scholarly journals Phenotype of early erythroblastic leukemias

Blood ◽  
1986 ◽  
Vol 68 (5) ◽  
pp. 1167-1174 ◽  
Author(s):  
JL Villeval ◽  
P Cramer ◽  
F Lemoine ◽  
A Henri ◽  
A Bettaieb ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
De Novo ◽  
Chromosomal Abnormalities ◽  
Blast Crisis ◽  
Down's Syndrome ◽  
Down’S Syndrome ◽  
Intermediate Phenotype ◽  
Erythroid Progenitor ◽  
Frequent Event

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.

scholarly journals Phenotype of early erythroblastic leukemias

Blood ◽  
1986 ◽  
Vol 68 (5) ◽  
pp. 1167-1174 ◽  
Author(s):  
JL Villeval ◽  
P Cramer ◽  
F Lemoine ◽  
A Henri ◽  
A Bettaieb ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
De Novo ◽  
Chromosomal Abnormalities ◽  
Blast Crisis ◽  
Down's Syndrome ◽  
Down’S Syndrome ◽  
Intermediate Phenotype ◽  
Erythroid Progenitor ◽  
Frequent Event

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.

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
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Chromosomal Abnormalities ◽  
Blast Crisis ◽  
Extra Chromosome ◽  
Chromosome Analysis ◽  
Growth Patterns ◽  
Terminal Phase ◽  
Aneuploid Cell ◽  
Low Levels

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.

scholarly journals Clonal evolution of AML1-ETO coexisting with BCR-ABL and additional chromosome abnormalities in a blastic transformation of chronic myeloid leukemia

2020 ◽  
Vol 48 (5) ◽  
pp. 030006052091923 ◽  
Author(s):  
Cheng-Cheng Ma ◽  
Ye Chai ◽  
Hui ling Chen ◽  
Xin Wang ◽  
Ying Gao ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Copy Number ◽  
Myeloid Leukemia ◽  
Kinase Inhibitor ◽  
Chromosomal Abnormalities ◽  
Blast Crisis ◽  
Clonal Evolution ◽  
Molecular Genetic ◽  
Chronic Phase ◽  
Interesting Case

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.

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
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Chromosomal Abnormalities ◽  
Blast Crisis ◽  
Extra Chromosome ◽  
Chromosome Analysis ◽  
Growth Patterns ◽  
Terminal Phase ◽  
Aneuploid Cell ◽  
Low Levels

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.

scholarly journals Pediatric Chronic Myeloid Leukemia with Megakaryocytic Blast Crisis as Initial Presentation: Case Report and Review of Literature

2021 ◽  
Vol 5 (4) ◽  
pp. 171-174
Author(s):  
Tuba Iqbal ◽  
◽  
Amber Younus ◽  
Uzma Zaidi ◽  
Jawad Hassan ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Kinase Inhibitor ◽  
De Novo ◽  
Pediatric Population ◽  
Blast Crisis ◽  
Chronic Phase ◽  
Transcript Level ◽  
Young Female

Abstract: Background: Pediatric Chronic Myeloid Leukemia (CML) is a rare entity accounting for 2-3% of pediatric malignancies. CML rarely presents as Blast Crisis (BC) at the time of diagnosis, and megakaryocytic blast crisis is even rarer. Case Presentation: We herein, report a case of a young female, 10-year-old who presented with anemia, leukocytosis and massive splenomegaly. Clinical features, peripheral film and bone marrow findings were consistent with CML in megakaryocytic blast crisis. Bone marrow cytogenetic analysis revealed karyotype of 46, XX, t(9:22)(q34;q11.2) in 20 metaphases and BCR-ABL P210 by PCR was detected with transcript level of 83%, which further confirmed our diagnosis. Conclusion: De novo presentation of chronic myeloid leukemia with megakaryocytic blast crisis is rarely observed in pediatric population with very few cases published till now. We are presenting this case because of its rarity, likelihood of misdiagnosis as AML (M7) and poor prognosis, if not treated precisely. Keywords: Chronic Myeloid Leukemia (CML), Acute Myeloid Leukemia (AML), Blast Crisis (BC), Acute Megakaryocytic Leukemia (AMKL), Chronic Phase (CP), Accelerated Phase (AP), Tyrosine Kinase Inhibitor (TKI).

scholarly journals A Rare Chromosome Abnormality with der(16)t(1;16)(q12;q11.2) in Blast Crisis of Chronic Myeloid Leukemia

2020 ◽  
Vol 13 (2) ◽  
pp. 1020-1025
Author(s):  
Ryo Yanagiya ◽  
Daisuke Ishikawa ◽  
Tomomi Toubai ◽  
Tsubasa Ichikawa ◽  
Naofumi Kawaguchi ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Disease Progression ◽  
Chromosomal Abnormality ◽  
Myeloid Leukemia ◽  
Poor Prognosis ◽  
Kinase Inhibitors ◽  
Chromosomal Abnormalities ◽  
Chromosome Abnormality ◽  
Blast Crisis ◽  
Cytotoxic Agents

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).

Sign in / Sign up

Export Citation Format

Share Document