Positive 111In-granulocyte scintigraphy in a patient with focal leukemic blast cell infiltrations

1985 ◽  
Vol 10-10 (11-12) ◽  
Author(s):  
Martti Syrj�l� ◽  
Kari Remes ◽  
Timo Paavonen ◽  
Kristian Liewendahl
Keyword(s):  
Blast Cell ◽  
Leukemic Blast ◽  
Leukemic Blast Cell ◽  
Granulocyte Scintigraphy

scholarly journals PGK1, a promising biomarker and therapeutic target for patients with acute myeloid leukemia who are susceptible to disease relapse

2020 ◽  
Author(s):  
Junyan Gao ◽  
Xinran Chu ◽  
Shan He ◽  
Li Gao ◽  
Hui Hou ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Cell Lines ◽  
Therapeutic Target ◽  
Myeloid Leukemia ◽  
Blast Cell ◽  
High Expression ◽  
Leukemic Blast ◽  
Leukemic Blast Cell ◽  
Healthy Control ◽  
Acute Myeloid

Abstract Background: Glycolysis, a multi-step enzymatic reaction, is considered to be the root of cancer development and progression. The aim of this study is to figure out the glycolytic enzyme, phosphoglycerate kinase 1 (PGK1) whether participate in the progression of acute myeloid leukemia (AML) and its possible mechanisms. Methods: Four datasets (GSE106096, GSE75086, GSE107968 and GSE106748) containing 30 leukemic blast cell samples of AML at diagnosis, 17 leukemic blast cell samples of AML relapse and 3 bone marrow CD34+ cell samples of healthy donors were downloaded from Gene Expression Omnibus (GEO) database and PGK1 was screened out as a potential survival biomarker in AML. Then we did a series of clinical sample verifications and gene set enrichment analysis (GSEA) focusing on PGK1. We further knocked down expression of PGK1 in myelogenous leukemia cell lines and explored its potential effects. Results: PGK1 expression was up-regulated among AML at diagnosis versus healthy control, AML relapse versus AML at diagnosis and AML relapse versus healthy control datasets. Through a serial of bioinformatic analyses (differentially expressed genes [DEGs] selection, function and pathway enrichments and protein-protein interaction [PPI] network establishment), PGK1 was identified as the most meaningful gene in AML progression. Furthermore, the generally high expression of PGK1 was confirmed in AML samples comparing with healthy controls in our single center and the high-expression PGK1 was associated with a comparatively low complete remission (CR) rate, a significantly high 5-year cumulative incidence of relapse (CIR), a poor 5-year event-free survival (EFS) rate, and a poor 5-year overall survival (OS) rate. The GSEA revealed that high-expression PGK1 in AML was associated with many pathways including cytosolic DNA sensing, pentose phosphate, base excision repair and DNA replication. In vitro, the transfected U937 and K562 cells with PGK1 knock-down showed decreased cell viability and increased apoptotic rate. PGK1 inhibition could greatly decrease the half maximal inhibitory concentrations (IC50) of cytarabine (Ara-C) and daunorubicin (DNR) in U937 and K562 cell lines.Conclusions: High-expression PGK1 was associated with poor prognosis in AML. PGK1 may serve to predict the AML progression and provide a novel therapeutic target for AML.

scholarly journals Effect of cytosine arabinoside on leukemic blast cell colonies

1986 ◽  
Vol 22 (2) ◽  
pp. 219-220 ◽  
Author(s):  
P. Lacopino ◽  
M. Comis ◽  
M. R. Abenavoli ◽  
A. Neri
Keyword(s):  
Cytosine Arabinoside ◽  
Blast Cell ◽  
Leukemic Blast ◽  
Leukemic Blast Cell

scholarly journals Autologous leukemia-specific T-cell-mediated lymphocytotoxicity in patients with acute myelogenous leukemia.

1978 ◽  
Vol 147 (3) ◽  
pp. 912-922 ◽  
Author(s):  
S K Lee ◽  
R T Oliver
Keyword(s):  
Acute Myelogenous Leukemia ◽  
Blast Cell ◽  
Third Party ◽  
Myelogenous Leukemia ◽  
Target Antigen ◽  
Leukemic Blast ◽  
Crossover Studies ◽  
Acute Myelogenous ◽  
Blast Cells ◽  
Short Term Culture

Short-term culture of acute myelogenous leukemia patient's remission lymphocytes with inactivated autologous leukemic blast cells plus allogeneic lymphocytes, generated effector T lymphocytes which were cytotoxic for the specific autologous blast cell in 11 of 14 patients studied. Experiments using Daudi and Molt 4 lymphoblastoid cell lines as third-party helper cell suggest that an HLA D locus incompatability is necessary to provide effective help in this system. Cold target inhibition experiments, crossover studies between pairs of patients, and experiments with allogeneic leukemic blast cells as priming stimulus suggest that the target antigen is only present on the specific autologous blast cell.

scholarly journals Autocrine growth mechanisms of the progenitors of blast cells in acute myeloblastic leukemia

Blood ◽  
1989 ◽  
Vol 74 (1) ◽  
pp. 35-41
Author(s):  
I Murohashi ◽  
S Tohda ◽  
T Suzuki ◽  
K Nagata ◽  
Y Yamashita ◽  
...  
Keyword(s):  
Blast Cell ◽  
Leukemic Cells ◽  
Cell Fraction ◽  
Leukemic Blast ◽  
Colony Stimulating Factor ◽  
Growth Mechanisms ◽  
Autocrine Growth ◽  
Blast Cells ◽  
Cell Subpopulations ◽  
Stimulating Factor

Autocrine growth mechanisms of leukemic blast progenitors in acute myeloblastic leukemia (AML) were investigated. Colony formation of leukemic blast progenitors was observed in 14 of 14 patients tested when purified blast cell fraction depleted of both T cells and monocytes was plated in methylcellulose without any colony-stimulating factor (CSF). However, there existed a minimal cell density required to initiate blast progenitor growth with marked patient-to-patient variation. To clarify the role of cell density on the spontaneous growth of blast progenitors, we tested whether leukemic cells produced and secreted some stimulatory humoral factor(s). Production of colony- stimulating activity (CSA) by blast cells was observed in 17 of 18 patients tested. Following further depletion of monocytes, the CSA levels decreased markedly in 14 patients, indicating that blast cells with monocytoid differentiation were responsible for CSA production. We also confirmed granulocyte colony-stimulating factor (G-CSF) and/or granulocyte macrophage-colony-stimulating factor (GM-CSF) production by leukemic blasts using specific immunologic assays. When leukemic cells were divided into nonadherent nonphagocytic cell fraction and adherent cell fraction, only nonadherent nonphagocytic cells showed clonogenecity and adherent blast cells lacked the colony-forming capacity. The results indicate that there are at least two blast cell subpopulations in AML: one is proliferating subpopulation with self- renewal capacity and the other is supporting subpopulation with functions such as CSF production. The quite intimate relationship between these two blast cell subpopulations in AML may play an important role on the growth of leukemic blast progenitors in vitro.

scholarly journals Autocrine growth mechanisms of the progenitors of blast cells in acute myeloblastic leukemia

Blood ◽  
1989 ◽  
Vol 74 (1) ◽  
pp. 35-41 ◽  
Author(s):  
I Murohashi ◽  
S Tohda ◽  
T Suzuki ◽  
K Nagata ◽  
Y Yamashita ◽  
...  
Keyword(s):  
Blast Cell ◽  
Leukemic Cells ◽  
Cell Fraction ◽  
Leukemic Blast ◽  
Colony Stimulating Factor ◽  
Growth Mechanisms ◽  
Autocrine Growth ◽  
Blast Cells ◽  
Cell Subpopulations ◽  
Stimulating Factor

Abstract Autocrine growth mechanisms of leukemic blast progenitors in acute myeloblastic leukemia (AML) were investigated. Colony formation of leukemic blast progenitors was observed in 14 of 14 patients tested when purified blast cell fraction depleted of both T cells and monocytes was plated in methylcellulose without any colony-stimulating factor (CSF). However, there existed a minimal cell density required to initiate blast progenitor growth with marked patient-to-patient variation. To clarify the role of cell density on the spontaneous growth of blast progenitors, we tested whether leukemic cells produced and secreted some stimulatory humoral factor(s). Production of colony- stimulating activity (CSA) by blast cells was observed in 17 of 18 patients tested. Following further depletion of monocytes, the CSA levels decreased markedly in 14 patients, indicating that blast cells with monocytoid differentiation were responsible for CSA production. We also confirmed granulocyte colony-stimulating factor (G-CSF) and/or granulocyte macrophage-colony-stimulating factor (GM-CSF) production by leukemic blasts using specific immunologic assays. When leukemic cells were divided into nonadherent nonphagocytic cell fraction and adherent cell fraction, only nonadherent nonphagocytic cells showed clonogenecity and adherent blast cells lacked the colony-forming capacity. The results indicate that there are at least two blast cell subpopulations in AML: one is proliferating subpopulation with self- renewal capacity and the other is supporting subpopulation with functions such as CSF production. The quite intimate relationship between these two blast cell subpopulations in AML may play an important role on the growth of leukemic blast progenitors in vitro.

Diagnosis of chronic osteomyelitis by combined 99mTc-bone and 99mTc-anti-granulocyte scintigraphy

2016 ◽  
Vol 55 (06) ◽  
pp. N60-N61
Author(s):  
Anne Frölich ◽  
Gotthard Knoll ◽  
Manfred Bähre ◽  
Christoph Neumann
Keyword(s):  
Chronic Osteomyelitis ◽  
Granulocyte Scintigraphy

High Fibrinopeptide A (FPA) Levels in Acute Non-Lymphocytic Leukemia Are Reduced by Heparin Administration

1984 ◽  
Vol 52 (03) ◽  
pp. 301-304 ◽  
Author(s):  
L Gugliotta ◽  
Silvana Viganò ◽  
A D’Angelo ◽  
Anna Guarini ◽  
S Tura ◽  
...  
Keyword(s):  
Body Temperature ◽  
Blast Cell ◽  
Lymphocytic Leukemia ◽  
Healthy Controls ◽  
Intravenous Bolus ◽  
Fibrinopeptide A ◽  
Cell Counts ◽  
Heparin Administration ◽  
Blast Cells ◽  
Baseline Values

SummaryPlasma levels of fibrinopeptide A (FPA) in 30 untreated patients with acute non-lymphocytic leukemia (ANLL) were significantly higher than in 30 healthy controls (p <0.001). Patients without laboratory signs of disseminated intravascular coagulation (DIC) had levels of FPA higher than controls (p <0.02) but markedly lower than patients with DIC (p <0.001). Five patients with M3 leukemia had a higher mean FPA level (p <0.02) and a lower peripheral blast cell count (p <0.05) than patients with other cytological subtypes of ANLL. When patients with M3 were excluded, a significant correlation was observed between the peripheral blast cell counts and the FPA levels (r = 0.66, p <0.001). FPA levels were similar with body temperature either above or below 38° C. After intravenous bolus of heparin FPA dropped to normal levels in 14 out of 17 patients who had high baseline values. These findings indicate that intravascular thrombin formation, which probably result from the expression of procoagulant activities of blast cells, is the main cause of high FPA in the majority of patients with acute non-lymphocytic leukemia.

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