pentose/sarcoma

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Targeting oxidative pentose phosphate pathway prevents recurrence in mutant Kras colorectal carcinomas.

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Recurrent tumors originate from cancer stem cells (CSCs) that survive conventional treatments. CSCs consist of heterogeneous subpopulations that display distinct sensitivity to anticancer drugs. Such a heterogeneity presents a significant challenge in preventing tumor recurrence. In the current

IDH Mutation Analysis in Ewing Sarcoma Family Tumors.

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BACKGROUND Isocitrate dehydrogenase (IDH) catalyzes the oxidative decarboxylation of isocitrate to yield α-ketoglutarate (α-KG) with production of reduced nicotinamide adenine dinucleotide (NADH). Dysfunctional IDH leads to reduced production of α-KG and NADH and increased production of

2',5'-Bis-O-(tert-butyldimethylsilyl)-3'-spiro-5''-(4''-amino-1'',2''- oxathiole-2'',2'-dioxide)pyrimidine (TSAO) nucleoside analogues: highlyselective inhibitors of human immunodeficiency virus type 1 that are targeted at the viral reverse transcriptase.

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A series of pyrimidine nucleoside analogues containing [2',5'-bis-O-(tert-butyldimethylsilyl)-3'-spiro-5''-(4''-amino- 1'',2''-oxathiole-2'',2''-dioxide)]-beta-D-ribofuranose as the pentose were found to inhibit human immunodeficiency virus type 1 [HIV-1(IIIB)] replication at a concentration of

Effect of methionine on glycolysis in tumor cells: in vivo and in vitro NMR studies.

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Inhibition of glycolysis by methionine is a phenomenon previously shown in transformed cells growing in culture. In a recent paper, [Collet V. et al., Q. Magn. Res. Biol. Med. 11, 127-134 (1995)] we investigated this effect in vivo by 13C nuclear magnetic resonance spectroscopy, but the results did

Chemoprevention of spontaneous tumorigenesis in nullizygous p53-deficient mice by dehydroepiandrosterone and its analog 16alpha-fluoro-5-androsten-17-one.

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Transgenic mice with both alleles of the p53 tumor suppressor gene product 'knocked out' by gene targeting are susceptible to early development of tumors, chiefly lymphomas and sarcomas. Compared with the control group, administration of dehydroepiandrosterone (DHEA) at 0.3% of the diet to male

SMYD1 and G6PD modulation are critical events for miR-206-mediated differentiation of rhabdomyosarcoma.

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Rhadomyosarcoma (RMS) is the most common soft tissue sarcoma of childhood. RMS cells resemble fetal myoblasts but are unable to complete myogenic differentiation. In previous work we showed that miR-206, which is low in RMS, when induced in RMS cells promotes the resumption of differentiation by

Histoenzymology of the lung. V. Histoenzymatic analysis of sixty lung tumors.

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A series of sixty lung tumors operated during 1977 were histoenzymatically investigated (12 macrocellular carcionomas, 4 microcellular, 18 epidermoid, 18 cylindrocubic, 2 bronchiolo-alveolar cell carcinomas, 4 lung fibroblastic sarcomas, and 2 benign lung tumors: a haemangioma and a carcinoid

Global metabolic profiling of infection by an oncogenic virus: KSHV induces and requires lipogenesis for survival of latent infection.

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Like cancer cells, virally infected cells have dramatically altered metabolic requirements. We analyzed global metabolic changes induced by latent infection with an oncogenic virus, Kaposi's Sarcoma-associated herpesvirus (KSHV). KSHV is the etiologic agent of Kaposi's Sarcoma (KS), the most common

Metabolic Enzymes in Sarcomagenesis: Progress Toward Biology and Therapy.

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Cellular metabolism reprogramming is an emerging hallmark of cancer, which provides tumor cells with not only necessary energy but also crucial materials to support growth. Exploiting the unique features of cancer metabolism is promising in cancer therapies. The growing interest in this field has

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