| Deoxycytidine kinase inactivation enhances gemcitabine resistance and sensitizes mitochondrial metabolism interference in pancreatic cancer. | Deoxycytidine kinase inactivation enhances gemcitabine resistance and sensitizes mitochondrial metabolism interference in pancreatic cancer.
Dash S, Ueda T, Komuro A, Honda M, Sugisawa R, Okada H., Free PMC Article | 02/17/2024 |
| Drug resistance to nelarabine in leukemia cell lines might be caused by reduced expression of deoxycytidine kinase through epigenetic mechanisms. | Drug resistance to nelarabine in leukemia cell lines might be caused by reduced expression of deoxycytidine kinase through epigenetic mechanisms.
Yoshida K, Fujita A, Narazaki H, Asano T, Itoh Y. | 02/26/2022 |
| Combination of azacytidine and curcumin is a potential alternative in decitabine-resistant colorectal cancer cells with attenuated deoxycytidine kinase. | Combination of azacytidine and curcumin is a potential alternative in decitabine-resistant colorectal cancer cells with attenuated deoxycytidine kinase.
Hosokawa M, Seiki R, Iwakawa S, Ogawara KI. | 01/29/2022 |
| Deoxycytidine Kinase (DCK) Mutations in Human Acute Myeloid Leukemia Resistant to Cytarabine. | Deoxycytidine Kinase (DCK) Mutations in Human Acute Myeloid Leukemia Resistant to Cytarabine.
Wu B, Mao ZJ, Wang Z, Wu P, Huang H, Zhao W, Zhang L, Zhang Z, Yin H, Gale RP, Yin B. | 11/22/2021 |
| Human equilibrative nucleoside transporter-1 and deoxycytidine kinase can predict gemcitabine effectiveness in Egyptian patients with Hepatocellular carcinoma. | Human equilibrative nucleoside transporter-1 and deoxycytidine kinase can predict gemcitabine effectiveness in Egyptian patients with Hepatocellular carcinoma.
Attia F, Fathy S, Anani M, Hassan A, Attia F, Ibrahim G, Elazab M., Free PMC Article | 09/11/2021 |
| DCK is an Unfavorable Prognostic Biomarker and Correlated With Immune Infiltrates in Liver Cancer. | DCK is an Unfavorable Prognostic Biomarker and Correlated With Immune Infiltrates in Liver Cancer.
Hu SF, Lin X, Xu LP, Chen HG, Guo JF, Jin L., Free PMC Article | 01/9/2021 |
| study suggests that DCK knockdown facilitates apoptosis while inhibiting proliferation and tumorigenicity in vivo of cervical cancer HeLa cells. | Effects of DCK knockdown on proliferation, apoptosis and tumorigenicity in vivo of cervical cancer HeLa cells.
Shang QY, Wu CS, Gao HR. | 06/16/2018 |
| Phosphorylated and activated DCK can inhibit radiation-induced cell death including apoptosis and mitotic catastrophe, and promote radiation-induced autophagy through PI3K/Akt/mTOR pathway. | The Role of Deoxycytidine Kinase (dCK) in Radiation-Induced Cell Death.
Zhong R, Xin R, Chen Z, Liang N, Liu Y, Ma S, Liu X., Free PMC Article | 04/8/2017 |
| Low deoxycytidine kinase expression is associated with periampullary adenocarcinoma. | Prognostic effect of hENT1, dCK and HuR expression by morphological type in periampullary adenocarcinoma, including pancreatic cancer.
Elebro J, Ben Dror L, Heby M, Nodin B, Jirström K, Eberhard J., Free PMC Article | 12/17/2016 |
| expression and A9846G AA genotype significantly associated with reduced mortality in pancreatic ductal adenocarcinoma | dCK Expression and Gene Polymorphism With Gemcitabine Chemosensitivity in Patients With Pancreatic Ductal Adenocarcinoma: A Strobe-Compliant Observational Study.
Xiong J, Altaf K, Ke N, Wang Y, Tang J, Tan C, Li A, Zhang H, He D, Liu X., Free PMC Article | 11/12/2016 |
| recently described a human deoxycytidine kinase mutant (G12) that sensitizes cancer cell lines to treatment with gemcitabine. Here, starting from the G12 variant, we identified a mutant that triggers even greater sensitisation to gemcitabine than G12. | Potent Sensitisation of Cancer Cells to Anticancer Drugs by a Quadruple Mutant of the Human Deoxycytidine Kinase.
Coulibaly ST, Rossolillo P, Winter F, Kretzschmar FK, Brayé M, Martin DP, Lener D, Negroni M., Free PMC Article | 06/28/2016 |
| RNA expression of deoxycytidine kinase (DCK), human equilibrative nucleoside transporter-1 (ENT1) and ribonucleotide reductase M1 (RRM1) were significantly higher and cytidine deaminase (CDA) was significantly lower in ex vivo Ara-C sensitive samples. | RNA expression of genes involved in cytarabine metabolism and transport predicts cytarabine response in acute myeloid leukemia.
Abraham A, Varatharajan S, Karathedath S, Philip C, Lakshmi KM, Jayavelu AK, Mohanan E, Janet NB, Srivastava VM, Shaji RV, Zhang W, Abraham A, Viswabandya A, George B, Chandy M, Srivastava A, Mathews V, Balasubramanian P., Free PMC Article | 04/16/2016 |
| n the multivariate Cox regression analysis, we found that age at diagnosis, wild-type genotype of the CDA A79C polymorphism, and wild-type genotype of the dCK C360G polymorphism were the most significant prognostic factors for predicting the risk of death | Role of Genetic Polymorphisms of Deoxycytidine Kinase and Cytidine Deaminase to Predict Risk of Death in Children with Acute Myeloid Leukemia.
Medina-Sanson A, Ramírez-Pacheco A, Moreno-Guerrero SS, Dorantes-Acosta EM, Sánchez-Preza M, Reyes-López A., Free PMC Article | 03/19/2016 |
| results strongly suggest that (1) the E197K alteration in DCK causes inactivation of DCK, and that (2) loss of the normal E197 allele is the crucial mechanism in acquisition of gemcitabine resistance in the RMKN28 tumor cell line | Acquisition of chemoresistance to gemcitabine is induced by a loss-of-function missense mutation of DCK.
Nakano T, Saiki Y, Kudo C, Hirayama A, Mizuguchi Y, Fujiwara S, Soga T, Sunamura M, Matsumura N, Motoi F, Unno M, Horii A. | 12/12/2015 |
| DCK rs12648166 and DCK rs4694362 SNPs were associated with hematologic toxicity (OR = 2.63, CI 95% = 1.37-5.04, P = 0.0036 and OR = 2.53, CI 95% = 1.34-4.80, P = 0.0044, respectively). | Impact of single nucleotide polymorphisms of cytarabine metabolic genes on drug toxicity in childhood acute lymphoblastic leukemia.
Gabor KM, Schermann G, Lautner-Csorba O, Rarosi F, Erdelyi DJ, Endreffy E, Berek K, Bartyik K, Bereczki C, Szalai C, Semsei AF. | 06/20/2015 |
| These findings indicate that the decitabine metabolic pathway affects its therapeutic effects, lower hENT1 expression may induce primary resistance and down-regulated DCK expression may be related to secondary resistance. | The hENT1 and DCK genes underlie the decitabine response in patients with myelodysplastic syndrome.
Wu P, Geng S, Weng J, Deng C, Lu Z, Luo C, Du X. | 03/28/2015 |
| induction after hypoxia plays a role in the progression of pulmonary fibrosis by contributing to alveolar epithelial cell proliferation | Hypoxia-induced deoxycytidine kinase contributes to epithelial proliferation in pulmonary fibrosis.
Weng T, Poth JM, Karmouty-Quintana H, Garcia-Morales LJ, Melicoff E, Luo F, Chen NY, Evans CM, Bunge RR, Bruckner BA, Loebe M, Volcik KA, Eltzschig HK, Blackburn MR., Free PMC Article | 02/21/2015 |
| DCK expression levels are prognostic and had predictive value for sensitivity to 5-FU in pancreatic cancer. | dCK expression correlates with 5-fluorouracil efficacy and HuR cytoplasmic expression in pancreatic cancer: a dual-institutional follow-up with the RTOG 9704 trial.
McAllister F, Pineda DM, Jimbo M, Lal S, Burkhart RA, Moughan J, Winter KA, Abdelmohsen K, Gorospe M, Acosta Ade J, Lankapalli RH, Winter JM, Yeo CJ, Witkiewicz AK, Iacobuzio-Donahue CA, Laheru D, Brody JR., Free PMC Article | 01/24/2015 |
| DCK could regulate the migration and invasion of fibroblast-like synoviocytes through AKT pathway in rheumatoid arthritis patients. | Deoxycytidine kinase promotes the migration and invasion of fibroblast-like synoviocytes from rheumatoid arthritis patients.
Fan W, Zhou ZY, Huang XF, Bao CD, Du F., Free PMC Article | 08/9/2014 |
| PP2A constitutively dephosphorylates dCK in cells and negatively regulates its activity. | Protein phosphatase 2A regulates deoxycytidine kinase activity via Ser-74 dephosphorylation.
Amsailale R, Beyaert M, Smal C, Janssens V, Van Den Neste E, Bontemps F. | 04/19/2014 |
| Report genetic variation in deoxycytidine kinase and subsequent gemcitabine metabolism. | Pharmacogenomics of gemcitabine metabolism: functional analysis of genetic variants in cytidine deaminase and deoxycytidine kinase.
Baker JA, Wickremsinhe ER, Li CH, Oluyedun OA, Dantzig AH, Hall SD, Qian YW, Ring BJ, Wrighton SA, Guo Y. | 07/13/2013 |
| It is evident that the DCK and CDA polymorphisms might be the important markers for the AML patients' therapy outcomes in a Chinese population. | Association of polymorphisms of cytosine arabinoside-metabolizing enzyme gene with therapeutic efficacy for acute myeloid leukemia.
Xu PP, Chen BA, Feng JF, Cheng L, Xia GH, Li YF, Qian J, Ding JH, Lu ZH, Wang XM, Xu K, Schultz M. | 01/5/2013 |
| Hematologic toxicity such as neutropenia, thrombocytopenia, and anemia were not associated with three tagged single-nucleotide polymorphisms of deoxycytidine kinase or haplotypes. Genetic variations did not affect survival of the patients. | Lack of association of genetic variations of deoxycytidine kinase with toxicity or survival of non-small-cell lung cancer patients treated with gemcitabine plus cisplatin.
Ryu JS, Kim HJ, Shin ES, Nam HS, Cho JH, Lee JE. | 12/8/2012 |
| High levels of dCK in pancreatic ductal adenocarcinoma predict longer survival times in patients treated with adjuvant gemcitabine. | Levels of gemcitabine transport and metabolism proteins predict survival times of patients treated with gemcitabine for pancreatic adenocarcinoma.
Maréchal R, Bachet JB, Mackey JR, Dalban C, Demetter P, Graham K, Couvelard A, Svrcek M, Bardier-Dupas A, Hammel P, Sauvanet A, Louvet C, Paye F, Rougier P, Penna C, André T, Dumontet C, Cass CE, Jordheim LP, Matera EL, Closset J, Salmon I, Devière J, Emile JF, Van Laethem JL. | 11/17/2012 |
| These results indicate that the inactivation of DCK is one of the crucial mechanisms in acquisition of gemcitabine resistance. | DCK is frequently inactivated in acquired gemcitabine-resistant human cancer cells.
Saiki Y, Yoshino Y, Fujimura H, Manabe T, Kudo Y, Shimada M, Mano N, Nakano T, Lee Y, Shimizu S, Oba S, Fujiwara S, Shimizu H, Chen N, Nezhad ZK, Jin G, Fukushige S, Sunamura M, Ishida M, Motoi F, Egawa S, Unno M, Horii A. | 06/23/2012 |