Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.5.4.4 (
adenosine deaminase
)
5,136
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
We studied the activity of serum
adenosine deaminase
(
ADA
) and its isozyme in 36 leukemic patients (16 ANLL, 11 ALL, and 9
CML
) and 8 MDS. Isozyme was measured by erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA) inhibitory assay. This assay was simple and reliable. The appearance rate of abnormally high
ADA
value were 81.24% for ANLL, 100% for ALL, 77.8% for
CML
and 37.5% for MDS. The
ADA
level became high when MDS turned into overt leukemia. In isozyme pattern, there was a clear difference between ANLL and ALL. The isozyme I/II ratio was significantly higher (p less than 0.001) in ALL than ANLL. Lymphoblastic crisis of
CML
also had a high isozyme I/II ratio. There was a correlation between isozyme I and absolute number of peripheral blasts in ALL (r = 0.768). When observed time sequentially,
ADA
and isozyme changed correlatively with the number of blasts counts. Serum
ADA
and its isozyme are useful parameters both for leukemic diagnosis and treatment.
...
PMID:[Serum adenosine deaminase and its isozyme activity in leukemia and MDS]. 223 54
We have analyzed the distribution and prognostic significance of terminal deoxynucleotidyl transferase (TdT) and
adenosine deaminase
(
ADA
) in connection with conventional cytology, cytogenetics, response to therapy, and survival. The study population consisted of 78 patients with AML, 44 patients with Ph1 +
CML
in chronic phase, and 35 adult patients with Ph1 +
CML
in blastic phase, among which 5 cases presented as Ph1 + acute leukemia. Nine percent of the AML cases were positive for TdT and were characterized by a high percentage of blast cells in bone marrow, myeloid features by cytochemistry and absence of the Philadelphia chromosome. The median
ADA
values of the TdT+ AML cases were several times higher than those obtained for the TdT- cases. The survival calculated for the two groups of AML cases subdivided according to
ADA
levels was significantly longer (p less than 0.025) for the patients with low levels of
ADA
(less than 250 U/10(8) cells). In chronic phase of
CML
, TdT was absent and
ADA
values were increased over normal controls only in cases with early signs of transformation. In blastic phase, 31% of the 35 cases were positive for TdT, and
ADA
values were significantly higher (p less than 0.001) in TdT+ than TdT- cases. The survival calculated from the onset of transformation was significantly longer for the TdT+ acute phase (10.4 mo) compared to the TdT- patients (4.8 mo; p less than 0.025). Four cases presenting as Ph1 + acute leukemia were TdT+ and had elevated levels of
ADA
; 3 of them responded to ALL therapy, reverting to a stable phase of
CML
.
...
PMID:Prognostic significance of terminal transferase and adenosine deaminase in acute and chronic myeloid leukemia. 704 66
The content of nuclear high mobility group (HMG) proteins, activities of ornithine decarboxylase (ODC),
adenosine deaminase
(
ADA
) and purine nucleoside phosphorylase (PNP) and also glycosaminoglycan (GAG) content and composition were studied in leukocytes of patients with chronic myelogenous leukemia in the phase of blast crisis (BC
CML
). Myeloid and lymphoid cytochemical variants of BC
CML
differ by biochemical parameters. It is suggested, that the content of HMG-proteins, activities of ODC and PNP, and electrophoretic patterns of GAGs could be used in diagnostics of two main variants of BC
CML
.
...
PMID:[Certain biochemical features of leukocytes in blast crisis of chronic myelogenous leukemia]. 970 28
Post-transcriptional adenosine-to-inosine RNA editing mediated by
adenosine deaminase
acting on RNA1 (ADAR1) promotes cancer progression and therapeutic resistance. However, ADAR1 editase-dependent mechanisms governing leukemia stem cell (LSC) generation have not been elucidated. In blast crisis chronic myeloid leukemia (BC
CML
), we show that increased JAK2 signaling and BCR-ABL1 amplification activate ADAR1. In a humanized BC
CML
mouse model, combined JAK2 and BCR-ABL1 inhibition prevents LSC self-renewal commensurate with ADAR1 downregulation. Lentiviral ADAR1 wild-type, but not an editing-defective ADAR1(E912A) mutant, induces self-renewal gene expression and impairs biogenesis of stem cell regulatory let-7 microRNAs. Combined RNA sequencing, qRT-PCR, CLIP-ADAR1, and pri-let-7 mutagenesis data suggest that ADAR1 promotes LSC generation via let-7 pri-microRNA editing and LIN28B upregulation. A small-molecule tool compound antagonizes ADAR1's effect on LSC self-renewal in stromal co-cultures and restores let-7 biogenesis. Thus, ADAR1 activation represents a unique therapeutic vulnerability in LSCs with active JAK2 signaling.
...
PMID:ADAR1 Activation Drives Leukemia Stem Cell Self-Renewal by Impairing Let-7 Biogenesis. 2749 66
