|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
DI-87 is a promising new compound for use in combination therapy against tumors expressing dCK.
|
31812677 |
2020 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Low deoxycytidine kinase expression in tumour biopsies from patients treated with gemcitabine, assessed by immunostaining and image analysis, correlates with a poor prognosis, but there is no such correlation in tumour biopsies from a Phase I cohort treated with NUC-1031.
|
31113993 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
SIGNIFICANCE: A new molecular MRI method that detects deoxycytidine kinase activity using its natural substrate deoxycytidine has great translational potential for clinical assessment of tumor resistance and prediction of treatment efficacy.
|
30940660 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
<sup>18</sup>F-clofarabine might be used to measure dCK expression and thus serve as a predictive biomarker for tumor responses to dCK-dependent prodrugs or small-molecule dCK inhibitors, respectively.
|
27811125 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Patients with brain (17), colon (24), and breast (30) tumors, 53, 67, and 73%, respectively, had an elevated T/N value (Specific Activity of tumor/ Specific Activity of normal tissue) involving dCK and dCMPD suggesting chemotherapy with 5-fluorodeoxycytidine (5-FdC) alone or in combination with thymidine plus deoxytetrahydrouridine, or with the radiosensitizer, 5-chlorodeoxycytidine (5-CldC) plus tetrahydrouridine (H4U).
|
27745548 |
2017 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We propose that dCK activity in tumor vasculature renders it gemcitabine sensitive, which is sufficient to invoke a tumor response and permit tumor cell kill in gemcitabine-resistant tumors.
|
25224279 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Using [(18)F]-FAC, a dCK-specific positron emission tomography (PET) probe, we visualized and quantified dCK activation in tumor xenografts after IR, indicating that dCK activation could serve as a biomarker for ATM function and DNA damage response in vivo.
|
25101980 |
2014 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Bladder tumour specimens showed an heterogeneous gene expression pattern and patients with higher levels of dCK and hENT1 had better response.
|
16868547 |
2006 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The role of drug transport and metabolism on gemcitabine cytotoxicity was examined with specific inhibitors, whereas transcription analysis of human equilibrative nucleoside transporter-1 (hENT1), deoxycytidine kinase (dCK), 5'-nucleotidase (5'-NT), cytidine deaminase (CDA), and ribonucleotide reductase subunits M1 and M2 (RRM1 and RRM2) was done by quantitative reverse transcription-PCR in tumor tissue isolated by laser microdissection from surgical or biopsy samples of 102 patients.
|
16585222 |
2006 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Sequencing of the entire dCK coding sequence in 17 cell lines and 9 patients' cancer tissues with disease progression while on gemcitabine did not identify any mutations, suggesting that genetic alterations of dCK are not a common mechanism of resistance to gemcitabine for this tumor type.
|
16638857 |
2006 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The LC is a rapid and reliable method for quantitation of dCK mRNA levels in tumors to predict clinical gemcitabine sensitivity.
|
15327832 |
2004 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Activities of dCK and CDA were measured in a panel of eight gemcitabine-sensitive and -resistant tumors of a different origin (pancreas, lung, colon, ovary, and head and neck) grown as s.c. tumors in mice.
|
12477049 |
2002 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Retroviral transfer of deoxycytidine kinase into tumor cell lines enhances nucleoside toxicity.
|
8625309 |
1996 |
|
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 |