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 |
Viral Load result
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Association Between Single-Nucleotide Polymorphisms in HLA Alleles and Human Immunodeficiency Virus Type 1 Viral Load in Demographically Diverse, Antiretroviral Therapy-Naive Participants From the Strategic Timing of AntiRetroviral Treatment Trial.
|
31219150 |
2019 |
Red cell distribution width determination
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
RDW - Red blood cell distribution width result
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
HUMAN IMMUNODEFICIENCY VIRUS TYPE 1, SUSCEPTIBILITY TO
|
0.100 |
GeneticVariation
|
disease |
GWASCAT |
Association Between Single-Nucleotide Polymorphisms in HLA Alleles and Human Immunodeficiency Virus Type 1 Viral Load in Demographically Diverse, Antiretroviral Therapy-Naive Participants From the Strategic Timing of AntiRetroviral Treatment Trial.
|
31219150 |
2019 |
HIV-1, RESISTANCE TO
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Association Between Single-Nucleotide Polymorphisms in HLA Alleles and Human Immunodeficiency Virus Type 1 Viral Load in Demographically Diverse, Antiretroviral Therapy-Naive Participants From the Strategic Timing of AntiRetroviral Treatment Trial.
|
31219150 |
2019 |
ACQUIRED IMMUNODEFICIENCY SYNDROME, PROGRESSION TO
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Association Between Single-Nucleotide Polymorphisms in HLA Alleles and Human Immunodeficiency Virus Type 1 Viral Load in Demographically Diverse, Antiretroviral Therapy-Naive Participants From the Strategic Timing of AntiRetroviral Treatment Trial.
|
31219150 |
2019 |
AIDS, PROGRESSION TO
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Association Between Single-Nucleotide Polymorphisms in HLA Alleles and Human Immunodeficiency Virus Type 1 Viral Load in Demographically Diverse, Antiretroviral Therapy-Naive Participants From the Strategic Timing of AntiRetroviral Treatment Trial.
|
31219150 |
2019 |
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Genomic profiling uncovered deletion of the deoxycytidine kinase (DCK) gene in both MOLM-13- and SHI-1-derived cytarabine-resistant variants and in an AML patient sample.
|
27833094 |
2017 |
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 |
Leukemia, Myelocytic, Acute
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In conclusion, our data reveal that hypoxia-induced downregulation of deoxycytidine kinase represents one stroma-cell-independent mechanism of drug resistance to cytarabine in acute myeloid leukaemia.
|
26613208 |
2016 |
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
Dck-defective leukemic cells may become prednisolone sensitive indicating prednisolone may be an effective adjuvant therapy in some cases of DCK-negative AML.
|
27808171 |
2016 |
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
DCK rs4643786 may serve as an independent predictor of drug response and AML outcome.
|
27548009 |
2016 |
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
Expression Levels of Human Equilibrative Nucleoside Transporter 1 and Deoxycytidine Kinase Enzyme as Prognostic Factors in Patients with Acute Myeloid Leukemia Treated with Cytarabine.
|
27119162 |
2016 |
Leukemia, Myelocytic, Acute
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Higher DCK and RRM1 expression in AML patient's blast correlated with better DFS.
|
26083014 |
2015 |
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Role of Genetic Polymorphisms of Deoxycytidine Kinase and Cytidine Deaminase to Predict Risk of Death in Children with Acute Myeloid Leukemia.
|
26090398 |
2015 |
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 |
Leukemia, Myelocytic, Acute
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We analyzed the expression of deoxycytidine kinase (dCK), UMP/CMP-kinase (UMP/CMP-K), nucleotide diphosphokinase (NDPK-B) and 5'-nucleotidases cN-II, cN-III, cdN and mdN by quantitative polymerase chain reaction at diagnosis in leukemic blasts from 96 patients with acute myeloid leukemia (AML) treated with ara-C. Our results show that high mRNA levels of cN-II and low mRNA levels of cN-III are correlated with a worse clinical outcome and suggest that these enzymes may have a role in sensitivity to ara-C in AML patients.
|
16330448 |
2005 |