fenretinide and Bone-Neoplasms

fenretinide has been researched along with Bone-Neoplasms* in 5 studies

Other Studies

5 other study(ies) available for fenretinide and Bone-Neoplasms

ArticleYear
Langerhans cell histiocytosis in a patient with stage 4 neuroblastoma receiving oral fenretinide.
    Pediatric blood & cancer, 2009, Volume: 53, Issue:6

    Langerhans cell histiocytosis (LCH) has previously been reported in association with other malignancies. The pathogenesis of LCH and its relationship to other malignancies is poorly understood. We present a novel case of a child who developed an LCH bone lesion while receiving a Phase I protocol therapy with oral fenretinide/Lym-X-Sorb (4-HPR/LXS) powder for neuroblastoma.

    Topics: Bone Neoplasms; Child; Fenretinide; Histiocytosis, Langerhans-Cell; Humans; Male; Neuroblastoma

2009
Manipulation of oxidative stress to induce cell death in Ewing's sarcoma family of tumours.
    European journal of cancer (Oxford, England : 1990), 2008, Volume: 44, Issue:15

    Ewing's sarcoma family of tumours (ESFT) are childhood cancers whose aggressive behaviour and propensity to relapse prompts the need for new treatment approaches. In this study, the role of cellular antioxidants in determining the sensitivity of ESFT cell lines to the cytotoxicity of the antineoplasic agent fenretinide was investigated with a view to identifying targets for the development of new treatment strategies. ESFT cell lines differentially express cellular antioxidants, although cellular glutathione (GSH) was identified as the major determinant of sensitivity to fenretinide. The importance of GSH in ESFT physiology was demonstrated by the depletion of intracellular GSH using l-buthionine (S,R) sulphoximine (BSO), which decreased cell viability. Furthermore, pre-treatment of ESFT cells with BSO sensitised them to fenretinide-induced death. Overall, these results demonstrate that ESFT cells are sensitive to changes in intracellular redox environment, and that targeting specific cellular antioxidants might be a viable strategy in treating ESFT.

    Topics: Antineoplastic Agents; Antioxidants; Bone Neoplasms; Buthionine Sulfoximine; Cell Death; Dose-Response Relationship, Drug; Enzyme Inhibitors; Fenretinide; Glutathione; Humans; Oxidation-Reduction; Oxidative Stress; Oxidoreductases; Reactive Oxygen Species; Sarcoma, Ewing; Tumor Cells, Cultured

2008
BAY 11-7082 induces cell death through NF-kappaB-independent mechanisms in the Ewing's sarcoma family of tumours.
    Cancer letters, 2008, Sep-18, Volume: 268, Issue:2

    The role of NF-kappaB in the Ewing's sarcoma family of tumours (ESFT) and their response to fenretinide has been investigated. Basal levels of phosphorylated NF-kappaB were low in all ESFT cells. BAY 11-7082 decreased cell viability, which was accompanied by caspase-3 cleavage. This was independent of the increase in reactive oxygen species, p38(MAPK) phosphorylation and expression of NF-kappaB target proteins. NF-kappaB knockdown did not induce death under normal growth conditions, but did reduce TNFalpha-dependent cell survival. Fenretinide-induced apoptosis was independent of NF-kappaB. BAY 11-7082-induced cell death through an NF-kappaB-independent mechanism and enhanced cell death when combined with fenretinide.

    Topics: Apoptosis; Bone Neoplasms; Cell Line, Tumor; Fenretinide; Humans; I-kappa B Proteins; NF-kappa B; NF-KappaB Inhibitor alpha; Nitriles; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Reactive Oxygen Species; Sarcoma, Ewing; Sulfones; Transcription Factor RelA; Tumor Necrosis Factor-alpha

2008
N-(4-Hydroxyphenyl)retinamide and nitric oxide pro-drugs exhibit apoptotic and anti-invasive effects against bone metastatic breast cancer cells.
    Carcinogenesis, 2006, Volume: 27, Issue:3

    Breast cancer most frequently metastasizes to bone causing decreased quality of life and morbidity. Since current treatments are palliative, strategies to prevent bone metastases in breast cancer patients are required. There is substantial evidence indicating that high levels of nitric oxide (NO) suppress tumor growth and metastasis in vivo. We hypothesize that agents that produce high concentrations of NO could prevent the spread of breast cancer to bone. We previously demonstrated that the synthetic retinoid N-(4-hydroxyphenyl)retinamide (4-HPR) produces high levels of NO via the induction of NO synthases. NO pro-drugs are designed to produce large amounts of NO without inducing NO synthases but upon metabolism by their intracellular targets. The objective of this study was to determine the effectiveness of 4-HPR and an NO pro-drug, diethylamineNONOate/AM (NONO-AM), in inhibiting the growth and invasiveness of bone metastatic breast cancer cells. Parental MDA-MB-231 breast cancer cells were resistant to 4-HPR-induced apoptosis at clinically relevant doses, whereas 4-HPR-induced apoptosis in a dose-dependent manner in MDA-MB-231/F10 bone metastatic breast cancer cells. Unlike 4-HPR, NONO-AM induced apoptosis in a dose-dependent manner in both parental MDA-MB-231 cells and F10 cells. The bone metastatic F10 cells were more sensitive to the anti-invasive effects of 4-HPR and NONO-AM than were MDA-MB-231 cells. Although suppression of matrix metalloprotease-9 activity may be one mechanism by which 4-HPR decreases the invasion of F10 cells, it does not appear to be the anti-invasion mechanism of NONO-AM. These in vitro results suggest that 4-HPR and NO pro-drugs may be effective chemopreventive agents against bone metastatic breast cancer.

    Topics: Anticarcinogenic Agents; Apoptosis; Bone Neoplasms; Breast Neoplasms; Dose-Response Relationship, Drug; Enzyme Induction; Female; Fenretinide; Humans; Hydrazines; Neoplasm Invasiveness; Nitric Oxide; Nitric Oxide Donors; Nitric Oxide Synthase; Nitrogen Oxides; Tumor Cells, Cultured

2006
Dietary 4-HPR suppresses the development of bone metastasis in vivo in a mouse model of prostate cancer progression.
    Clinical & experimental metastasis, 2000, Volume: 18, Issue:5

    The effects of the synthetic retinoid N-(4-hydroxyphenyl) retinamide (4-HPR) on prostate cancer metastasis in vivo were evaluated in the mouse prostate reconstitution (MPR) model. MPRs were produced by infection of either heterozygous (+/-) or nullizygous (-/-) p53-mutant fetal prostatic epithelial cells with the recombinant retrovirus Zipras/myc 9. Previous studies have documented that loss of p53 function potentiates metastasis in this model system. MPRs were grafted into homozygous (+/+) p53 male mice, fed a 4-HPR containing diet or a control diet and maintained until the status of tumor progression dictated sacrifice. Under these experimental conditions, treatment with 4-HPR did not have a significant effect on primary tumor wet weight for either p53 +/- or p53 -/- MPRs. For, p53 +/- MPRs the animals fed the 4-HPR diet had a slight improvement in survival and a significant reduction in the number of mesenteric metastases (P = 0.0477, t-test). Notably, in p53 +/- MPRs the incidence of metastasis to lumbar spine and sternum was 92% in the control animals compared to 54% in the 4-HPR treated animals (P = 0.035, chi2-test). In p53 -/- MPRs there was a trend toward a reduction in the number of soft tissue metastases to lung and liver in the 4-HPR group relative to the control diet group and a statistically significant reduction in the incidence of metastasis to bone was demonstrated in that 50% of control animals versus 30% of 4-HPR treated p53 -/- animals harbored bone metastases (P = 0 < 0.05, chi2-test). Cell lines were established from portions of the primary tumor and from selected metastatic deposits in each experimental group. Clonal analysis, by retroviral integration pattern, indicated increased clonal diversity in both the primary tumors and metastasis-derived cell lines from 4-HPR treated animals relative to the control animals. In vitro treatment with 4-HPR did not reveal discriminating differences between cell lines derived from primary tumors and bone metastases or control and treatment groups in regard to growth arrest or apoptotic responses. Overall these studies indicate limited anti-tumor and anti-metastatic activity in this highly aggressive in vivo mouse model of prostate cancer, yet 4-HPR treatment significantly suppressed the development of bone metastases in p53 +/- and p53 -/- MPRs revealing a novel and potentially clinically useful activity of this retinoid.

    Topics: Animals; Antineoplastic Agents; Bone Neoplasms; Cell Division; Diet; Disease Models, Animal; Fenretinide; Male; Mice; Prostatic Neoplasms; Survival Rate; Tumor Cells, Cultured; Tumor Suppressor Protein p53

2000
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