|1.||Greene, Warner C: 3 articles (02/2007 - 05/2005)|
|2.||Soros, Vanessa B: 3 articles (02/2007 - 05/2005)|
|3.||Bergman, A M: 2 articles (01/2009 - 02/2004)|
|4.||Peters, G J: 2 articles (01/2009 - 02/2004)|
|5.||Prochnow, Courtney: 1 article (08/2012)|
|6.||Pham, Phuong: 1 article (08/2012)|
|7.||Goodman, Myron F: 1 article (08/2012)|
|8.||Chen, Xiaojiang S: 1 article (08/2012)|
|9.||Mu, Yunxiang: 1 article (08/2012)|
|10.||Tsuchida, Akihiko: 1 article (07/2012)|
10/01/1987 - "Deoxycytidine deaminase is present in all the tissues which were analyzed, although its activity is lower in some of the tumor samples. "
04/01/2007 - "Its unnatural stereochemistry renders it insensitive to some mechanisms of resistance of tumor cells to D-nucleosides, such as deamination by deoxycytidine deaminase and decreased active uptake by nucleoside transporters. "
05/01/1987 - "A critical feature of this chemotherapeutic strategy using FdCyd plus H4Urd was that the elevated level of cytidine deaminase in LLC tumor tissue was inhibited less than 10% by the administration of 25 mg/kg H4Urd, whereas deoxycytidine deaminase activities in normal tissues (including bone marrow and intestine) were inhibited greater than 93%.(ABSTRACT TRUNCATED AT 400 WORDS)"
01/01/2009 - "The aim of this phase 0 study was to investigate whether gemcitabine passes the blood-tumor barrier, and is phosphorylated in the tumor by deoxycytidine kinase (dCK) to gemcitabine nucleotides in order to enable radiosensitization, and whether it is deaminated by deoxycytidine deaminase (dCDA) to dFdU. "
04/01/1982 - "The activities of cytidine triphosphate synthetase, deoxycytidine monophosphate deaminase, uridine kinase, thymidine kinase, thymidine monophosphate kinase and DNA polymerase were markedly increased in tumor tissues, compared with those in the corresponding normal tissues, while the activities of deoxycytidine kinase, cytidine deaminase and deoxycytidine deaminase were only slightly increased. "
01/01/2008 - "APOBEC3G (A3G), a deoxycytidine deaminase, is a potent host antiviral factor that can restrict HIV-1 infection. "
02/01/2007 - "APOBEC3G (A3G), a deoxycytidine deaminase, is a powerful host antiretroviral factor that can restrict HIV-1 infection. "
06/01/2006 - "APOBEC3G (A3G), a deoxycytidine deaminase, is a powerful host antiretroviral factor that can restrict HIV-1 infection. "
05/05/2005 - "Here we show that the anti-retroviral deoxycytidine deaminase APOBEC3G strongly protects unstimulated peripheral blood CD4+ T cells against HIV-1 infection. "
04/01/1977 - "Induction of deoxycytidine deaminase activity in mammalian cell lines by infection with herpes simplex virus type 1."
|3.||Acute Myeloid Leukemia (Acute Myelogenous Leukemia)
09/01/1997 - "Activity of thymidine kinase and of polymerase alpha as well as activity and gene expression of deoxycytidine deaminase in leukemic blasts are correlated with clinical response in the setting of granulocyte-macrophage colony-stimulating factor-based priming before and during TAD-9 induction therapy in acute myeloid leukemia."
06/01/1987 - "Deoxycytidine kinase and deoxycytidine deaminase values correspond closely to clinical response to cytosine arabinoside remission induction therapy in patients with acute myelogenous leukemia."
01/01/2012 - "No deoxycytidine deaminase activity was detected in either of the leukemias. "
02/01/2004 - "1-beta-D-arabinofuranosylcytosine (ara-C) is a deoxycytidine analog with activity in leukemia, which requires phosphorylation by deoxycytidine kinase (dCK) to allow formation of its active phosphate 1-beta-D-arabinofuranosylcytosine triphosphate, but can be deaminated by deoxycytidine deaminase. "
|5.||Hyper-IgM Immunodeficiency Syndrome (Hyper-IgM Syndrome)
|7.||Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF)
|9.||Ribonucleotide Reductases (Ribonucleotide Reductase)
|2.||Drug Therapy (Chemotherapy)