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A glucose-targeted mixed micellar formulation outperforms Genexol in breast cancer cells.

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Breast cancer represents the top cancer among women, accounting 521.000 deaths per year. Development of targeted nanomedicines to breast cancer tissues represents a milestone to reduce chemotherapy side effects. Taking advantage of the over-expression of glucose (Glu) membrane transporters in breast

Safe chemotherapy and hormone therapy for treating early breast cancer in a glucose 6-phosphate dehydrogenase-deficient patient: case report.

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Breast cancer is the leading cause of neoplasia-related deaths among women, but no data are available in the literature on the safe use of oncological treatments in glucose 6-phosphate dehydrogenase (G6PD)-deficient patients. This case report describes, for the first time, the treatment of a

Case report: a glucose responsive insulinoma--implication for the diagnosis of insulin secreting tumors.

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Normal insulin secretagogues, including glucose, usually have little influence on insulin secretion from insulinomas. Therefore, insulinomas typically cause fasting hypoglycemia with relative hyperinsulinemia. This report describes a patient with hyperinsulinemia due to an islet cell adenoma with

Safe neoadjuvant trastuzumab-based treatment in HER2 + inflammatory early breast cancer in a glucose 6-phosphate dehydrogenase-deficient postmenopausal woman: A case report and review of the literature.

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Glucose 6-phosphate dehydrogenase (G6PD) is a basic antioxidant pathway for erythrocytes, being its deficiency the most common gene mutation worldwide. As breast cancer is one of the most frequent tumors, many of these patients may present with G6PD deficiency prior treatment without

A glucose carbonate apatite complex exhibits in vitro and in vivo anti-tumour effects.

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Tumour targeting nanotechnology has recently made therapeutic progress and several therapeutic nanoparticles have been approved for clinical application. However, an ideal nanotechnology based therapeutic for solid tumours, particularly for systemic administration, still remains a challenge in

Metformin inhibits gastric cancer cells metastatic traits through suppression of epithelial-mesenchymal transition in a glucose-independent manner.

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Epithelial-mesenchymal transition (EMT), which is mainly recognized by upregulation of mesenchymal markers and movement of cells, is a critical stage occurred during embryo development and spreading cancerous cells. Metformin is an antidiabetic drug used in treatment of type 2 diabetes. EMT

Anticancer strategy targeting the energy metabolism of tumor cells surviving a low-nutrient acidic microenvironment (R1)

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Objective: Tumor cells experience hypoxia, acidosis, and hypoglycemia. Metabolic adaptation to a glucose shortage is essential to maintain tumor cell survival because of their high glucose requirement. This study aimed to study the

Tyrosine kinase inhibitor imatinib modulates the viability and apoptosis of castrate-resistant prostate cancer cells dependently on the glycolytic environment.

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The tyrosine kinase inhibitor imatinib has been used in prostate cancer treatment with outcomes that did not follow the in vitro findings. The glycolytic environment has been shown to influence the efficacy of anti-cancer drugs. This study aimed to evaluate the effect of imatinib on

Metabolic signature genes associated with susceptibility to pyruvate kinase, muscle type 2 gene ablation in cancer cells.

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Pyruvate kinase, muscle type 2 (PKM2), is a key factor in the aerobic glycolysis of cancer cells. In our experiments, liver cancer cell lines exhibited a range of sensitivity to PKM2 knockdown-mediated growth inhibition. We speculated that this differential sensitivity is attributable to the

INI1 and GLUT-1 expression in epithelioid sarcoma and its cutaneous neoplastic and nonneoplastic mimics.

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The morphological features of epithelioid sarcoma may closely mimic those of epithelial neoplasms, such as squamous cell carcinoma, mesenchymal tumors, such as benign fibrous histiocytoma, and nonneoplastic lesions, such as granuloma annulare. Immunohistochemistry, particularly for epithelial

Biochemical studies on rats with insulin-secreting islet cell tumors induced by streptozotocin: with special reference to physiological response to oral glucose load in the course of and after tumor induction.

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Pancreatic islet cell tumors were induced in 32 of 49 male Wistar rats (73%) surviving 9 months or longer following treatment with streptozotocin alone, with streptozotocin and nicotinamide, or with streptozotocin and picolinamide. Serial oral glucose tolerance tests in rats treated with

Screening of plant constituents for effect on glucose transport activity in Ehrlich ascites tumour cells.

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The effect of plant extracts on D-glucose uptake by Ehrlich ascites tumour cells was examined. Among the 23 extracts of medicinal plants, five samples inhibited, and six samples activated, the uptake significantly. From one of the active plants, Lagerstroemia speciosa, two triterpenoids, colosolic

Parallel antitumor, granuloma-forming and tumor-necrosis-factor-priming activities of mycoloyl glycolipids from Nocardia rubra that differ in carbohydrate moiety: structure-activity relationships.

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Multiple intravenous injections (30 micrograms, ten times) in ICR mice of trehalose dimycolate and glucose monomycolate from Nocardia rubra, containing C36-48 mycolic acids, showed a prominent antitumor effect on a subcutaneously implanted sarcoma-180, an allogeneic sarcoma of mice with a

Macrocyclic triamine derived glucose analogues for 99m Tc(CO)3 labeling: synthesis and biological evaluation as potential tumor-imaging agents.

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[99m Tc(CO)3 (H2 O)3 ]+ has attracted great attention among 99m Tc-labeling techniques, due to its ease of preparation, readily substituted water molecules of the precursor fac-[99m Tc(CO)3 (H2 O)3 ]+ by a variety of functional groups, small size and inertness. Bifunctional chelator based on a

[The effect of membrane-active compounds on the radiation-modifying effect of glucose in x-irradiated ascitic tumor cells].

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A study was made of the influence of membrane-active agents with different mechanisms of action (quercetin, amiloride, valinomycin, and digitonin), that modify the transmembrane transfer of inorganic ions, on a modifying effect of a glucose loading in X-irradiated Ehrlich ascites tumor cells. The

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