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Specific association of thiamine-coated gadolinium nanoparticles with human breast cancer cells expressing thiamine transporters.

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Thiamine (vitamin B(1)) was investigated as a tumor-specific ligand for gadolinium nanoparticles. Solid nanoparticles containing gadolinium hexanedione (1.5 mg/mL) were engineered from oil-in-water microemulsion templates and coated with thiamine ligands. Thiamine ligands were synthesized by

Thiamine transporter gene expression and exogenous thiamine modulate the expression of genes involved in drug and prostaglandin metabolism in breast cancer cells.

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In previous studies, we have shown that RNA levels of the thiamine transporter THTR2 were down-regulated in breast cancer tumors in comparison with normal tissues and that THTR2-mediated increases in thiamine uptake activity contributed to increased apoptosis after exposure to ionizing radiation. To

Bioinformatic and metabolomic analysis reveals miR-155 regulates thiamine level in breast cancer.

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microRNA-155 (miR-155) is one of the well-known oncogenic miRNA implicated in various types of tumors. Thiamine, commonly known as vitamin B1, is one of critical cofactors for energy metabolic enzymes including pyruvate dehydrogenase, alpha ketoglutarate dehydrogenase, and transketolase. Here we

The Effects of Thiamine on Breast Cancer Cells.

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(1) Background: Thiamine is an important cofactor for multiple metabolic processes. Its role in cancer has been debated for years. Our aim is to determine if thiamine can convert the cellular metabolic state of breast cancer cells from anaerobic to aerobic, thus reducing their growth. (2) Methods:

Hypoxia induced upregulation and function of the thiamine transporter, SLC19A3 in a breast cancer cell line.

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Adaptive responses within hypoxic tumor microenvironments require the altered expression of Solute Carrier (SLC) transporters to maintain nutrient uptake in support of cellular metabolism and biosynthesis. Using a real time PCR array strategy to further characterize changes in transporter expression

Down-regulation of thiamine transporter THTR2 gene expression in breast cancer and its association with resistance to apoptosis.

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The recent molecular identification of two thiamine transporters, SLC19A2 (THTR1) and SLC19A3 (THTR2), has provided the opportunity to study thiamine transporter gene expression in human malignancies. We compared RNA levels of both THTR1 and THTR2 in a panel of human breast tumors and corresponding

Role of HIF-1α in the hypoxia inducible expression of the thiamine transporter, SLC19A3.

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Ensuring continuous intracellular supply of thiamine is essential to maintain metabolism. Cellular homeostasis requires the function of the membrane bound thiamine transporters THTR1 and THTR2. In the absence of increased dietary intake of thiamine, varying intracellular levels to meet metabolic

Graft failure of autologous peripheral blood stem cell transplantation due to acute metabolic acidosis associated with total parenteral nutrition in a patient with relapsed breast cancer.

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A 32-year-old female had been diagnosed as having relapsed breast cancer and liver metastasis. She underwent high-dose chemotherapy followed by autologous peripheral blood stem cell transplantation (PBSCT) with 5.8 x 10(6)/kg CD34+ cells. She was supported by total parenteral nutrition (TPN) without

Up-regulation of vitamin B1 homeostasis genes in breast cancer.

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An increased carbon flux and exploitation of metabolic pathways for the rapid generation of biosynthetic precursors is a common phenotype observed in breast cancer. To support this metabolic phenotype, cancer cells adaptively regulate the expression of glycolytic enzymes and nutrient transporters.

Transketolase protein TKTL1 overexpression: A potential biomarker and therapeutic target in breast cancer.

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Malignant tumors degrade glucose to lactate even in the presence of oxygen via the pentose phosphate pathway (ppp). The non-oxidative part of the ppp is controlled by thiamine-dependant transketolase enzyme reactions. Overexpression of the transketolase-like-1-gene (TKTL1) in urothelial and

Metabolic effects of acute thiamine depletion are reversed by rapamycin in breast and leukemia cells.

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Thiamine-dependent enzymes (TDEs) control metabolic pathways that are frequently altered in cancer and therefore present cancer-relevant targets. We have previously shown that the recombinant enzyme thiaminase cleaves and depletes intracellular thiamine, has growth inhibitory activity against

Micronutrients Involved in One-Carbon Metabolism and Risk of Breast Cancer Subtypes.

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BACKGROUND Vitamins involved in one-carbon metabolism are hypothesized to influence breast cancer (BC) risk. However, epidemiologic studies that examined associations between B vitamin intake and BC risk have provided inconsistent results. We prospectively examined, in the Italian ORDET cohort,

Low-thiamine diet increases mammary tumor latency in FVB/N-Tg(MMTVneu) mice.

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We have previously described the down-regulation of thiamine transporter gene expression in breast cancer, and others have shown an epidemiologic relationship between obesity and breast cancer. To further explore the relationship of thiamine, fat, and breast cancer, we exposed

Biotin uptake by T47D breast cancer cells: functional and molecular evidence of sodium-dependent multivitamin transporter (SMVT).

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The objective of this study was to investigate functional and molecular evidence of carrier mediated system responsible for biotin uptake in breast cancer (T47D) cells and to delineate mechanism of intracellular regulation of this transporter. Cellular accumulation of [3H] biotin was studied in T47D

Sensitivity of breast cancer cell lines to recombinant thiaminase I.

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OBJECTIVE We have previously shown that the expression of the thiamine transporter THTR2 is decreased sevenfold in breast cancer, which may leave breast cancer cells vulnerable to acute thiamine starvation. This concept was supported by the observation that MDA231 breast cancer xenografts

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