DCK, deoxycytidine kinase, 1633

N. diseases: 102; N. variants: 6
Source: ALL
Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0027651
Disease: Neoplasms
Neoplasms
0.100 AlteredExpression group BEFREE DI-87 is a promising new compound for use in combination therapy against tumors expressing dCK. 31812677 2020
CUI: C0027651
Disease: Neoplasms
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
CUI: C0027651
Disease: Neoplasms
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
CUI: C0376705
Disease: Viral Load result
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
CUI: C1836231
Disease: HIV-1, RESISTANCE TO
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
CUI: C1836233
Disease: AIDS, PROGRESSION TO
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
CUI: C0023467
Disease: Leukemia, Myelocytic, Acute
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
CUI: C0027651
Disease: Neoplasms
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
CUI: C0027651
Disease: Neoplasms
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
CUI: C0023467
Disease: Leukemia, Myelocytic, Acute
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
CUI: C0023467
Disease: Leukemia, Myelocytic, Acute
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
CUI: C0023467
Disease: Leukemia, Myelocytic, Acute
Leukemia, Myelocytic, Acute
0.100 GeneticVariation disease BEFREE DCK rs4643786 may serve as an independent predictor of drug response and AML outcome. 27548009 2016
CUI: C0023467
Disease: Leukemia, Myelocytic, Acute
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
CUI: C0023467
Disease: Leukemia, Myelocytic, Acute
Leukemia, Myelocytic, Acute
0.100 AlteredExpression disease BEFREE Higher DCK and RRM1 expression in AML patient's blast correlated with better DFS. 26083014 2015
CUI: C0023467
Disease: Leukemia, Myelocytic, Acute
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
CUI: C0027651
Disease: Neoplasms
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
CUI: C0027651
Disease: Neoplasms
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
CUI: C0027651
Disease: Neoplasms
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
CUI: C0027651
Disease: Neoplasms
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
CUI: C0027651
Disease: Neoplasms
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
CUI: C0023467
Disease: Leukemia, Myelocytic, Acute
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