword(s):  
Bone Marrow ◽  
Chronic Myelogenous Leukemia ◽  
Bone Marrow Cells ◽  
Chronic Phase ◽  
Myelogenous Leukemia ◽  
Blastic Crisis ◽  
Cytogenetic Studies ◽  
Chromosomal Breakpoints ◽  
Variant Translocation ◽  
Marrow Cells

Cytogenetic studies were performed on nine patients with acute promyelocytic leukemia. Every patient had an identical translocation (15;17) or, in one case, a variant three-way rearrangement between chromosomes 7, 15, and 17. Another patient with chronic myelogenous leukemia was examined at the time of blastic crisis when the patient's bone marrow was infiltrated by hypergranular promyelocytes and blasts. Bone marrow cells contained a t(15;17) as well as a Ph1 chromosome. Only the latter abnormality was observed in the chronic phase of the disease. The translocation (15;17) was detected in all ten patients when bone marrow or peripheral blood cells were cultured for 24 hours prior to making chromosome preparations. However, the t(15;17) was not seen in three of these same cases when bone marrow cells were processed directly. These findings indicate that the t(15;17) is closely associated with acute proliferation of leukemic promyelocytes and that detection of this karyotypic defect may be influenced by the particular cytogenetic processing method used in different laboratories. An analysis of the banding pattern in the variant translocation provided additional evidence favoring chromosomal breakpoints at or very near the junction between bands 17q12 and 17q21 and at 15q22.

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