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glutamine/sarcoma

Krækjan er vistuð á klemmuspjaldið
Bls 1 frá 106 niðurstöður

The inhibition of glutamine synthetase sensitizes human sarcoma cells to L-asparaginase.

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OBJECTIVE To evaluate the activity of the antitumor enzyme L: -asparaginase (ASNase) on tumor cells of mesenchymal origin and the contribution of glutamine synthetase (GS) to the adaptation to the metabolic stress caused by the anti-tumor enzyme. METHODS We studied the effects of ASNase in six human

Antagonizing Bcl-2 family members sensitizes neuroblastoma and Ewing's sarcoma to an inhibitor of glutamine metabolism.

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Neuroblastomas (NBL) and Ewing's sarcomas (EWS) together cause 18% of all pediatric cancer deaths. Though there is growing interest in targeting the dysregulated metabolism of cancer as a therapeutic strategy, this approach has not been fully examined in NBL and EWS. In this study, we first tested a

gamma-Glutamyl hydrolase from human sarcoma HT-1080 cells: characterization and inhibition by glutamine antagonists.

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Elevated gamma-glutamyl hydrolase (GGH) activity as a contributing factor in mechanisms of acquired and intrinsic antifolate resistance has been reported for several cultured cell lines. Despite this, little is known about this enzyme, especially the human species. Using the human HT-1080 sarcoma
Ewing sarcoma (EWS) is a soft tissue and bone tumor that occurs primarily in adolescents and young adults. In most cases of EWS, the chimeric transcription factor, EWS-FLI1 is the primary oncogenic driver. The epigenome of EWS cells reflects EWS-FLI1 binding and activation or repression of

Targeting glutamine metabolism slows soft tissue sarcoma growth.

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Tumour cells frequently utilize glutamine to meet bioenergetic and biosynthetic demands of rapid cell growth. However, glutamine dependence can be highly variable between in vitro and in vivo settings, based on surrounding microenvironments and complex adaptive responses to glutamine deprivation.

Glutamine synthetase is necessary for sarcoma adaptation to glutamine deprivation and tumor growth.

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Despite a growing body of knowledge about the genomic landscape and molecular pathogenesis of sarcomas, translation of basic discoveries into targeted therapies and significant clinical gains has remained elusive. Renewed interest in altered metabolic properties of cancer cells has led to an

[CONDITION OF THE AMMONIA-GLUTAMINE-GLUTAMIC ACID SYSTEM IN THE RAT BRAIN DURING THE DEVELOPMENT OF M-1 SARCOMA].

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[CONTENT OF AMMONIA, GLUTAMINE AND GLUTAMIC ACID IN THE RAT BRAIN IN EXTRACEREBRAL SARCOMA].

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Fused in sarcoma/translocated in liposarcoma: a multifunctional DNA/RNA binding protein.

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The fused in sarcoma/translocated in liposarcoma (FUS/TLS) gene was initially identified as a component of a fusion pro-oncogene resulting from a chromosomal translocation seen in liposarcomas. FUS/TLS belongs to a sub-family of RNA binding proteins, encoding an N-terminal

Polymerase-defective mutant of the Bryan high-titer strain of Rous sarcoma virus.

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A mutant of the Bryan high-titer strain of Rous sarcoma virus defective in reverse transcriptase is known as type alpha (BH-RSV alpha). BH-RSV alpha virion particles do not contain any polymerase-related proteins but they direct the synthesis of a normal sized Pr180 gag-pol polyprotein precursor in
OBJECTIVE Histological grading is currently one of the best predictors of tumor behavior and outcome in soft tissue sarcoma. However, occasionally there is significant disagreement even among expert pathologists. An alternative method that gives more reliable and non-subjective diagnostic
Kaposi's sarcoma-associated herpesvirus (KSHV, human herpesvirus-8) is aetiologically associated with Kaposi's sarcoma and several other lymphoproliferative disorders. The latent nuclear antigen (LNA) encoded by KSHV ORF73 has important functions in virus latent infection and shows molecular

Characterization of the protease of a fish retrovirus, walleye dermal sarcoma virus.

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Three fish retroviruses infecting walleyes constitute the recently recognized genus called epsilonretrovirus. The founding member of this group, walleye dermal sarcoma virus (WDSV), induces benign skin tumors in the infected fish and replicates near 4 degrees C. While the viral genomic sequence is
Kaposi's sarcoma-associated herpesvirus (KSHV)-induced activation of nuclear factor erythroid 2-related factor 2 (Nrf2) is essential for both the expression of viral genes (latency) and modulation of the host antioxidant machinery. Reactive oxygen species (ROS) are also regulated by the ubiquitously

Fused in Sarcoma: Properties, Self-Assembly and Correlation with Neurodegenerative Diseases.

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Fused in sarcoma (FUS) is a DNA/RNA binding protein that is involved in RNA metabolism and DNA repair. Numerous reports have demonstrated by pathological and genetic analysis that FUS is associated with a variety of neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS),
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