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adenosine 5 monophosphate/cáncer

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In vitro evaluation of adenosine 5'-monophosphate as an imaging agent of tumor metabolism.

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Adenosine appears to play an important role in tumor growth and metastasis. Synthesized (11)C-adenosine 5'-monophosphate (AMP) has recently been reported as a potential tumor-imaging radiotracer. METHODS A variety of human tumor cell lines (SKOV-3, SCC-15, U251, U87, Raji, and Daudi) were incubated
Flavokawain B (FKB), a natural kava chalcone, shows potent antitumor activity in various types of cancer, although the mechanism of action remains unclear. In this study, we report that FKB has profound effects on the metabolic state of human thyroid cancer (TCa) cells, leading to high autophagy

A central role for neuronal adenosine 5'-monophosphate-activated protein kinase in cancer-induced anorexia.

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The pathogenesis of cancer anorexia is multifactorial and associated with disturbances of the central physiological mechanisms controlling food intake. However, the neurochemical mechanisms responsible for cancer-induced anorexia are unclear. Here we show that chronic infusion of

Metformin promotes survivin degradation through AMPK/PKA/GSK-3β-axis in non-small cell lung cancer.

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Metformin, a first-line antidiabetic drug, has been reported with anticancer activities in many types of cancer. However, its molecular mechanisms remain largely unknown. As a member of inhibitor of apoptosis proteins, survivin plays an important role in the regulation of cell death. In the present
Sitagliptin is an emerging oral hypoglycemic agent that inhibits the development of a wide variety of tumors. Current researches indicate that the abnormal activation of Yes-associated protein (YAP) promotes the proliferation and poor prognosis of multiple tumors. However, the ability of sitagliptin

Synthesis and biodistribution of [11C]adenosine 5'-monophosphate ([11C]AMP).

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OBJECTIVE Imaging purine receptors and adenylate biodistribution in vivo may be of clinical importance not only for the investigation of normal adenylate metabolism but also in pathological conditions where adenylate uptake and/or release from certain tissues and organs may be altered, such as some

Combined Use of Metformin and Everolimus Is Synergistic in the Treatment of Breast Cancer Cells.

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Everolimus inhibits mammalian target of rapamycin (mTOR) and leads to decreased protein synthesis and decreased cancer cell proliferation in many experimental systems. Adenosine 5'-monophosphate-activated protein kinase (AMPK) activators such as metformin have similar actions in keeping with the
UNASSIGNED It is hypothesized that metabolism plays a strong role in cancer cell regulation. We have recently demonstrated improved progression-free survival in patients with glioblastoma who received metformin as an antidiabetic substance during chemoradiation. Although metformin is

Cytotoxic effect of 8-amino adenosine 3',5'-cyclic monophosphate on FM3A mouse mammary tumor cells.

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Derivatives of adenosine 3',5'-cyclic monophosphate (cAMP) with modifications at the 8-position were synthesized and examined for their cytotoxic effects on FM3A mouse mammary tumor cells and ZR-75 human mammary tumor cells. On in vitro tests of these derivatives, 8-amino (8-NH2) cAMP was the most

Generation of extracellular ATP in blood and its mediated inhibition of host weight loss in tumor-bearing mice.

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Intraperitoneal injections of adenosine 5'-monophosphate (AMP) or adenosine 5'-triphosphate (ATP), but not of adenosine, inorganic phosphate or pyrophosphate, were shown to inhibit tumor growth and host weight loss in tumor-bearing murine hosts. The inhibition of tumor growth and host weight loss

Experimental cancer therapy in mice by adenine nucleotides.

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Adenosine 5'-monophosphate (AMP), adenosine 5'-diphosphate (ADP) and adenosine 5'-triphosphate (ATP), injected intraperitoneally into tumor-bearing (s.c. implanted footpad tumors) mice, exhibited significant anticancer activity. Daily treatments (for 10 days) inhibited the growth of the

Metformin induces apoptotic cytotoxicity depending on AMPK/PKA/GSK-3β-mediated c-FLIPL degradation in non-small cell lung cancer.

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Background
Metformin, a first-line antidiabetic drug, has recently been reported with anticancer activities in various cancers; however, the underlying mechanisms remain elusive. The aim of the present study was to investigate the role of cellular FADD-like IL-1β-converting

Metformin and rapamycin have distinct effects on the AKT pathway and proliferation in breast cancer cells.

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Rapamycin and its analogues inhibit mTOR, which leads to decreased protein synthesis and decreased cancer cell proliferation in many experimental systems. Adenosine 5'- monophosphate-activated protein kinase (AMPK) activators such as metformin have similar actions, in keeping with the TSC2/1 pathway

Diabetes and cancer: the mechanistic implications of epidemiological analyses from the Hong Kong Diabetes Registry.

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Diabetes is a disorder of energy metabolism associated with increased cancer risk, but the underlying mechanism is poorly understood. In a prospective cohort of patients enrolled in the Hong Kong Diabetes Registry, we explored risk factors for cancer including drug usage in type 2 diabetes. In a

Aspirin disrupts the mTOR-Raptor complex and potentiates the anti-cancer activities of sorafenib via mTORC1 inhibition.

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Aspirin is associated with a reduced risk of cancer and delayed progression of malignant disease. Adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)-mTOR signaling is believed to partially contribute to these anticancer effects, although the mechanism is unclear. In this study, we
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