Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.30.2 (endonuclease)
 18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The previously established fact of low activity of Ca, Mg-dependent endonucleolysis of cell nucleus DNA in lymphoproliferative diseases (CME-activity) brought the authors to study intranuclear characteristics of lymphoid cells in childhood acute lymphoblastic leukemia (ALL). The intensity of DNA-endonucleolysis was measured in 0.7% agarose gel using electrophoresis. Peripheral blood and bone marrow samples from 13 untreated ALL patients and 23 children in remission were examined. The age of the patients ranged from 4 to 14 years. CME-activity before treatment appeared to be 2-10 times less than normal in 8 out of 13 patients. In bone marrow cell nuclei CME-activity was universally reduced 3-20-fold. In ALL remission endonuclease activity in blood and bone marrow cells returned to normal.
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PMID:[Changes in the activity of endonucleolysis of nuclear DNA in children with acute leukemia]. 764 86

We studied 98 female patients in remission (2-240 months) from childhood ALL to determine the clonality status of their hematopoiesis. Thirty-one (31.6%) were heterozygous at the PGK locus for the BstX1 endonuclease restriction site, permitting X-linked clonality assays to be performed. Two patients were in relapse at the time of study and were excluded. We used the PGK-PCR clonality assay (PPCA) to analyze DNA from PMN and mononuclear cells of the remaining 29 female patients. All (29/29) patients demonstrated polyclonal hematopoiesis. These data show that remission from childhood ALL involves reestablishment of polyclonally derived hematopoiesis in all patients studied.
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PMID:Clonality analysis of childhood ALL in remission: no evidence of clonal hematopoiesis. 810 90

The most common gene fusion (up to 25%) in childhood acute lymphoblastic leukemia (ALL) is that between ETV6 and RUNX1 (previously TEL and AML1, respectively; we here use the old nomenclature, for ease of reference to the literature). We determined the incidence of TEL/AML1 translocation with reverse transcriptase polymerase chain reaction (RT-PCR) and flow-cytometric immunophenotyping of newly diagnosed pediatric acute lymphoblastic leukemia patients in Thailand. The TEL/AML1 fusion genes were cloned into plasmids and sequenced. The variant found was confirmed with restriction fragment length polymorphism (RFLP) using SphI restriction endonuclease. Of 35 ALL patients, we found an incidence of 8.6% of TEL/AML1 translocation in ALL patients (12% of B-lineage ALL), which is lower than that reported in caucasians but is similar to that reported in Japanese and Koreans. All the translocation-positive patients had B-lineage common ALL, expressing CD10+. Interestingly, the two TEL/AML1 subclones were CD20 negative, and one subclone expressed a myelocytic marker (CD33+). Two TEL/AML1 subclones from bone marrow of ALL patients were isolated and sequenced. One was a wild type and the other was a variant having A --> G substitution at nucleotide 73 from the 5' end. The substitution nucleotide was located in the AML1 region. The clinical relevance of the variant is to be investigated.
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PMID:Cloning and sequencing of ETV6/RUNX1 (TEL/AML1) variant in acute lymphoblastic leukemia. 1510 90