scholarly journals Discordant patterns of chromosome changes and myeloblast proliferation during the terminal phase of chronic myeloid leukemia

Blood ◽  
1976 ◽  
Vol 47 (3) ◽  
pp. 347-353 ◽  
Author(s):  
JA Gall ◽  
DR Boggs ◽  
PA Chervenick ◽  
S Pan ◽  
RB Fleming

Abstract A patient with Ph1 positive chronic myeloid leukemia (CML) developed blastic transformation which by morphologic criteria appeared to be localized to the lymphatic system. Chromosome analysis at this time, however, revealed new chromosomal abnormalities in addition to the existing Ph1 in all tissues studied (lymph node, blood, and bone marrow) consisting primarily of extra chromosome numbers 19 and 9 and a second Ph1. Therapy resulted in clinical remission with significant decrease in the aneuploid cell lines. However, these reappeared with recurrence of the blast crisis. Colony formation in semisolid culture of blood and marrow cells at the time of initial blast crisis yielded growth patterns characteristic of CML. On recurrence of the blast crisis after therapy, growth patterns were characteristic of CML in blast crisis or acute myeloblastic leukemia even though blood and marrow still showed relatively low levels of myeloblasts and promyelocytes. Possible explanations are discussed for the disparity in distribution between morphologic and chromosomal abnormalities in this patient.

Blood ◽  
1976 ◽  
Vol 47 (3) ◽  
pp. 347-353
Author(s):  
JA Gall ◽  
DR Boggs ◽  
PA Chervenick ◽  
S Pan ◽  
RB Fleming

A patient with Ph1 positive chronic myeloid leukemia (CML) developed blastic transformation which by morphologic criteria appeared to be localized to the lymphatic system. Chromosome analysis at this time, however, revealed new chromosomal abnormalities in addition to the existing Ph1 in all tissues studied (lymph node, blood, and bone marrow) consisting primarily of extra chromosome numbers 19 and 9 and a second Ph1. Therapy resulted in clinical remission with significant decrease in the aneuploid cell lines. However, these reappeared with recurrence of the blast crisis. Colony formation in semisolid culture of blood and marrow cells at the time of initial blast crisis yielded growth patterns characteristic of CML. On recurrence of the blast crisis after therapy, growth patterns were characteristic of CML in blast crisis or acute myeloblastic leukemia even though blood and marrow still showed relatively low levels of myeloblasts and promyelocytes. Possible explanations are discussed for the disparity in distribution between morphologic and chromosomal abnormalities in this patient.


2020 ◽  
Vol 48 (5) ◽  
pp. 030006052091923 ◽  
Author(s):  
Cheng-Cheng Ma ◽  
Ye Chai ◽  
Hui ling Chen ◽  
Xin Wang ◽  
Ying Gao ◽  
...  

Blast crisis develops in a minority of patients with chronic myeloid leukemia even in the era of tyrosine kinase inhibitor (TKI) therapy. Reports suggest that we know little about the mechanism of BCR-ABL and AML1-ETO co-expression in blast crisis of chronic myeloid leukemia, and that other chromosomal abnormalities also coexist. Here, we document an unusual and interesting case of a 51-year-old female diagnosed in the chronic phase of chronic myeloid leukemia. After undergoing TKI treatment for 3 months, her bone marrow aspirates in the chronic phase had transformed to blast crisis. Molecular genetic testing indicated she was positive for p210 form of BCR-ABL (copy number decreased from 108.91% to 56.96%) and AML1-ETO fusion (copy number, 5.65%) genes and had additional chromosomal abnormalities of t(8; 21)(q22; q22)/t(9; 22)(q34; q11), t(2; 5)(p24; q13) and an additional +8 chromosome.


Blood ◽  
1977 ◽  
Vol 49 (6) ◽  
pp. 913-923
Author(s):  
JS Senn ◽  
GB Price

Blast crisis, closely resembling acute leukemia, is the usual terminal event in chronic myeloid leukemia. Using physical (“fingerprint”) and cultural (colony-forming) methods, we have demonstrated distinctive patterns in the stable phase of chronic myeloid leukemia and in blast crisis. An unusual fingerprint alteration preceding the onset of the terminal phase is noted, and cell culture perturbation is evident at different stages of the disease. Our findings indicate that the application of these methods to the study of hemopoietic disorders is valid, and suggest that the use of such techniques may allow a better understanding of the complex cellular events occurring in the course of chronic myeloid leukemia.


Blood ◽  
1986 ◽  
Vol 68 (5) ◽  
pp. 1167-1174 ◽  
Author(s):  
JL Villeval ◽  
P Cramer ◽  
F Lemoine ◽  
A Henri ◽  
A Bettaieb ◽  
...  

Nine cases of early erythroblastic leukemia, unidentified by usual criteria, have been diagnosed using a panel of antibodies. Three cases arose in patients with Down's syndrome, one in a patient with therapy- related leukemia, and four patients were in blast crisis of chronic myeloid leukemia; only one case arose de novo. Blast cells could be assigned to two main stages of erythroid differentiation: presence of all erythroid-specific proteins in two patients, a phenotype corresponding to an immature erythroblast; absence of the erythroid markers such as glycophorin A and spectrin in the presence of carbonic anhydrase isoenzyme I, ABH group antigens, and the antigen defined by FA6 152 monoclonal antibody in six patients, a phenotype related to a late erythroid progenitor (CFU-E). One patient had an intermediate phenotype. All patients except one demonstrated a megakaryocytic component. In three patients, chromosomal abnormalities were present, detected both in blasts and in erythroid colonies. In conclusion, these findings indicate that most “cryptic erythroleukemias” are blocked at a “CFU-E-like” stage of differentiation, it may be a frequent event in Down's syndrome and chronic myeloid leukemia, and these erythroleukemias are phenotypically heterogeneous.


Blood ◽  
1977 ◽  
Vol 49 (6) ◽  
pp. 913-923 ◽  
Author(s):  
JS Senn ◽  
GB Price

Abstract Blast crisis, closely resembling acute leukemia, is the usual terminal event in chronic myeloid leukemia. Using physical (“fingerprint”) and cultural (colony-forming) methods, we have demonstrated distinctive patterns in the stable phase of chronic myeloid leukemia and in blast crisis. An unusual fingerprint alteration preceding the onset of the terminal phase is noted, and cell culture perturbation is evident at different stages of the disease. Our findings indicate that the application of these methods to the study of hemopoietic disorders is valid, and suggest that the use of such techniques may allow a better understanding of the complex cellular events occurring in the course of chronic myeloid leukemia.


Blood ◽  
1983 ◽  
Vol 61 (4) ◽  
pp. 640-644 ◽  
Author(s):  
JD Griffin ◽  
R Tantravahi ◽  
GP Canellos ◽  
JS Wisch ◽  
EL Reinherz ◽  
...  

Abstract There is little evidence to suggest that T lymphocytes are involved in the leukemic process in chronic myeloid leukemia (CML). A case of CML in blast phase is described in which T-cell surface antigens were detected by immunofluorescence on the patient's blasts using monoclonal antibodies. In order to determine that the T-cell blasts were derived from the original CML clone, cells bearing the T3 antigen were isolated by fluorescence-activated cell sorting and chromosome analysis was performed. All metaphases examined had the Philadelphia chromosome, confirming their origin from CML.


Blood ◽  
1983 ◽  
Vol 61 (4) ◽  
pp. 640-644 ◽  
Author(s):  
JD Griffin ◽  
R Tantravahi ◽  
GP Canellos ◽  
JS Wisch ◽  
EL Reinherz ◽  
...  

There is little evidence to suggest that T lymphocytes are involved in the leukemic process in chronic myeloid leukemia (CML). A case of CML in blast phase is described in which T-cell surface antigens were detected by immunofluorescence on the patient's blasts using monoclonal antibodies. In order to determine that the T-cell blasts were derived from the original CML clone, cells bearing the T3 antigen were isolated by fluorescence-activated cell sorting and chromosome analysis was performed. All metaphases examined had the Philadelphia chromosome, confirming their origin from CML.


Blood ◽  
1986 ◽  
Vol 68 (5) ◽  
pp. 1167-1174 ◽  
Author(s):  
JL Villeval ◽  
P Cramer ◽  
F Lemoine ◽  
A Henri ◽  
A Bettaieb ◽  
...  

Abstract Nine cases of early erythroblastic leukemia, unidentified by usual criteria, have been diagnosed using a panel of antibodies. Three cases arose in patients with Down's syndrome, one in a patient with therapy- related leukemia, and four patients were in blast crisis of chronic myeloid leukemia; only one case arose de novo. Blast cells could be assigned to two main stages of erythroid differentiation: presence of all erythroid-specific proteins in two patients, a phenotype corresponding to an immature erythroblast; absence of the erythroid markers such as glycophorin A and spectrin in the presence of carbonic anhydrase isoenzyme I, ABH group antigens, and the antigen defined by FA6 152 monoclonal antibody in six patients, a phenotype related to a late erythroid progenitor (CFU-E). One patient had an intermediate phenotype. All patients except one demonstrated a megakaryocytic component. In three patients, chromosomal abnormalities were present, detected both in blasts and in erythroid colonies. In conclusion, these findings indicate that most “cryptic erythroleukemias” are blocked at a “CFU-E-like” stage of differentiation, it may be a frequent event in Down's syndrome and chronic myeloid leukemia, and these erythroleukemias are phenotypically heterogeneous.


2020 ◽  
Vol 13 (2) ◽  
pp. 1020-1025
Author(s):  
Ryo Yanagiya ◽  
Daisuke Ishikawa ◽  
Tomomi Toubai ◽  
Tsubasa Ichikawa ◽  
Naofumi Kawaguchi ◽  
...  

Although tyrosine kinase inhibitors markedly improve the clinical outcome of chronic myeloid leukemia (CML), blast crisis in CML (CML-BC) still has a poor prognosis. Many chromosomal abnormalities have been reported in CML-BC and may contribute to therapeutic resistance, disease progression, and prognosis. Herein, we report a rare chromosome abnormality with der(16)t(1;16)(q12;q11.2) in CML-BC. It has been demonstrated that this chromosomal abnormality is associated with disease progression and poor prognosis in other malignancies, such as Ewing sarcoma. A 70-year-old man with CML who had been treated with imatinib and dasatinib was admitted to our hospital after complaining for several weeks of fatigue and dyspnea and diagnosed with CML-BC. His tumor cells presented additional chromosomal abnormality with der(16)t(1;16)(q12;q11.2), which has never been reported in CML cases. We successfully treated him using cytotoxic agents combined with ponatinib, and this chromosome abnormality was detected via G-banding. Our patient has lived for over 8 months without any progression with ponatinib treatment alone. Although the biological function of this chromosomal abnormality remains unclear, the satellite DNA of 1q12, which induces genomic instability in other malignancies, and the loss of 16q may contribute to the disease progression of CML in this case. In conclusion, this paper is the first to report on the case of CML-BC with der(16)t(1;16)(q12;q11.2).


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