scholarly journals Granulocytic sarcoma of the brain in a patient with acute myeloid leukemia

2004 ◽  
Vol 51 (3) ◽  
pp. 129-131 ◽  
Author(s):  
Natasa Colovic ◽  
Milica Colovic ◽  
Vesna Cemerikic-Martinovic ◽  
Tatjana Terzic ◽  
Svetlana Ivanovic ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Granulocytic Sarcoma ◽  
Chromosome Translocation ◽  
Leukemic Cells ◽  
Extramedullary Tumor ◽  
Large Round ◽  
Neurosurgical Operation ◽  
The Brain ◽  
Acute Myeloid

Granulocytic sarcoma is extramedullary tumor composed of immature leukemic cells most frequently located in close proximity to bone, but it also can be found in the skin, breast, gastrointesti- nal tract, ovaries and brain. Granulocytic sarco- ma may arise during the course of leukemia or precede its development in the bone marrow. The majority of reported cases of granulocytic sarcomas in acute myleoid leukemia have chromosome translocation t(8;21). We report a 46-year-old man with acute myeloid leukemia, type M2 involving the marrow and peripheral blood and chromosome t(8;21) who developed granulocytic sarcoma in the brain, as a first manifestation of relapse 6 months after complete remission was achieved. During a neurosurgical operation a cortically located tumor (3.5x5 cm) in the brain was partially removed. Histology showed tumor consisted of homogenous infiltrate of blasts, admixed with more mature haematopoietic cells. The blasts have large round to oval nuclei, delicate chromatin, one or more small well-defined nucleoli and scant basophilic cytoplasm. Immunohistochemistry showed that blast cells were myeloperoxidase positive, confirming the diagnosis of myeloblastic sarcoma in the brain. The patient died two days after surgery.

scholarly journals Thrombopoietin/MPL participates in initiating and maintaining RUNX1-ETO acute myeloid leukemia via PI3K/AKT signaling

Blood ◽  
2012 ◽  
Vol 120 (4) ◽  
pp. 868-879 ◽  
Author(s):  
John Anto Pulikkan ◽  
Dmitri Madera ◽  
Liting Xue ◽  
Paul Bradley ◽  
Sean Francis Landrette ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Leukemia Virus ◽  
Myeloproliferative Disorders ◽  
Chromosome Translocation ◽  
Leukemic Cells ◽  
Cytokine Signaling ◽  
Wild Type ◽  
Downstream Signaling ◽  
Acute Myeloid

Abstract Oncogenic mutations in components of cytokine signaling pathways elicit ligand-independent activation of downstream signaling, enhancing proliferation and survival in acute myeloid leukemia (AML). The myeloproliferative leukemia virus oncogene, MPL, a homodimeric receptor activated by thrombopoietin (THPO), is mutated in myeloproliferative disorders but rarely in AML. Here we show that wild-type MPL expression is increased in a fraction of human AML samples expressing RUNX1-ETO, a fusion protein created by chromosome translocation t(8;21), and that up-regulation of Mpl expression in mice induces AML when coexpressed with RUNX1-ETO. The leukemic cells are sensitive to THPO, activating survival and proliferative responses. Mpl expression is not regulated by RUNX1-ETO in mouse hematopoietic progenitors or leukemic cells. Moreover, we find that activation of PI3K/AKT but not ERK/MEK pathway is a critical mediator of the MPL-directed antiapoptotic function in leukemic cells. Hence, this study provides evidence that up-regulation of wild-type MPL levels promotes leukemia development and maintenance through activation of the PI3K/AKT axis, and suggests that inhibitors of this axis could be effective for treatment of MPL-positive AML.

scholarly journals The 8;21 chromosome translocation in acute myeloid leukemia is always detectable by molecular analysis using AML1

Blood ◽  
1993 ◽  
Vol 81 (6) ◽  
pp. 1573-1579 ◽  
Author(s):  
N Maseki ◽  
H Miyoshi ◽  
K Shimizu ◽  
C Homma ◽  
M Ohki ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Molecular Analysis ◽  
Myeloid Leukemia ◽  
Southern Hybridization ◽  
Chromosome Translocation ◽  
Leukemic Cells ◽  
Hybridization Method ◽  
Essential Step ◽  
Aml1 Gene ◽  
Acute Myeloid

The AML1 gene was rearranged in leukemic cells with t(8;21)(q22;q22) or its variant, complex t(8;V;21) translocations from 33 acute myeloid leukemia (AML) patients. The AML1 rearrangement was also detected in three AML patients without t(8;21); two had a normal diploid karyotype, and one had a karyotype of 45,X, - X. The AML1 rearrangement in the t(8;21) breakpoint cluster region was not detected in leukemic cells with cytogenetic abnormalities other than t(8;21), or with normal diploidy obtained from 23 AML patients. Because leukemic cells of the five patients with complex t(8;V;21) translocations had a der(8)t(8;21) chromosome with a break in band 8q22 in common, the juxtaposition of the 5' side of AML1 to a predicted counterpart gene located in the breakpoint region of 8q22 may be an essential step in the leukemogenesis of AML with t(8;21). Our findings show that the 8;21 translocation, its variants, and the masked t(8;21) may all be detectable by the Southern hybridization method using the AML1 probes.

scholarly journals The 8;21 chromosome translocation in acute myeloid leukemia is always detectable by molecular analysis using AML1

Blood ◽  
1993 ◽  
Vol 81 (6) ◽  
pp. 1573-1579 ◽  
Author(s):  
N Maseki ◽  
H Miyoshi ◽  
K Shimizu ◽  
C Homma ◽  
M Ohki ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Molecular Analysis ◽  
Myeloid Leukemia ◽  
Southern Hybridization ◽  
Chromosome Translocation ◽  
Leukemic Cells ◽  
Hybridization Method ◽  
Essential Step ◽  
Aml1 Gene ◽  
Acute Myeloid

Abstract The AML1 gene was rearranged in leukemic cells with t(8;21)(q22;q22) or its variant, complex t(8;V;21) translocations from 33 acute myeloid leukemia (AML) patients. The AML1 rearrangement was also detected in three AML patients without t(8;21); two had a normal diploid karyotype, and one had a karyotype of 45,X, - X. The AML1 rearrangement in the t(8;21) breakpoint cluster region was not detected in leukemic cells with cytogenetic abnormalities other than t(8;21), or with normal diploidy obtained from 23 AML patients. Because leukemic cells of the five patients with complex t(8;V;21) translocations had a der(8)t(8;21) chromosome with a break in band 8q22 in common, the juxtaposition of the 5' side of AML1 to a predicted counterpart gene located in the breakpoint region of 8q22 may be an essential step in the leukemogenesis of AML with t(8;21). Our findings show that the 8;21 translocation, its variants, and the masked t(8;21) may all be detectable by the Southern hybridization method using the AML1 probes.

scholarly journals Acute myeloid leukemia with leukemic pleural effusion and high levels of pleural adenosine deaminase: A case report and review of literature

Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 387-396
Author(s):  
Sing-Ting Wang ◽  
Chieh-Lung Chen ◽  
Shih-Hsin Liang ◽  
Shih-Peng Yeh ◽  
Wen-Chien Cheng
Keyword(s):  
Acute Myeloid Leukemia ◽  
Pleural Effusion ◽  
Adenosine Deaminase ◽  
Myeloid Leukemia ◽  
Diagnostic Yield ◽  
Leukemic Cells ◽  
Pleural Effusions ◽  
Diagnostic Dilemma ◽  
True Incidence ◽  
Acute Myeloid

Abstract Pleural effusions are rarely observed in association with acute myeloid leukemia (AML), and their true incidence remains unknown. Given the low diagnostic yield from cytopathologic analysis of malignant pleural effusions and the fact that patients with leukemia are often thrombocytopenic and unable to tolerate invasive procedures, the incidence of leukemic effusions may be underestimated. Here, we report a rare case of pleural effusion in a patient with newly diagnosed AML. Initial analysis revealed an exudative, lymphocyte-predominant effusion. High levels of adenosine deaminase (ADA) were detected in pleural fluid, consistent with a diagnosis of tuberculosis. However, the analysis of pleural cytology revealed leukemic cells, permitting the diagnosis of leukemic effusion to be made. The patient underwent induction chemotherapy and pleural effusion resolved without recurrence. This case emphasizes the diagnostic dilemma presented by high levels of ADA in a leukemic pleural effusion, as this association has not been previously considered in the literature.

scholarly journals Ocular Granulocytic Sarcoma: A Case Report and Literature Review of Ocular Extramedullary Acute Myeloid Leukemia

2013 ◽  
Vol 13 (1) ◽  
pp. 93-96 ◽  
Author(s):  
Maro Ohanian ◽  
Gautam Borthakur ◽  
Alfonso Quintas-Cardama ◽  
Michael Mathisen ◽  
Jorge E. Cortés ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Case Report ◽  
Literature Review ◽  
Myeloid Leukemia ◽  
Granulocytic Sarcoma ◽  
Acute Myeloid

Granulocytic Sarcoma of Bladder in an 18-mo-old Child with Acute Myeloid Leukemia

2014 ◽  
Vol 81 (10) ◽  
pp. 1118-1119
Author(s):  
C. G. Delhi Kumar ◽  
V. Thilagavathy ◽  
Thirunavukkarasu Arun Babu
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Granulocytic Sarcoma ◽  
Acute Myeloid

scholarly journals Evidence for malignant transformation in acute myeloid leukemia at the level of early hematopoietic stem cells by cytogenetic analysis of CD34+ subpopulations

Blood ◽  
1995 ◽  
Vol 86 (8) ◽  
pp. 2906-2912 ◽  
Author(s):  
D Haase ◽  
M Feuring-Buske ◽  
S Konemann ◽  
C Fonatsch ◽  
C Troff ◽  
...  
Keyword(s):  
Stem Cells ◽  
Acute Myeloid Leukemia ◽  
Hematopoietic Stem Cells ◽  
Malignant Transformation ◽  
Cell Sorting ◽  
Myeloid Leukemia ◽  
De Novo ◽  
Leukemic Cells ◽  
Hematopoietic Stem ◽  
Acute Myeloid

Acute myeloid leukemia (AML) is a heterogenous disease according to morphology, immunophenotype, and genetics. The retained capacity of differentiation is the basis for the phenotypic classification of the bulk population of leukemic blasts and the identification of distinct subpopulations. Within the hierarchy of hematopoietic development and differentiation it is still unknown at which stage the malignant transformation occurs. It was our aim to analyze the potential involvement of cells with the immunophenotype of pluripotent stem cells in the leukemic process by the use of cytogenetic and cell sorting techniques. Cytogenetic analyses of bone marrow aspirates were performed in 13 patients with AML (11 de novo and 2 secondary) and showed karyotype abnormalities in 10 cases [2q+, +4, 6p, t(6:9), 7, +8 in 1 patient each and inv(16) in 4 patients each]. Aliquots of the samples were fractionated by fluorescence-activated cell sorting of CD34+ cells. Two subpopulations, CD34+/CD38-(early hematopoietic stem cells) and CD34+/CD38+ (more mature progenitor cells), were screened for karyotype aberations as a marker for leukemic cells. Clonal abnormalities and evaluable metaphases were found in 8 highly purified CD34+/CD38-populations and in 9 of the CD34+/CD38-specimens, respectively. In the majority of cases (CD34+/CD38-, 6 of 8 informative samples; CD34+/CD38+, 5 of 9 informative samples), the highly purified CD34+ specimens also contained cytogenetically normal cells. Secondary, progression-associated chromosomal changes (+8, 12) were identified in the CD34+/CD38-cells of 2 patients. We conclude that clonal karyotypic abnormalities are frequently found in the stem cell-like (CD34+/CD38-) and more mature (CD34+/CD38+) populations of patients with AML, irrespective of the phenotype of the bulk population of leukemic blasts and of the primary or secondary character of the leukemia. Our data suggest that, in AML, malignant transformation as well as disease progression may occur at the level of CD34+/CD38-cells with multilineage potential.

scholarly journals High expression of bcl-2 protein in acute myeloid leukemia cells is associated with poor response to chemotherapy

Blood ◽  
1993 ◽  
Vol 81 (11) ◽  
pp. 3091-3096 ◽  
Author(s):  
L Campos ◽  
JP Rouault ◽  
O Sabido ◽  
P Oriol ◽  
N Roubi ◽  
...  
Keyword(s):  
Cell Death ◽  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Mitochondrial Protein ◽  
High Expression ◽  
Leukemic Cells ◽  
Stem Cell Marker ◽  
Cell Counts ◽  
Response To Chemotherapy ◽  
Acute Myeloid

The BCL-2 proto-oncogene encodes a mitochondrial protein that blocks programmed cell death. High amounts of bcl-2 protein are found not only in lymphoid malignancies, but also in normal tissues characterized by apoptotic cell death, including bone marrow. Using a monoclonal antibody to bcl-2 protein, we analyzed 82 samples of newly diagnosed acute myeloid leukemia. The number of bcl-2+ cells in each sample was heterogeneous (range, 0% to 95%), with a mean of 23%. The percentage of bcl-2+ cells was higher in M4 and M5 types, according to French- American-British classification, and in cases with high white blood cell counts. bcl-2 expression was also correlated with that of the stem cell marker CD34. In vitro survival of leukemic cells maintained in liquid culture in the absence of growth factors was significantly longer in cases with a high percentage of bcl-2+ cells. High expression of bcl-2 was associated with a low complete remission rate after intensive chemotherapy (29% in cases with 20% or more positive cells v 85% in cases with less than 20% positive cells, P < 10(-5)) and with a significantly shorter survival. In multivariate analysis, the percentage of bcl-2+ cells (or the blast survival in culture), age, and the percentage of CD34+ cells were independently associated with poor survival.

Sign in / Sign up

Export Citation Format

Share Document