Reticulosarcoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Characterization of an adenosine deaminase-deficient human histiocytic lymphoma cell line (DHL-9) and selection of mutants deficient in adenosir kinase and deoxycytidine kinase.
|
6303563 |
1983 |
Diffuse Large B-Cell Lymphoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Characterization of an adenosine deaminase-deficient human histiocytic lymphoma cell line (DHL-9) and selection of mutants deficient in adenosir kinase and deoxycytidine kinase.
|
6303563 |
1983 |
Histiocytic sarcoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Characterization of an adenosine deaminase-deficient human histiocytic lymphoma cell line (DHL-9) and selection of mutants deficient in adenosir kinase and deoxycytidine kinase.
|
6303563 |
1983 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Approximately 3 days after the end of the 5-Aza-C infusion, the HDara-C regimen was given again with the idea that the induced DNA hypomethylation in the leukemic cells may have increased the dCk activity and that a reversal of the tumor drug resistance to ara-C could have occurred.
|
2473850 |
1989 |
Acute lymphocytic leukemia
|
0.030 |
Biomarker
|
disease |
BEFREE |
Reexpression of dCk could increase the cellular ara-CTP concentrations and the sensitivity to ara-C. A total of 17 pediatric patients with refractory acute lymphocytic leukemia (ALL) received a continuous infusion of 5-Aza-C at 150 mg/m2 daily for 5 days after not responding to (13/17) or relapsing from (4/17) an HDara-C regimen (3 g/m2 over 3 h, every 12 h, x 8 doses).
|
2473850 |
1989 |
leukemia
|
0.030 |
GeneticVariation
|
disease |
BEFREE |
Resistance to 1,25-dihydroxyvitamin D3 of a deoxycytidine kinase-deficient variant of human leukemia HL60 cells.
|
1426045 |
1992 |
Childhood Leukemia
|
0.030 |
GeneticVariation
|
disease |
BEFREE |
Resistance to 1,25-dihydroxyvitamin D3 of a deoxycytidine kinase-deficient variant of human leukemia HL60 cells.
|
1426045 |
1992 |
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We conclude that structural alteration of the coding region of the dCK gene represents one possible mechanism for ara-C resistance in vivo, but, considering the frequency of this event, other mechanisms may play a more important role for clinical resistance to ara-C in patients with AML.
|
7514246 |
1994 |
Acute monocytic leukemia
|
0.030 |
GeneticVariation
|
disease |
BEFREE |
We conclude that structural alteration of the coding region of the dCK gene represents one possible mechanism for ara-C resistance in vivo, but, considering the frequency of this event, other mechanisms may play a more important role for clinical resistance to ara-C in patients with AML.
|
7514246 |
1994 |
Refractory cancer
|
0.010 |
GeneticVariation
|
phenotype |
BEFREE |
We conclude that structural alteration of the coding region of the dCK gene represents one possible mechanism for ara-C resistance in vivo, but, considering the frequency of this event, other mechanisms may play a more important role for clinical resistance to ara-C in patients with AML.
|
7514246 |
1994 |
Acute myeloid leukaemia refractory
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
In order to define the relevance of this mechanism in vivo, we analyzed the dCK gene in 16 adult patients with relapsed/refractory acute myeloid leukemia (AML) and clinical resistance to standard-dose and/or high-dose ara-C. Southern blot analysis using genomic DNA from peripheral blood or bone marrow samples containing > or = 70% leukemic blasts and agarose gel electrophoresis of cDNA obtained by RT-PCR did not reveal gross rearrangements of the dCK gene.
|
7514246 |
1994 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Retroviral transfer of deoxycytidine kinase into tumor cell lines enhances nucleoside toxicity.
|
8625309 |
1996 |
Malignant Neoplasms
|
0.050 |
GeneticVariation
|
group |
BEFREE |
These data suggest that viral vector transduction of the dCK gene followed by treatment with ara-C represents a new chemosensitization strategy for cancer gene therapy.
|
8616717 |
1996 |
Malignant Neoplasms
|
0.050 |
Biomarker
|
group |
BEFREE |
Because many tumors have relatively low levels of dCK, it is possible that dCK gene transfer will be a useful adjunct to the treatment of these malignancies.
|
8625309 |
1996 |
Primary malignant neoplasm
|
0.040 |
GeneticVariation
|
group |
BEFREE |
These data suggest that viral vector transduction of the dCK gene followed by treatment with ara-C represents a new chemosensitization strategy for cancer gene therapy.
|
8616717 |
1996 |
Herpes Simplex Infections
|
0.020 |
AlteredExpression
|
group |
BEFREE |
To develop gene therapy for targeting metastatic lung adenocarcinoma, the toxic activity of herpes simplex virus type 1-thymidine kinase, Escherichia coli cytosine deaminase, and human deoxycytidine kinase were investigated in metastatic human lung adenocarcinoma cell lines H1437 and H2122.
|
8640820 |
1996 |
Glioma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Viral vector transduction of the human deoxycytidine kinase cDNA sensitizes glioma cells to the cytotoxic effects of cytosine arabinoside in vitro and in vivo.
|
8616717 |
1996 |
Adenocarcinoma of lung (disorder)
|
0.010 |
Biomarker
|
disease |
BEFREE |
To develop gene therapy for targeting metastatic lung adenocarcinoma, the toxic activity of herpes simplex virus type 1-thymidine kinase, Escherichia coli cytosine deaminase, and human deoxycytidine kinase were investigated in metastatic human lung adenocarcinoma cell lines H1437 and H2122.
|
8640820 |
1996 |
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
The p16 and dCK CpG islands were also unmethylated in the 8 AML specimens.
|
9808523 |
1998 |
Herpes Simplex Infections
|
0.020 |
Biomarker
|
group |
BEFREE |
Herpes simplex virus thymidine kinase and ganciclovir (HSV-TK/GCV), Escherichia coli cytosine deaminase and 5-fluorocytosine (CD/5FC), E coli nitroreductase and CB1954 (NTR/CB1954), and human deoxycytidine kinase and cytosine arabinoside (dCK/AraC) were employed.
|
9673364 |
1998 |
Hematopoietic Neoplasms
|
0.010 |
Biomarker
|
group |
BEFREE |
In our study, we used sodium bisulfite sequencing to generate high resolution maps of 5-methylcytosine in the CpG islands associated with p15, p16 and dCK in normal human bone marrow (BM), peripheral blood lymphocytes (PBL) and cytosine arabinoside (ara-C)-resistant acute myeloid leukemia (AML) patients, and established human hematopoietic tumor cell lines.
|
9808523 |
1998 |
Down Syndrome
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
Transcripts of deoxycytidine kinase were 2.6-fold higher in DS compared with non-DS cells and may be a factor in the enhanced metabolism of ara-C in DS cells.
|
10438727 |
1999 |
Complete Trisomy 21 Syndrome
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
Transcripts of deoxycytidine kinase were 2.6-fold higher in DS compared with non-DS cells and may be a factor in the enhanced metabolism of ara-C in DS cells.
|
10438727 |
1999 |
Leukemia, Myelocytic, Acute
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
These findings suggest that the presence of inactive, alternatively spliced dCK mRNA transcripts in resistant AML blasts may contribute to the process of AraC resistance in patients with AML.(Blood.2000;96:1517-1524)
|
10942400 |
2000 |
Leukemia, Myelocytic, Acute
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
To improve research concerning the involvement of dCK inactivation in patients with acute myeloid leukemia (AML), we have set up a protocol that allows direct assessment of dCK expression and activity in primary human cells.
|
10995016 |
2000 |