Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuroblastoma is the second most common solid tumor in children. So far few tumor models for this cancer have been reported in mice. We have created a murine tumor model for studying human neuroblastoma based on surgical orthotopic implantation in scid mice. Small fragments of subcutaneous tumors of SK-N-BE(2) human neuroblastoma cells expressing enhanced green fluorescent protein were surgically implanted near the left adrenal gland of scid mice. One hundred percent of the animals (n = 21) successfully implanted developed a large retroperitoneal tumor and became moribund between 22 and 57 days after implantation (mean survival time = 41 days). At the time of sacrifice the presence of bone marrow metastasis was detected by RT-PCR for green fluorescent protein in 95% of the cases. The growth of small tumor implants could be easily visualized and quantified by surveillance MR imaging, with a resolution of 117 x 117 x 750 microm in two orthogonal planes allowing accurate volume measurements, as well as assessment of necrosis and tissue invasion. This novel model should be a valuable tool to study the biology and therapeutic approaches to neuroblastoma.
Clin Exp Metastasis 2000
PMID:Magnetic resonance imaging for the evaluation of a novel metastatic orthotopic model of human neuroblastoma in immunodeficient mice. 1159 2

The diagnosis of acute, non-traumatic diseases of the lower respiratory tract requires exact knowledge of the specific anatomy, physiology and pathology of the pediatric chest. The absolutely and relatively smaller airways, as compared with those of adults, and the undeveloped collateral ventilation result in radiological appearances that are unique in children. Viral pneumonia is predominant only in small children up to an age of 2 years. With increasing age, there is a higher incidence of bacterial pneumonia. The differentiation of viral and bacterial etiology of a pneumonia is not possible on the basis of chest radiographs. In acute pediatric imaging, possible aspiration of foreign bodies has to be considered. Since most foreign bodies cannot be detected radiographically, indirect features such as hyperinflation or mediastinal shifts have to be evaluated. Primary lung tumors are rare in children. More common are metastases with known primary tumors. Neuroblastoma or lymphomas may mimic intrapulmonary pathologies.
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PMID:[Acute, atraumatic changes of the lower respiratory tract in the child in thoracic roentgen imaging. Recognition and appreciation of radiological changes]. 1196 32

Neuroblastoma and Wilms' tumor are the most common noncentral nervous system solid tumors in children. Imaging plays a crucial role in the evaluation of the primary tumor and regional and metastatic disease. There is a growing body of literature supporting the use of MRI as the technique of choice for the evaluation of local and regional disease in children with suspected neuroblastoma; however, in children with suspected Wilms' tumor, MRI will likely continue to play a role as a problem-solver when the results of CT are equivocal or indeterminant.
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PMID:Imaging of neuroblastoma and Wilms' tumor. 1242 47

Neuroblastoma is the most frequent solid extracranial neoplasm of childhood, with a median age of presentation of under 2 years. This tumour is highly malignant in patients older than 12 months of age with metastatic disease. Clinical studies have confirmed that amplification of the MYCN proto-oncogene is one of the best prognostic indicators of poor outcome. Approximately 30% of neuroblastoma tumours present MYCN amplification at diagnosis. Far less is known about the incidence and consequences of overrepresentation of the gene due to duplication or rearrangement of the chromosome arm in which the gene is situated. This study has analysed 110 neuroblastomas by FISH and has detected a gain of 1-3 copies per cell of MYCN in 8% of MYCN-non-amplified tumours. In these primary tumours, cells gained small numbers of additional MYCN genes by two mechanisms: formation of an isochromosome 2p, or an unbalanced translocation involving the short arm of chromosome 2 (with MYCN) and various partner chromosomes. Quantitative RT-PCR showed three- to seven-fold elevated MYCN expression in three tumours. Although the follow-up time to date is still short, clinical outcome suggests that low-level overexpression of the MYCN gene does not enhance tumour aggressiveness and rapidity of disease progression, as is often seen in neuroblastoma with MYCN amplification. It is hypothesized that the small elevation in MYCN expression could alter the regulation of apoptosis, as has been shown in experimental models.
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PMID:MYCN gene overrepresentation detected in primary neuroblastoma tumour cells without amplification. 1243 19

Neuroblastic tumors are a broad biological and clinical spectrum of neoplastic disease that has long captured the attention of clinicians and scientists alike. It is the most common solid extracranial tumor in children and accounts for 8-10% of all childhood tumors. Tumors are derived from neural crest cells and neural differentiation is common. Neuroblastoma is unique in that it presents with at least three distinct patterns of disease. Locoregional disease (Stage 1, 2, 3) does not metastasize to bone or bone marrow. Stage 4 is a systemic disease with widespread metastasis that responds to chemotherapy but many develop resistance. Stage 4s presents in infancy, is widespread and can spontaneously regress with no intervention, leaving a focus of fibrosis or calcification. Prognosis correlates with age, stage and tumor biological profile. The goal of this review is to provide an overview of the disease and highlight diagnostic, prognostic and therapeutic advances in neuroblastoma. Recommendations and resources for the evaluation and treatment of this disease are outlined.
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PMID:Genomic medicine and neuroblastoma. 1252 63

Neuroblastoma (NB) is the most common extracranial solid tumor of childhood. In advanced disease stages, prognosis is poor and treatments have limited efficacy, thus novel strategies are warranted. The synthetic retinoid Fenretinide (HPR) induces apoptosis in NB and melanoma cell lines. We reported an in vitro potentiation of HPR effects on melanoma cells when the drug is incorporated into GD2-targeted immunoliposomes (anti-GD2-SIL-HPR). We investigated the antitumor activity of anti-GD2-SIL-HPR against NB cells, both in vitro and in vivo. Anti-GD2-SIL showed specific, competitive binding to and uptake by, various NB cell lines. In in vitro cytotoxicity studies, NB cells, incubated with 30 microM HPR entrapped in anti-GD2-immunoliposomes, showed a significant reduction in cellular growth compared to free HPR, HPR entrapped in Ab-free liposomes or anti-GD2 empty liposomes. In an in vivo NB metastatic model, we demonstrated that anti-GD2-SIL-HPR completely inhibited the development of macroscopic and microscopic metastases in comparison to controls. Similar, but significantly less potent, antitumor effect was observed also in mice treated with anti-GD2 immunoliposomes without HPR (anti-GD2-SIL-blank) or anti-GD2 MAb alone (p = 0.0297 and p = 0.0294, respectively, vs. anti-GD2-SIL-HPR). Moreover, our results clearly demonstrated that although anti-GD2 MAb had a strong antitumor effect in this in vivo NB model, 100% curability was obtained only after treatment with anti-GD2-SIL-HPR (p < 0.0001). Anti-GD2 liposomal HPR should receive clinical evaluation as adjuvant therapy of neuroblastoma.
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PMID:In vitro and in vivo antitumor activity of liposomal Fenretinide targeted to human neuroblastoma. 1259 10

Neuroblastoma is a tumour derived from primitive cells of the sympathetic nervous system and is the most common solid tumour in childhood. Interestingly, most infants experience complete regression of their disease with minimal therapy, even with metastatic disease. However, older patients frequently have metastatic disease that grows relentlessly, despite even the most intensive multimodality therapy. Recent advances in understanding the biology and genetics of neuroblastomas have allowed classification into low-, intermediate- and high-risk groups. This allows the most appropriate intensity of therapy to be selected - from observation alone to aggressive, multimodality therapy. Future therapies will focus increasingly on the genes and biological pathways that contribute to malignant transformation or progression.
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PMID:Neuroblastoma: biological insights into a clinical enigma. 1261 55

Neuroblastoma is the second most frequent malignancy in childhood. We investigated whether screening for neuroblastoma at 1 year of age reduces the incidence of metastatic disease or mortality. Screening was offered in 6 of the 16 German states from 1995 to 2000 with the remaining states serving as controls. We studied 2,581,188 children in the screening area born between 1994 and 1999 and 2,117,600 in the control area. We compared mortality from neuroblastoma and the incidence of disseminated disease in the two groups. The screened group and the control group had similar rates of stage 4 neuroblastoma and mortality due to neuroblastoma. Comparison of the screened group and the control area revealed substantial over diagnosis in the screened participants. The present findings provide no support for mass screening for neuroblastoma at 1 year of age.
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PMID:Children may not benefit from neuroblastoma screening at 1 year of age. Updated results of the population based controlled trial in Germany. 1288 Sep 55

Neuroblastoma (NB) is the most common extracranial solid tumor of childhood. In advanced disease stages, prognosis is poor and treatments have limited efficacy, thus novel strategies are warranted. The synthetic retinoid fenretinide (HPR) induces apoptosis in NB and melanoma cell lines. We reported an in vitro potentiation of HPR effects on melanoma cells when the drug is incorporated into GD2-targeted immunoliposomes (anti-GD2-SIL-HPR). Here, we investigated the antitumor activity of anti-GD2-SIL-HPR against NB cells, both in vitro and in vivo. Anti-GD2-immunoliposomes (anti-GD2-SIL) showed specific, competitive binding to, and uptake by, various NB cell lines. Moreover, anti-GD2-SIL-HPR presented increased selectivity and efficacy in inhibiting NB cell proliferation through the induction of apoptosis, compared to free drug and SL-HPR. In an in vivo NB metastatic model, we demonstrated that anti-GD2-SIL-HPR completely inhibited the development of macroscopic and microscopic metastases in comparison to controls. However, similar, but significantly less potent antitumor effect was observed also in mice treated with anti-GD2 immunoliposomes without HPR (anti-GD2-SIL-blank) or anti-GD2 mAb alone (P=0.0297 and P=0.0294, respectively, vs. anti-GD2-SIL-HPR). Moreover, our results clearly demonstrated that, although anti-GD2 mAb had a strong antitumor effect in this in vivo NB model, 100% curability was obtained only following treatment with anti-GD2-SIL-HPR (P<0.0001). Anti-GD2 liposomal HPR should receive clinical evaluation as adjuvant therapy of neuroblastoma.
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PMID:Immunoliposomal fenretinide: a novel antitumoral drug for human neuroblastoma. 1288 Sep 75

Thalidomide has previously been shown to have anti-angiogenic properties. More recently, clinical efficacy of this agent has been demonstrated in multiple myeloma and prostate cancer. Neuroblastoma is the most frequent solid tumor of the abdomen of childhood, yet children with this disease frequently have metastases at presentation. Such patients have a very poor prognosis with current therapies. Thus, new approaches are needed. We have previously shown that VEGF antagonists can inhibit neoangiogenesis and tumor growth in experimental neuroblastoma. In this study, we investigated the anti-angiogenic and anti-tumor properties of thalidomide in a xenograft model of human neuroblastoma. Tumors were induced in athymic mice using the human neuroblastoma cell line NGP. Intraperitoneal thalidomide (100 mg/kg/dose) or vehicle was administered beginning one week after implantation, and animals euthanized at six weeks. Thalidomide treatment did not significantly alter tumor growth as compared with controls. However, thalidomide suppressed angiogenesis, as demonstrated both by fluorescein angiography and immunohistochemical staining, and induced apoptosis of endothelial cells in neuroblastoma xenografts. Quantification of microvessel density demonstrated a significant reduction of vasculature in treated tumors (p<0.004). Thalidomide induced co-option of host vasculature, an effect noted previously after VEGF blockade. This study demonstrates that thalidomide has anti-angiogenic properties in experimental neuroblastoma.
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PMID:Thalidomide is anti-angiogenic in a xenograft model of neuroblastoma. 1461 37


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