ceramide/ساركومة

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الصفحة 1 من عند 21 النتائج

Enhanced phosphorylation of sphingosine and ceramide sustains the exuberant proliferation of endothelial progenitors in Kaposi sarcoma.

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Endothelial colony-forming cells (ECFCs), a unique endothelial stem cell population, are highly increased in the blood of Kaposi sarcoma (KS) patients. KS-derived ECFCs (KS-ECFCs) are also endowed with increased proliferative and vasculogenic potential, thus suggesting that they may be precursors of

Quantifying Fluorescently Labeled Ceramide Levels in Human Sarcoma Cell Lines in Response to a Sphingomyelin Synthase Inhibitor.

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Sphingolipid metabolism is an important process in sustaining the growth needs of rapidly dividing cancer cells. Enzymes that synthesize sphingolipids have become attractive targets in cancer pharmacology. Ceramide is a precursor for synthesizing sphingolipids such as sphingomyelin,

Fenretinide cytotoxicity for Ewing's sarcoma and primitive neuroectodermal tumor cell lines is decreased by hypoxia and synergistically enhanced by ceramide modulators.

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Patients with disseminated Ewing's family of tumors (ESFT) often experience drug-resistant relapse. We hypothesize that targeting minimal residual disease with the cytotoxic retinoid N-(4-hydroxyphenyl) retinamide (4-HPR; fenretinide) may decrease relapse. We determined the following: (a) 4-HPR

Developing new ceramide analogs and identifying novel sphingolipid controlled genes against a virus-associated lymphoma

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Primary effusion lymphoma (PEL) is an aggressive malignancy with poor prognosis even under chemotherapy, usually infected by Kaposi's sarcoma-associated herpesvirus (KSHV), one of human oncogenic viruses. Currently, there is no specific treatment for PEL, therefore developing new therapies is of

Cytotoxic effects of sphingolipids as single or multi-modality agents on human melanoma and soft tissue sarcoma in vitro.

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We evaluated the cytotoxic effects of a cell-permeable ceramide (Cer), N-hexanoyl-D-sphingosine (C6-Cer) and of two related sphingoid bases, sphingosine (So) and dihydrosphingosine (sphinganine; Sa) on human melanoma cell lines and on soft tissue sarcoma lines recently established from fresh

Pazopanib radio-sensitization of human sarcoma tumors.

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Recent data in our laboratory indicate that engagement of host-derived microenvironmental elements impact tumor response to single high dose radiation therapy (SDRT). In these studies we showed that microvascular endothelial damage plays a critical role in tumor response as regulator of direct

Elevation of de novo ceramide synthesis in tumor masses and the role of microsomal dihydroceramide synthase.

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Ceramide is formed through sphingomyelin hydrolysis or de novo synthesis and may play a key role in cell growth, differentiation and apoptosis. To clarify which pathway tumor cells use to form ceramide and how its formation is regulated, we determined the levels of dihydroceramide and ceramide in

The human retinoblastoma gene product suppresses ceramide-induced apoptosis in human bladder tumor cells.

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The retinoblastoma gene product, Rb, has previously been implicated as an obligatory component in the antiproliferative effects mediated by the lipid second messenger, ceramide. We have evaluated both the apoptotic effects and the effects on cell cycle distribution of the exogenous cell-permeable

Viral oncomiR spreading between B and T cells is employed by Kaposi's sarcoma herpesvirus to induce non-cell-autonomous target gene regulation.

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The two human lymphotrophic γ-herpesviruses, Kaposi's sarcoma herpesvirus (KSHV) and Epstein-Barr virus (EBV), are a recognized cause of human cancer, encoding multiple miRs that are major players in carcinogenesis. Previously, we discovered that EBV-encoded miRs transfer between infected B and T

Ceramides promote apoptosis for virus-infected lymphoma cells through induction of ceramide synthases and viral lytic gene expression.

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Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiologic agent for several human cancers including primary effusion lymphoma (PEL), a rapidly progressive malignancy arising preferentially in immunocompromised patients. With conventional chemotherapy, PEL continues to portend high mortality,

THE ISOLATION AND PARTIAL CHARACTERIZATION OF THE GLYCOLIPIDS OF BP8/C3H ASCITES-SARCOMA CELLS.

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1. The total lipid was extracted from BP8/C3H ascites-sarcoma cells with acetone, light petroleum, pyridine and chloroform-methanol successively. Each extract was treated with mild alkali. The alkali-stable lipids from the pyridine and chloroform-methanol extracts, which included the glycolipids,

Enhancement of Soft Tissue Sarcoma Response to Gemcitabine through Timed Administration of a Short-Acting Anti-Angiogenic Agent

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Background/aims: Despite enormous effort, anti-angiogenic drugs have not lived up to the promise of globally-enhancing anti-cancer therapies. Clinically, anti-angiogenic drugs have been used to persistently suppress vascular endothelial

[The changes in the sphingenine/sphinganine ratio in sphingolipids of transplantable rat tumors depends on a transplantation organ].

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The content of sphingenine (sphingosine) and sphinganine was determined in the total pool of sphingomyelin and ceramide in the rat tumors transplanted subcutaneously and intrahepatically. The sphingenine/sphinganine ratio in the subcutaneously transplanted sarcoma M1 and cholangiocellular carcinoma

Ganglioside vaccines with emphasis on GM2.

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Gangliosides are neuraminic acid-containing glycosphingolipids that are anchored into the cell membrane lipid bilayer by lipophilic ceramide chains. They are overexpressed on tissues of neuroectodermal origin, and particularly in tumors such as melanomas, sarcomas, neuroblastomas, astrocytomas, and

Glycolipid synthesis in normal and virus-transformed hamster cell lines.

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Studies have been continued on the synthesis of glycolipids by the NIL 2 line of hamster cells. Several clones were isolated from this line. These clones vary in morphology, saturation density, and glycolipid composition. Contrary to expectation there was no correlation between saturation density

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