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Tamoxifen enhances erlotinib-induced cytotoxicity through down-regulating AKT-mediated thymidine phosphorylase expression in human non-small-cell lung cancer cells.

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Tamoxifen is a triphenylethylene nonsteroidal estrogen receptor (ER) antagonist used worldwide as an adjuvant hormone therapeutic agent in the treatment of breast cancer. However, the molecular mechanism of tamoxifen-induced cytotoxicity in non-small cell lung cancer (NSCLC) cells has not been

[Studies on the thymidine-triphosphate synthesis in malignant tumors. I. Effects of thymidine on deoxyribonucleoside triphosphate pools and deoxyribonucleic acid synthesis (author's transl)].

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Measurements of the deoxyribonucleoside triphosphate (dNTP) contents, the [14C] thymidine and deoxyuridine incorporation and the "key enzymes" of the thymidine triphosphate (dTTP) synthesis, thymidine kinase and ribonucleotide reductase, in diploid Ehrlich-ascites carcinoma, in Yoshida

Thymidine kinase in breast cancer.

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The enzyme thymidine kinase is associated with DNA synthesis. Thymidine kinase serum levels were studied in normal controls (n = 20), patients with primary breast cancer (n = 60), patients with systemic breast cancer (n = 20) and as a non-cancer disease control group in patients with inflammatory

Can thymidine kinase levels in breast tumors predict disease recurrence?

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BACKGROUND Our previous study of thymidine kinase (TK) levels in the serum of breast cancer patients demonstrated a statistically significant positive correlation with cancer stage. In postsurgical follow-up studies of 20 patients with primary breast cancer, total serum TK levels rose with disease

Positron imaging feasibility studies: selective tumor concentration of 3H-thymidine, 3H-uridine, and 14C-2-deoxyglucose.

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The potential usefulness of substrates for glycolysis and nucleic acid synthesis as tumor imaging agents was compared to that of 67Ga-citrate. In separate experiments, 3H-thymidine, 3H-uridine, 14C-2-deoxyglucose, and 67Ga-citrate were injected intraveneously into BALB/c mice with solid subcutaneous

Two forms of thymidine kinase in normal and tumor tissues of animals.

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The thymidine kinases extracted from the spleen of mice infected with Friend virus and from Yoshida sarcoma in rats were separated into two active peaks by diethylaminoethyl cellulose column chromatography, while those of normal tissues have been found to consist of only the first peak (P-1). The

Synthesis and evaluation of thymidine kinase 1-targeting carboranyl pyrimidine nucleoside analogs for boron neutron capture therapy of cancer.

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A library of sixteen 2nd generation amino- and amido-substituted carboranyl pyrimidine nucleoside analogs, designed as substrates and inhibitors of thymidine kinase 1 (TK1) for potential use in boron neutron capture therapy (BNCT) of cancer, was synthesized and evaluated in enzyme kinetic-, enzyme

N3-substituted thymidine bioconjugates for cancer therapy and imaging.

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The compound class of 3-carboranyl thymidine analogues (3CTAs) are boron delivery agents for boron neutron capture therapy (BNCT), a binary treatment modality for cancer. Presumably, these compounds accumulate selectively in tumor cells via intracellular trapping, which is mediated by hTK1.

Preparation and preliminary biological evaluation of novel (99m)Tc-labelled thymidine analogs as tumor imaging agents.

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Two kinds of novel thymidine derivatives, N-thymidine-yl-N′-methyl-N′-{N′′-[2-sulfanyl-(ethylamino)acetyl]-2-aminoethylsulfanyl-1-hexanamide}-ethanediamine (TMHEA) and N-thymidine-yl-N′-methyl-N′-{N′′-[2-sulfanyl-(ethylamino)acetyl]-2-aminoethylsulfanyl-1-hexanamide}-hexanediamine (TMHHA) were

Kinase-mediated trapping of bi-functional conjugates of paclitaxel or vinblastine with thymidine in cancer cells.

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In the present work, we explore the possibility of introducing selectivity to existing chemotherapeutics via the design of non-pro-drug, bi-functional molecules comprising a microtubule-binding agent and a substrate for a disease-associated kinase. The design, synthesis, and in vitro biological

Use of thymidine analogues to indicate vascular perfusion in tumours.

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Temporary reduction in blood-flow within tumour blood vessels can reduce oxygen supply leading to transient perfusion-limited hypoxia. Consequent selection of cells with mutations and reduced radiosensitivity can lead to disease progression and treatment-resistance. In the present study, we

Angiogenesis, thymidine phosphorylase, and resistance of squamous cell head and neck cancer to cytotoxic and radiation therapy.

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Thymidine phosphorylase (TP), an enzyme involved in the thymidine synthesis and degradation, has been shown to promote tumor angiogenesis. Both TP expression and tumor vascularization are putative postoperative prognostic markers of cancer. Because of its bifunctional role, TP may have interactions

Suppression of thymidine phosphorylase-mediated angiogenesis and tumor growth by 2-deoxy-L-ribose.

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Thymidine phosphorylase (TP), an enzyme involved in the reversible conversion of thymidine to thymine, is identical to an angiogenic factor, platelet-derived endothelial cell growth factor (PD-ECGF). Both TP and one of the TP-degradation products of thymidine 2-deoxy-D-ribose (dRib) display

Enhancement of hormonal synchronization and 5-fluorouracil cytotoxicity in breast cancer cells by low concentration of thymidine.

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A method is described that applies a low concentration of thymidine to achieve maximal hormonal synchronization in cultures of an established human breast cancer cell line, MCF-7. The method consists of sequential treatments with tamoxifen, estradiol, and thymidine. The increase (3.8 fold) in the

Synthesis and Biological Evaluation of Novel (99m)Tc(CO)₃-Labeled Thymidine Analogs as Potential Probes for Tumor Proliferation Imaging.

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Achieving a (99m)Tc labeled thymidine radiotracer for single photon emission tomography (SPECT) is considered to be of interest. In this study, four novel thymidine analogs, 6a, 6b, 6c and 6d, were successfully synthesized via "click reaction" route and then radiolabeled using a [(99m)Tc(CO)₃]⁺ core

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