l norleucine/neoplasms

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Feasibility and antitumor efficacy in vivo, of simultaneously targeting glycolysis, glutaminolysis and fatty acid synthesis using lonidamine, 6-diazo-5-oxo-L-norleucine and orlistat in colon cancer.

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The aim of the present study was to investigate in vivo the feasibility and efficacy of the combination of lonidamine (LND), 6-diazo-5-oxo-L-norleucine (DON) and orlistat to simultaneously target glycolysis, glutaminolysis and de novo synthesis of fatty acids, respectively. The doses of LND and DON

The combination of orlistat, lonidamine and 6-diazo-5-oxo-L-norleucine induces a quiescent energetic phenotype and limits substrate flexibility in colon cancer cells

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Cancer upregulates glycolysis, glutaminolysis and lipogenesis, and induces a catabolic state in patients. The concurrent inhibition of both tumor anabolism and host catabolism, and the energetic consequences of such an approach, have not previously been fully investigated. In the present study,

Tumor-Targeted Delivery of 6-Diazo-5-oxo-l-norleucine (DON) Using Substituted Acetylated Lysine Prodrugs.

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6-Diazo-5-oxo-l-norleucine (DON) is a glutamine antagonist with robust anticancer efficacy; however, its therapeutic potential was hampered by its biodistribution and toxicity to normal tissues, specifically gastrointestinal (GI) tissues. To circumvent DON's toxicity, we synthesized a series of

Reviving Lonidamine and 6-Diazo-5-oxo-L-norleucine to Be Used in Combination for Metabolic Cancer Therapy.

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Abnormal metabolism is another cancer hallmark. The two most characterized altered metabolic pathways are high rates of glycolysis and glutaminolysis, which are natural targets for cancer therapy. Currently, a number of newer compounds to block glycolysis and glutaminolysis are being developed;

Potential anti-cancer agents--II. A proposed mechanism for the anti-cancer action of L-azaserine and 6-diazo-5-oxo-L-norleucine.

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Pharmacokinetic and phase I study of intravenous DON (6-diazo-5-oxo-L-norleucine) in children.

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DON (6-diazo-5-oxo-L-norleucine), a glutamine antagonist, has been subjected to limited clinical trials since 1957. Use of the drug in adults has been curtailed due to sparse reports of effectiveness as well as its dose-limiting toxicities, i.e., severe nausea, vomiting and mucositis. In earlier

gamma-Glutamyl transpeptidase in rat ascites tumor cell LY-5. Lack of functional correlation of its catalytic activity with the amino acid transport.

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gamma-Glutamyl transpeptidase activity was detected in rat ascites tumor cells (LY-5) suspended in Hanks' balanced saline solution using L-gamma-glutamyl-p-nitroanilide as a substrate. Whole-cell suspension of the tumor cells exhibited full activity of the enzyme without detectable cell disruption

The rediscovery of DON (6-diazo-5-oxo-L-norleucine).

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DON (6-diazo-5-oxo-L-norleucine) and azotomycin are glutamine antagonists that were tested in human malignancies in the 1950s. Azotomycin demonstrated significant activity in colorectal cancer. DON is probably the active form of azotomycin. Recent impressive results for both of these agents in human

A Pilot Study of Metabolomic Pathways Associated With Fatigue in Survivors of Colorectal Cancer

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Background: Over 30% of cancer survivors experience chronic fatigue. An alteration in energy metabolism is one of the hypothesized mechanisms for cancer-related fatigue (CRF). No studies have evaluated for changes in metabolic profiles in

GFAT1/HBP/O-GlcNAcylation Axis Regulates β-Catenin Activity to Promote Pancreatic Cancer Aggressiveness.

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Reprogrammed glucose and glutamine metabolism are essential for tumor initiation and development. As a branch of glucose and metabolism, the hexosamine biosynthesis pathway (HBP) generates uridine diphosphate N-acetylglucosamine (UDP-GlcNAc) and contributes to the O-GlcNAcylation process. However,

Disrupting glutamine metabolic pathways to sensitize gemcitabine-resistant pancreatic cancer.

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Pancreatic cancer is a lethal disease with poor prognosis. Gemcitabine has been the first line systemic treatment for pancreatic cancer. However, the rapid development of drug resistance has been a major hurdle in gemcitabine therapy leading to unsatisfactory patient outcomes. With the recent

The homeostasis-maintaining metabolites from bacterial stress response to bacteriophage infection suppress tumor metastasis.

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The antiviral metabolites from bacterial stress response to bacteriophage infection can maintain homeostasis of host cells, while metabolism disorder is a remarkable characteristic of tumorigenesis. In the aspect of metabolic homeostasis, therefore, the antiviral homeostasis-maintaining metabolites

In vitro PET evaluations in lung cancer cell lines.

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One purpose of the study was to explore the PET tracer 11C-L-DOPA for the discrimination between small-cell lung cancer (SCLC) and non small-cell lung cancer (NSCLC). A further aim was to explore the potential antitumoral effects of 6-diazo-5-oxy-L-norleucine (DON) and the use of a PET proliferation

Enhancement of antitumor activity of glutamine antagonists 6-diazo-5-oxo-L-norleucine and acivicin in cell culture by glutaminase-asparaginase.

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Mouse P388 and L1210 leukemia cells grown in vitro were found to be 4 to 10 times more sensitive to 6-diazo-5-oxo-L-norleucine and 3 to 5 times more sensitive to Acivicin than were 3T3 and C57BL x DBA/2 F1 embryonic fibroblasts. The combined actions of succinylated Acinetobacter

[Inactivation of microbial glutamin-(asparagin-)ase by azaserine and 6-diazo-5-oxo-L-norleucine].

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The effect of substrate analogues on glutamin-(asparagin-)ase from Pseudomonas aurantiaca-548 has been studied. The enzyme was demonstrated to be highly sensitive to the the action of 6-diazo-5-oxo-L-norleucine and azaserine. L-isomers of glutamine, aspartate, glutamate and several other substrate

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