scholarly journals Blood group genotyping in multi-transfused patients

2021 ◽  
Vol 102 (5) ◽  
pp. 621-625
Author(s):  
N V Mineeva ◽  
I I Krobinets ◽  
S V Gavrovskaya ◽  
N N Bodrova ◽  
E A Sisoeva ◽  
...  
Keyword(s):  
Blood Group ◽  
Blood Cells ◽  
Myeloid Leukemia ◽  
Molecular Genetic ◽  
Primary Myelofibrosis ◽  
Beta Thalassemia ◽  
Blood Samples ◽  
Genetic Typing ◽  
Serological Typing ◽  
Hodgkin's Lymphomas

Aim. To assess the possibility of using blood group genotyping in recipients who received transfusions for 3 months. Methods. The study included blood samples from 95 patients who received 3 or more erythrocyte transfusions within 3 months. The patients had the following diagnoses: multiple myeloma (n=7), beta thalassemia (n=4), non-Hodgkin's lymphomas (n=11), chronic myeloid leukemia (n=16), primary myelofibrosis (n=9), myelodysplastic syndrome (n=22), acute leukemia (n=21), aplastic anemia (n=5). Red blood cells phenotyping was performed in Diaclon Rh Subgroups+K Gel Cards. The Rh and Kell genotyping was performed by using RBC SSP-PCR kits FluoGene vERYfy (Inno-train Diagnostics, Germany). The standard RHD/RHCE alleles, as well as polymorphisms associated with KEL1/KEL2 [T698C (Met198Thr)] of the KEL gene were genotyped. Results. The concordance rate between serological and molecular genetic typing of RhCE and Kell blood groups for donors was 100%, while the patients results were discordant in 45.3% of cases. Discrepancies in antigens of the Rh system were registered in 41 patients: one antigen of the Rh system in 30 patients, two in 9 patients. Ten patients who had been previously phenotyped as RhCc were genotyped as RHCE*CC. 2 patients who had been previously phenotyped as Rhee were genotyped as RHCE*EE. In 2 patients, antigens D and C were not detected in the phenotype but were identified in the genotype. Discrepancies in antigen K were recorded in 2 patients, and the antigen was absent in the phenotype but was present in the genotype. The genotyping results were confirmed by serological typing at subsequent hospitalizations. Сonclusion. Blood group genotyping is a useful adjunct to traditional methods when serological typing is limited.

High Mitochondrial Membrane Potential Identifies Patients with Myeloproliferative Neoplasms with a More Aggressive Natural History

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 1992-1992
Author(s):  
Jeffrey R Gardner ◽  
Omar Abdel-Wahab ◽  
Mark Frattini ◽  
Joseph G Jurcic ◽  
Kristina Knapp ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Polycythemia Vera ◽  
Mitochondrial Membrane Potential ◽  
Essential Thrombocythemia ◽  
Blood Cells ◽  
Myeloid Leukemia ◽  
Mitochondrial Membrane ◽  
Myeloproliferative Neoplasms ◽  
Primary Myelofibrosis ◽  
Acute Myeloid

Abstract Abstract 1992 The myeloproliferative neoplasms (MPN) can have a variable natural history. Polycythemia vera and essential thrombocythemia, in particular, are conditions that can extend over decades, but some patients have clinical progression to myelofibrosis or acute myeloid leukemia. As first articulated by Warburg, cancers are metabolically distinguished from normal tissues by the use of glycolysis under aerobic conditions. To metabolically characterize the blood cells of patients with myeloproliferative neoplasms, we measured the mitochondrial membrane potential using the cyanine dye, JC-1. In examining cells derived from the blood and/or marrow of 159 patients with primary myelofibrosis, polycythemia vera and essential thrombocythemia, we found that the mitochondrial membrane potential (FL2/FL1=electrochemical potential/mitochondrial mass) was elevated compared to the blood cells of normal individuals. Thirty five percent of patients with polycythemia vera and essential thrombocythemia had normal MMP. In contrast, 97% of patients with primary myelofibrosis, post-polycythemia myelofibrosis, post-essential thrombocythemia myelofibrosis and acute myeloid leukemia following an MPN had evidence of cell populations with higher mitochondrial membrane potential. Cells with distinctly higher mitochondrial membrane potential could be indentified in platelets and polymorphonuclear leukocytes; however the MMP of lymphocytes was normal, indicating that the alteration in metabolic state likely occurred in a multipotential myeloid stem cell. Cell populations were confirmed by co-staining with anti-CD19, -CD45, -GlycophorinA and -β3-integrin antibodies. Sequential analysis of patient samples found that the acquisition of higher mitochondrial membrane potential was stable and persistent over 2 years or more of follow up and that elevated membrane potential predisposed patients to disease progression. The balance of patients (65%) with ET had evidence of increased MMP suggesting the possibility of disease in an early state of evolution to a more aggressive condition. The increased MMP did not correlate with the presence of mutation in JAK2. These results indicate that clinically advanced MPN can be characterized by changes in mitochondrial physiology that might be identified non-invasively by flow cytometric staining with JC-1. In addition, the early nature of these changes may help to identify therapeutic targets. Disclosures: No relevant conflicts of interest to declare.

scholarly journals An Inheritable B-like Character in Persons of Blood Group A

Blood ◽  
1960 ◽  
Vol 16 (2) ◽  
pp. 1163-1172 ◽  
Author(s):  
JØRGEN ANDERSEN
Keyword(s):  
Blood Sample ◽  
Blood Group ◽  
Blood Cells ◽  
Group Character ◽  
Blood Samples ◽  
Blood Group A ◽  
The Family ◽  
Group A ◽  
Antigen A

Abstract In a previous paper the author reported investigations of a blood sample (Co) whose blood cells contained, in addition to a normal A antigen, a weak, atypical B-like antigen. The present paper deals with two blood samples, El and Do, which probably possessed the same weak, atypical B-like character. A study of El’s family showed that this blood group character, provisionally designated as Ab, may be inheritable, as it was found in two children and one grandchild of El’s. The serologic studies of the 5 Ab samples are reported, and on the basis of the family material the possible origin of the Ab character is discussed.

Enasidenib: First Mutant IDH2 Inhibitor for the Treatment of Refractory and Relapsed Acute Myeloid Leukemia

2019 ◽  
Vol 18 (14) ◽  
pp. 1936-1951 ◽  
Author(s):  
Raghav Dogra ◽  
Rohit Bhatia ◽  
Ravi Shankar ◽  
Parveen Bansal ◽  
Ravindra K. Rawal
Keyword(s):  
Clinical Trial ◽  
Bone Marrow ◽  
Overall Survival ◽  
Acute Myeloid Leukemia ◽  
Adverse Effects ◽  
Blood Cells ◽  
Myeloid Leukemia ◽  
White Blood Cells ◽  
Phase Iii ◽  
Acute Myeloid

Background: Acute myeloid leukemia is the collective name for different types of leukemias of myeloid origin affecting blood and bone marrow. The overproduction of immature myeloblasts (white blood cells) is the characteristic feature of AML, thus flooding the bone marrow and reducing its capacity to produce normal blood cells. USFDA on August 1, 2017, approved a drug named Enasidenib formerly known as AG-221 which is being marketed under the name Idhifa to treat R/R AML with IDH2 mutation. The present review depicts the broad profile of enasidenib including various aspects of chemistry, preclinical, clinical studies, pharmacokinetics, mode of action and toxicity studies. Methods: Various reports and research articles have been referred to summarize different aspects related to chemistry and pharmacokinetics of enasidenib. Clinical data was collected from various recently published clinical reports including clinical trial outcomes. Result: The various findings of enasidenib revealed that it has been designed to allosterically inhibit mutated IDH2 to treat R/R AML patients. It has also presented good safety and efficacy profile along with 9.3 months overall survival rates of patients in which disease has relapsed. The drug is still under study either in combination or solely to treat hematological malignancies. Molecular modeling studies revealed that enasidenib binds to its target through hydrophobic interaction and hydrogen bonding inside the binding pocket. Enasidenib is found to be associated with certain adverse effects like elevated bilirubin level, diarrhea, differentiation syndrome, decreased potassium and calcium levels, etc. Conclusion: Enasidenib or AG-221was introduced by FDA as an anticancer agent which was developed as a first in class, a selective allosteric inhibitor of the tumor target i.e. IDH2 for Relapsed or Refractory AML. Phase 1/2 clinical trial of Enasidenib resulted in the overall survival rate of 40.3% with CR of 19.3%. Phase III trial on the Enasidenib is still under process along with another trial to test its potency against other cell lines. Edasidenib is associated with certain adverse effects, which can be reduced by investigators by designing its newer derivatives on the basis of SAR studies. Hence, it may come in the light as a potent lead entity for anticancer treatment in the coming years.

Real-time Red Blood Cell Counting and Osmolarity Analysis using a Photoacoustic-based Microfluidic System

Lab on a Chip ◽  
2021 ◽  
Author(s):  
Wenxiu Zhao ◽  
Haibo Yu ◽  
Yangdong Wen ◽  
Hao Luo ◽  
Boliang Jia ◽  
...  
Keyword(s):  
Blood Cell ◽  
Physical Properties ◽  
Red Blood Cell ◽  
Blood Cells ◽  
Diagnostic Procedure ◽  
Microfluidic System ◽  
Cell Counting ◽  
Blood Samples ◽  
System P ◽  
Blood Cell Counting

Counting the number of red blood cells (RBCs) in blood samples is a common clinical diagnostic procedure, but conventional methods are unable to provide the size and other physical properties...

scholarly journals Loss of H3K27 methylation identifies poor outcomes in adult-onset acute leukemia

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
A. D. van Dijk ◽  
F. W. Hoff ◽  
Y. H. Qiu ◽  
J. Chandra ◽  
E. Jabbour ◽  
...  
Keyword(s):  
Acute Leukemia ◽  
Histone Methylation ◽  
Myeloid Leukemia ◽  
Outcome Prediction ◽  
Epigenetic Modification ◽  
Molecular Genetic ◽  
Proliferative Potential ◽  
Prognostic Impact ◽  
Adult Onset ◽  
H3k27 Methylation

Abstract Background Acute leukemia is an epigenetically heterogeneous disease. The intensity of treatment is currently guided by cytogenetic and molecular genetic risk classifications; however these incompletely predict outcomes, requiring additional information for more accurate outcome predictions. We aimed to identify potential prognostic implications of epigenetic modification of histone proteins, with a focus on H3K4 and H3K27 methylation marks in relation to mutations in chromatin, splicing and transcriptional regulators in adult-onset acute lymphoblastic and myeloid leukemia. Results Histone 3 lysine 4 di- and trimethylation (H3K4me2, H3K4me3) and lysine 27 trimethylation (H3K27me3) mark expression was evaluated in 241 acute myeloid leukemia (AML), 114 B-cell acute lymphoblastic leukemia (B-ALL) and 14T-cell ALL (T-ALL) patient samples at time of diagnosis using reverse phase protein array. Expression levels of the marks were significantly lower in AML than in B and T-ALL in both bone marrow and peripheral blood, as well as compared to normal CD34+ cells. In AML, greater loss of H3K27me3 was associated with increased proliferative potential and shorter overall survival in the whole patient population, as well as in subsets with DNA methylation mutations. To study the prognostic impact of H3K27me3 in the context of cytogenetic aberrations and mutations, multivariate analysis was performed and identified lower H3K27me3 level as an independent unfavorable prognostic factor in all, as well as in TP53 mutated patients. AML with decreased H3K27me3 demonstrated an upregulated anti-apoptotic phenotype. In ALL, the relative quantity of histone methylation expression correlated with response to tyrosine kinase inhibitor in patients who carried the Philadelphia cytogenetic aberration and prior smoking behavior. Conclusion This study shows that proteomic profiling of epigenetic modifications has clinical implications in acute leukemia and supports the idea that epigenetic patterns contribute to a more accurate picture of the leukemic state that complements cytogenetic and molecular genetic subgrouping. A combination of these variables may offer more accurate outcome prediction and we suggest that histone methylation mark measurement at time of diagnosis might be a suitable method to improve patient outcome prediction and subsequent treatment intensity stratification in selected subgroups.

Mitochondrial encephalopathies: molecular genetic diagnosis from blood samples

The Lancet ◽  
1991 ◽  
Vol 337 (8753) ◽  
pp. 1311-1313 ◽  
Author(s):  
S.R. Hammans ◽  
M.G. Sweeney ◽  
M. Brockington ◽  
J.A. Morgan-Hughes ◽  
A.E. Harding
Keyword(s):  
Molecular Genetic ◽  
Genetic Diagnosis ◽  
Blood Samples ◽  
Molecular Genetic Diagnosis

scholarly journals Molecular Genetic Analysis of the Human Lewis Histo-blood Group System

1996 ◽  
Vol 271 (16) ◽  
pp. 9830-9837 ◽  
Author(s):  
Takashi Kudo ◽  
Hiroko Iwasaki ◽  
Shoko Nishihara ◽  
Naoko Shinya ◽  
Takao Ando ◽  
...  
Keyword(s):  
Genetic Analysis ◽  
Blood Group ◽  
Molecular Genetic ◽  
Molecular Genetic Analysis ◽  
Blood Group System ◽  
Group System

Altered Growth Characteristics of Cord Blood Cells after in vivo Exposure to Maternal Acute Myeloid Leukemia and Chemotherapy

2005 ◽  
Vol 114 (2) ◽  
pp. 121-124
Author(s):  
T. Fietz ◽  
R. Arnold ◽  
G. Massenkeil ◽  
K. Rieger ◽  
B. Reufi ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Cord Blood ◽  
Blood Cells ◽  
Myeloid Leukemia ◽  
Growth Characteristics ◽  
Cord Blood Cells ◽  
Acute Myeloid

scholarly journals OCCURRENCE OF 19S AND 7S ANTI-IGGS DURING HYPERIMMUNIZATION OF RABBITS WITH STREPTOCOCCI

1972 ◽  
Vol 136 (4) ◽  
pp. 799-815 ◽  
Author(s):  
Viktor A. Bokisch ◽  
David Bernstein ◽  
Richard M. Krause
Keyword(s):  
Red Blood Cells ◽  
Blood Group ◽  
Pneumococcal Vaccine ◽  
Blood Cells ◽  
Genetic Influence ◽  
Group A

All 110 rabbits immunized with Group A, A-variant, and C streptococcal vaccines produced 19S anti-IgG in addition to antibodies to the streptococcal carbohydrates. 19S anti-IgG was detected by hemagglutination of rabbit red blood cells coated with rabbit anti-blood group F antibody. Antisera of 88 of these animals were also tested for 7S anti-IgG with a coprecipitation assay. This assay is based on the coprecipitation of 7S anti-IgG with complexes of streptococcal carbohydrate and anti-carbohydrate antibody. 50 of the 88 anti-Group C streptococcal antisera contained 7S anti-IgGs. In eight antisera the concentration was greater than 5 mg/ml. The data suggest a genetic influence on the occurrence of 7S anti-IgG. The eight rabbits which produced more than 5 mg/ml of 7S anti-IgG belonged to three related families. Moreover, there were families in which almost every member produced 7S anti-IgG and other families in which only 30% of the members manufactured 7S anti-IgG. The streptococcal vaccine was an especially efficient stimulus for the production of 19S anti-IgG, whereas the pneumococcal vaccine was much less effective in this respect. Furthermore, 7S anti-IgGs were not detected in antipneumococcal antisera, although the concentration of anti-capsular antibodies was similar to that of anti-carbohydrate antibodies in antistreptococcal antisera.

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